Wednesday, December 17, 2008

Magnesium Supplements May Help Lower High Blood Pressure

Magnesium Supplements May Help Lower High Blood Pressure:

"Magnesium supplements have a small but significant effect on lowering blood pressure, according to a study in this month's Hypertension: Journal of the American Heart Association."

Romantic comedies mar love lives-Health/Sci-The Times of India

Romantic comedies mar love lives-Health/Sci-The Times of India

LONDON: Romantic comedies
may have fired love lives of many for long. Yet, a new study has claimed that watching the popular flicks could spoil
relationships as they create unrealistic expectations.

Researchers in Edinburgh have carried out the study and found that people who watch romantic comedies are more likely to believe in predestined love than those who prefer to see other genres of movie.

According to them, unlikely happy endings, improbable plots and faux philosophy are to blame -- in fact, seeing even a single romantic comedy is enough to sway people's attitudes to romantic love.

"Marriage counsellors often see couples who believe that sex should always be perfect, and if someone is meant to be with you then they will know what you want without you needing to communicate it.

"We now have some emerging evidence that suggests popular media play a role in perpetuating these ideas in people's minds.

"The problem is that while most of us know that the idea of a perfect relationship is unrealistic, some of us are still more influenced by media portrayals than we realise," lead researcher Dr Bjarne Holmes said.

Saturday, December 13, 2008

Low Carbohydrate Diet Did Not Increase Bone Loss, Study Finds

Low Carbohydrate Diet Did Not Increase Bone Loss, Study Finds:

"A strict low-carbohydrate diet had no effect on bone loss for adults following an Adkins-type diet for weight loss, a three-month study by rheumatologists at the University of South Florida found. The clinical study was published this week in the online issue of the journal Osteoporosis International.

Low carbohydrate diets have become popular as a weight loss technique; however, critics contend such diets may have harmful side effects. One concern has been that low carbohydrate diets, which replace calories from carbohydrates with more consumption of high-protein foods like meat and eggs, alter the body's acid balance. This imbalance could lead to increased bone turnover (more rapid depletion than formation of bone) -- increasing the risk for osteoporosis.

"That's not what our study found," said lead author John D. Carter, assistant professor in the Division of Rheumatology, USF College of Medicine. "Patients on the low carbohydrate diet did lose weight, but the diet did not appear to compromise bone integrity or lead to bone loss." "

Friday, December 12, 2008

The Dana Foundation - The Prefrontal Cortex and Frontal Lobe Disorders : An Interview with Jordan Grafman, Ph.D.

The Dana Foundation - The Prefrontal Cortex and Frontal Lobe Disorders : An Interview with Jordan Grafman, Ph.D.

My research indicates that the human prefrontal cortex is especially designed to store in long-term memory the features that are unique to large structured sets of sequential events such as themes, morals, and plans. This enables us to put off immediate gratification, and allows us to out-think faster and stronger competitors. These observations form the foundation for the notion that the human prefrontal cortex is a crowning achievement of the human brain and that, like the rest of the brain, is a work in progress.

Q: You consider the prefrontal cortex to be the seat of “social cognition” and possibly “moral cognition” as well. What do these terms mean and what leads you to these conclusions?

A: Social cognition refers to the long-term memories we access when we interact socially with others, and that guide our social behaviors in routine and novel situations. These long-term memories contain information about how we accomplished social goals—from obtaining permission to do something, to taking leadership, to collaborating on a project —and incorporate information about perception and action. Moral cognition is a specific example of social cognition that pertains to ethical, legal, and “folk” justice, beliefs, and rules.

My colleagues and I (and others) have argued that the pre­frontal cortex is uniquely suited to manage social and moral cognition because it aids us in controlling our immediate reactions to a stimulus (like a face or gesture) and is critical for forecasting the consequences of a current behavior on a long-term goal. While other species have social cognitive abili­ties and some rudimentary features of moral cognition, social cognitive abilities reach their peak in humans (as does the anatomy and physiology of the prefrontal cortex). Like the prefrontal cortex, social cognition only matures in the second decade of life and shows some decline in old age.

In addition, brain damage in the prefrontal cortex due to head injuries, strokes, and dementing illnesses (among other brain disorders) often result in altered social cognitive abilities. Patients with lesions in the prefrontal cortex may behave inap­propriately in public, violating social rules such as personal space maintenance, social contracts, or inappropriate verbal­izations. The earliest example of this comes from the famous brain-injured patient Phineas Gage, but many modern-day Gages have been reported in great detail, highlighting the unfortunate case histories of these patients.

Thursday, December 11, 2008

Sugar Can Be Addictive: Animal Studies Show Sugar Dependence

Sugar Can Be Addictive: Animal Studies Show Sugar Dependence:

"A Princeton University scientist will present new evidence today 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.

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. "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."

Hoebel will report 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. The findings eventually could have implications for the treatment of humans with eating disorders, he said.

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. They consumed more sugar than they ever had before, suggesting craving and relapse behavior. Their motivation for sugar had grown. "In this case, abstinence makes the heart grow fonder," Hoebel said.

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. 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.

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.

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.

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 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."

Fructose Sets Table For Weight Gain Without Warning

Fructose Sets Table For Weight Gain Without Warning:

"Eating too much fructose can induce leptin resistance, a condition that can easily lead to becoming overweight when combined with a high-fat, high-calorie diet, according to a new study with rats.

Although previous studies have shown that being leptin resistant can lead to rapid weight gain on a high-fat, high-calorie diet, this is the first study to show that leptin resistance can develop as a result of high fructose consumption. The study also showed for the first time that leptin resistance can develop silently, that is, with little indication that it is happening.

Leptin is a hormone that plays a role in helping the body to balance food intake with energy expenditure. When leptin isn’t working -- that is, when the body no longer responds to the leptin it produces -- it’s called leptin resistance. Leptin resistance is associated with weight gain and obesity in the face of a high-fat, high-calorie diet.

Obesity has been a growing problem in the U.S. and in other parts of the world and fructose has been suspected of playing a role. Fructose is the sugar found in fruit, but it’s not the normal consumption of fruit that is the problem. Table sugar and high-fructose corn syrup are about 50% fructose and these ingredients have become increasingly common in many foods and beverages. With sugar and high-fructose corn syrup being added to many foods, people now eat much more fructose than ever before.

There was only one difference at the end of the six months: The rats on the high-fructose diet had higher levels of triglycerides in their blood.

The researchers discovered that the rats on the high-fructose diet were leptin resistant, that is, they did not lower their food intake when given leptin. The no-fructose animals responded normally to leptin by eating less.

This first six months of the study showed that leptin resistance can develop silently. “Usually, leptin resistance is associated with obesity, but in this case, leptin resistance developed without obesity,” Shapiro said. “This was very surprising.”

Role of diet

Having seen that leptin resistance could develop silently, the researchers next wanted to find out what would happen if they switched the rats to a high-fat, high-calorie diet -- the kind many Americans eat. They found that the animals exposed to the high-fructose diet, the leptin resistant rats, ate more and gained much more weight and fat than the leptin responsive animals on the fructose-free diet. All told, this study showed that leptin resistance can:

* develop by eating a lot of fructose
* develop silently, that is, with very little indication it is happening
* result in weight gain when paired with a high fat, calorie dense diet
"

Study Suggests A Possible Link Between High-Starch Diet And Pancreatic Cancer

Study Suggests A Possible Link Between High-Starch Diet And Pancreatic Cancer:

"A diet high in starchy foods such as potatoes, rice and white bread may increase the risk of pancreatic cancer in women who are overweight and sedentary, according to a new study by Dana-Farber Cancer Institute, Brigham and Women's Hospital and Harvard School of Public Health researchers.

Published in the Sept. 4 issue of the Journal of the National Cancer Institute, the study suggests that excess insulin – a substance used by the body to process the sugar in foods – can promote the development of pancreatic cancer.

Nearly 30,000 men and women in the United States are diagnosed with pancreatic cancer each year, and an equal number die from it. Pancreatic cancer typically is highly aggressive and is one of the least-curable malignancies. Only four percent of the people with pancreatic cancer are alive five years after diagnosis.

"Our findings add to the growing body of evidence that suggests that insulin may have a role in the development of pancreatic cancer," explains senior author Charles Fuchs, MD, of Dana-Farber. "Further research is needed, however, to track the connection in more detail."

Earlier laboratory studies have demonstrated that insulin encourages the growth of pancreatic cancer cells. Other studies have shown that people who are obese, physically inactive or have adult-onset diabetes mellitus tend to be "insulin resistant," causing them to produce larger-than-normal amounts of insulin to compensate and putting themselves at greater risk for pancreatic cancer. The new study explored whether women whose diets are heavy in foods that increase insulin production are likewise at elevated risk for pancreatic cancer. "

Too Much Fructose Could Leave Dieters Sugar Shocked

Too Much Fructose Could Leave Dieters Sugar Shocked

Dieters should focus on limiting the amount of fructose they eat instead of cutting out starchy foods such as bread, rice and potatoes, report the researchers, who propose using new dietary guidelines based on fructose to gauge how healthy foods are.

"There's a fair amount of evidence that starch-based foods don't cause weight gain like sugar-based foods and don't cause the metabolic syndrome like sugar-based foods," said Dr. Richard Johnson, the senior author of the report, which reviewed several recent studies on fructose and obesity. "Potatoes, pasta, rice may be relatively safe compared to table sugar. A fructose index may be a better way to assess the risk of carbohydrates related to obesity."

Many diets -- including the low-carb variety -- are based on the glycemic index, which measures how foods affect blood glucose levels. Because starches convert to glucose in the body, these diets tend to limit foods such as rice and potatoes.

While table sugar is composed of both glucose and fructose, fructose seems to be the more dangerous part of the equation, UF researchers say. Eating too much fructose causes uric acid levels to spike, which can block the ability of insulin to regulate how body cells use and store sugar and other nutrients for energy, leading to obesity, metabolic syndrome and type 2 diabetes, said Johnson, the division chief of nephrology and the J. Robert Cade professor of nephrology in the UF College of Medicine. UF researchers first detailed the role of uric acid on insulin resistance and obesity in a 2005 study in rats.

"Certainly we don't think fructose is the only cause of the obesity epidemic," Johnson said. "Too many calories, too much junk food and too much high-fat food are also part of the problem. But we think that fructose may have the unique ability to induce insulin resistance and features of the metabolic syndrome that other foods don't do so easily."

Cutting Caffeine May Help Control Diabetes

Cutting Caffeine May Help Control Diabetes: "Daily consumption of caffeine in coffee, tea or soft drinks increases blood sugar levels for people with type 2 diabetes and may undermine efforts to control their disease, say scientists at Duke University Medical Center.

The researchers found that when the participants consumed caffeine, their average daily sugar levels went up 8 per cent. Caffeine also exaggerated the rise in glucose after meals: increasing by 9 percent after breakfast, 15 percent after lunch and 26 per cent after dinner.

"We're not sure what it is about caffeine that drives glucose levels up, but we have a couple of theories," says Lane, who is the lead author of the study. "It could be that caffeine interferes with the process that moves glucose from the blood and into muscle and other cells in the body where it is used for fuel. It may also be that caffeine triggers the release of adrenaline -- the 'fight or flight" hormone that we know can also boost sugar levels."

Either way, he says, the higher sugar levels that result from caffeine are bad news for diabetic patients."

Type 1 Diabetes And Celiac Disease Linked

Type 1 Diabetes And Celiac Disease Linked:

"Type 1 (juvenile) diabetes and celiac disease appear to share a common genetic origin, scientists at the University of Cambridge and Barts and The London School of Medicine and Dentistry, have confirmed."

Monday, December 08, 2008

Can Amphetamines Help Cure Cocaine and Meth Addiction? - TIME

Can Amphetamines Help Cure Cocaine and Meth Addiction? - TIME

Proponents of stimulant maintenance treatment also note this significant detail: Many stimulant abusers suffer from attention-deficit/hyperactivity disorder (ADHD). While ADHD affects about 1% of the general population, according to Rush, it shows up in about 30% of cocaine and amphetamine addicts. Psychiatrists often hesitate to give hyperactivity drugs to patients with a history of addiction, but some studies suggest that maintenance may be exactly what this group needs — and that their drug abuse is an attempt to self-medicate. The studies that have included ADHD patients (many studies exclude them to avoid confounding) showed positive results. In one pilot study, conducted at Columbia University, maintenance treatment reduced cocaine use and craving in 12 cocaine addicts with ADHD.

Sunday, December 07, 2008

Obesity And Metabolism: Weight Gain And The Growing Risk Of Cancer

Obesity And Metabolism: Weight Gain And The Growing Risk Of Cancer:

"COLON CANCER

'Colorectal cancer and type II diabetes share a number of common factors, including obesity, so it is interesting to see the direct line between these two conditions,' said Andrew Flood, Ph.D., assistant professor in the Division of Epidemiology and Community Health at the University of Minnesota School of Public Health and the University of Minnesota Cancer Center 'In general, the idea is that if elevated insulin levels create a biochemical environment conducive to cancer growth, it provides one mechanism by which diet and lifestyle can really influence cancer risk.'

According to Flood, it is not exactly clear what aspect of diabetes is the underlying cause for this increased risk, but one hypothesis centers on the elevated concentration of insulin typically seen in people with type II diabetes. "In the early stages of the disease process, people become insulin resistant, meaning they must produce more and more insulin to regulate their blood sugar," Flood said.

"Even after frank diabetes begins, insulin levels remain chronically elevated for extended periods before the pancreas can no longer supply the level of insulin the body demands," Flood said. "If the elevated insulin is the problem, then pre-diabetics, who are also hyper-insulinemic, should also be at increased risk (for developing colorectal cancer)."

BREAST CANCER

"When looking at risk of diabetes and hypertension, breast cancer survivors really should talk to their oncologist about how to lower their insulin levels," said Melinda L. Irwin, Ph.D., M.P.H., assistant professor at Yale University's School of Public Health. "The simple message is that breast cancer patients should take proven steps to lower their blood insulin levels, including exercise and eating a diet rich in fruits and vegetables and low in fat."

Uh, don't you mean a diet low in carbohydrate. Any dummy can measure their blood sugar and see that carbs raise your blood sugar/insulin, and meat/fat doesn't


When looking at just women with invasive breast cancer, the risk of death among women with high C-peptide levels was three times higher than among women with low C-peptide levels. "Our findings clearly show that C-peptide and most likely insulin, in and of itself, is a marker for breast cancer prognosis," Irwin said.

PROSTATE CANCER

Association of C-peptide concentration with prostate cancer incidence in a prospective cohort

While studies have consistently shown that men with diabetes are at a decreased risk for prostate cancer, the reasons have been unclear. By evaluating prostate cancer data from a large, long-term cohort study, researchers at Johns Hopkins University have shown that those with high concentrations of C-peptide -- a marker of high insulin secretion that is a hallmark of diabetes -- had a measurable decrease in prostate cancer risk.

"Metabolic perturbations influence cancer risk, that much is becoming clear to us, and we are learning more about the fundamental issues in biology that guide prostate cancer development," said Gabriel Lai, a doctoral student in the Department of Epidemiology at Johns Hopkins Bloomberg School of Public Health. "One interesting possibility is that, over time, diabetics generally have less testosterone in their bloodstream than non-diabetics, which might lower risk of prostate cancer.""

Limiting Fructose May Boost Weight Loss, Researcher Reports

Limiting Fructose May Boost Weight Loss, Researcher Reports:

"One of the reasons people on low-carbohydrate diets may lose weight is that they reduce their intake of fructose, a type of sugar that can be made into body fat quickly, according to a researcher at UT Southwestern Medical Center.

[...]

"Our study shows for the first time the surprising speed with which humans make body fat from fructose," Dr. Parks said. Fructose, glucose and sucrose, which is a mixture of fructose and glucose, are all forms of sugar but are metabolized differently.

"All three can be made into triglycerides, a form of body fat; however, once you start the process of fat synthesis from fructose, it's hard to slow it down," she said.

In humans, triglycerides are predominantly formed in the liver, which acts like a traffic cop to coordinate the use of dietary sugars. It is the liver's job, when it encounters glucose, to decide whether the body needs to store the glucose as glycogen, burn it for energy or turn the glucose into triglycerides. When there's a lot of glucose to process, it is put aside to process later.

Fructose, on the other hand, enters this metabolic pathway downstream, bypassing the traffic cop and flooding the metabolic pathway.

"It's basically sneaking into the rock concert through the fence," Dr. Parks said. "It's a less-controlled movement of fructose through these pathways that causes it to contribute to greater triglyceride synthesis. The bottom line of this study is that fructose very quickly gets made into fat in the body."

Though fructose, a monosaccharide, or simple sugar, is naturally found in high levels in fruit, it is also added to many processed foods. Fructose is perhaps best known for its presence in the sweetener called high-fructose corn syrup or HFCS, which is typically 55 percent fructose and 45 percent glucose, similar to the mix that can be found in fruits. It has become the preferred sweetener for many food manufacturers because it is generally cheaper, sweeter and easier to blend into beverages than table sugar."

Keep in mind that regular sugar is 50% fructose also

Saturday, December 06, 2008

Lack Of Vitamin D Could Spell Heart Trouble

Lack Of Vitamin D Could Spell Heart Trouble:

"Vitamin D deficiency—which is traditionally associated with bone and muscle weakness—may also increase the risk of cardiovascular disease (CVD). A growing body of evidence links low 25-hydroxyvitamin D levels to common CVD risk factors such as hypertension, obesity and diabetes, as well as major cardiovascular events including stroke and congestive heart failure.

"Vitamin D deficiency is an unrecognized, emerging cardiovascular risk factor, which should be screened for and treated," said James H. O'Keefe, M.D., cardiologist and director of Preventive Cardiology at the Mid America Heart Institute, Kansas City, MO. "Vitamin D is easy to assess, and supplementation is simple, safe and inexpensive."

It is estimated that up to half of U.S. adults and 30 percent of children and teenagers have vitamin D deficiency, which is defined as a 25(OH)D level of <20ng/ml. Low vitamin D levels activate the renin-angiostensin-aldosterone system and, in doing so, predispose patients to hypertension and a stiffening and thickening of the heart and blood vessels. Vitamin D deficiency also alters hormone levels and immune function, which can increase the risk of diabetes, a major contributor to CVD.

Recent data from the Framingham Heart Study suggest patients with vitamin D levels below 15 ng/ml were twice as likely to experience a heart attack, stroke or other CV event within the next five years compared to those with higher levels. This risk remained even when researchers adjusted for traditional CV risk factors.

Treating Vitamin D Deficiency

In the absence of clinical guidelines, the authors outline specific recommendations for restoring and maintaining optimal vitamin D levels in CV patients. These patients should initially be treated with 50,000 IU of vitamin D2 or D3 once weekly for 8 to 12 weeks. Maintenance therapy should be continued using one of the following strategies:

* 50,000 IU vitamin D2 or D3every 2 weeks;
* 1,000 to 2,000 IU vitamin D3 daily;
* Sunlight exposure for 10 minutes for Caucasian patients (longer for people with increased skin pigmentation) between the hours of 10 a.m. to 3 p.m.

Vitamin D supplements appear to be safe. In rare cases, vitamin D toxicity (causing high calcium levels and kidney stones) is possible, but only when taking in excess of 20,000 units a day."

Body Shape and Heart Disease Risk: Apple Or Pear Shape Is Not Main Culprit To Heart Woes -- It's Liver Fat

Body Shape and Heart Disease Risk: Apple Or Pear Shape Is Not Main Culprit To Heart Woes -- It's Liver Fat:

"For years, pear-shaped people who carry weight in the thighs and backside have been told they are at lower risk for high blood pressure and heart disease than apple-shaped people who carry fat in the abdomen. But new findings from nutrition researchers at Washington University School of Medicine in St. Louis suggest body-shape comparisons don't completely explain risk.

In two studies, they report excess liver fat appears to be the real key to insulin resistance, cholesterol abnormalities and other problems that contribute to diabetes and cardiovascular disease. Having too much fat stored in the liver is known as nonalcoholic fatty liver disease.

"Since obesity is so much more common now, both in adults and in children, we are seeing a corresponding increase in the incidence of nonalcoholic fatty liver disease," says senior investigator Samuel Klein, M.D., the Danforth Professor of Medicine and Nutritional Science. "That can lead to serious liver disorders such as cirrhosis in extreme cases, but more often it tends to have metabolic consequences."

[...]


The researchers determined that children with fatty liver disease also had abnormalities in glucose and fat metabolism, including lower levels of HDL cholesterol, the so-called good cholesterol. Those without a fatty liver did not have markers of metabolic problems. Whether shaped like pears or apples, it was fat in the liver that influenced metabolic risk.

"Abdominal fat is not the best marker for risk," says Klein, who also directs the Nutrition Support Service at Barnes-Jewish Hospital. "It appears liver fat is the real marker. Abdominal fat probably has been cited in the past because it tends to track so closely with liver fat. But if you look at people where the two don't correspond — with excess fat in the liver but not in the abdomen and vice versa — the only thing that consistently predicts metabolic derangements is fat in the liver."

In a second study, Klein's team found nonalcoholic fatty liver disease was related to the release of larger amounts of fatty acids into the bloodstream that were, in turn, linked to elevated triglycerides and to insulin resistance, a key precursor to type 2 diabetes.

"Multiple organ systems become resistant to insulin in these adolescent children with fatty liver disease," he says. "The liver becomes resistant to insulin and muscle tissue does, too. This tells us fat in the liver is a marker for metabolic problems throughout the entire system."

The findings indicate that children and adults with fatty liver disease should be targeted for intensive interventions, according to Klein. Those who are obese but don't have fatty liver disease still should be encouraged to lose weight, but those with evidence of fatty liver are at particularly high risk for heart disease and diabetes. They need to be treated aggressively with therapies to help them lose weight because weight loss can make a big difference.

"Fatty liver disease is completely reversible," he says. "If you lose weight, you quickly eliminate fat in your liver. As little as two days of calorie restriction can improve the situation dramatically, and as fat in the liver is reduced, insulin sensitivity and metabolic problems improve.""

Attention Deficit Disorder and dating

95-174 (Attention Deficit Disorder)

The study also showed that ADD teens had more trouble than the learning disabled group with social skills such as dating and getting along with peers. ADD teens also had lower levels of communication abilities such as writing a letter or addressing an envelope. Those who fared worst in social skill levels were the 18 ADD teens with conduct disorders. They had the lowest abilities to get along with others and the greatest behavioral and emotional difficulties.

Friday, December 05, 2008

Low-carb Diets Alter Glucose Formation By The Liver

Low-carb Diets Alter Glucose Formation By The Liver


In contrast to previous reports, the present study showed similar hepatic glucose production among the dietary groups. The low-carbohydrate group was able to maintain hepatic glucose production at the levels observed for the weight-stable and low-calorie groups by increasing glucose formation using lactate or amino acids to match the reduction in glucose formation from glycerol.

"This observation is reminiscent of 'hepatic autoregulation' by which endogenous glucose production remains unchanged in the setting of altered gluconeogenesis or glycogenolysis because the two pathways tend to compensate for each other," the authors report.

They noted it was interesting that the increased glucose formation using lactate or amino acids in the low-carbohydrate group was not associated with increased TCA cycle flux (i.e. energy production.) However, they did not measure absolute rates of fatty acid delivery to the liver or ketone body production, limiting their ability to further interpret that finding.

"We have shown that the sources from which endogenous glucose is produced are dependent upon dietary macronutrient composition," the authors write. They suggest that the shift in glucose metabolism associated with a low carbohydrate diet could be beneficial in individuals with non-alcoholic fatty liver disease (NAFLD) due to improved disposal of hepatic fat.

In conclusion, these findings may partly explain the correlation between carbohydrate intake and severity of liver disease in individuals with NAFLD.

Wartime diet of regular fasting slashes prostate cancer risk | Mail Online

Wartime diet of regular fasting slashes prostate cancer risk | Mail Online:

"Rationing food intake every few weeks could slash men's risk of prostate cancer, scientists believe.

Men who halve the amount they normally eat for a week or two once a month could markedly lower their chances of a tumour at a young age.

In human terms, researchers said, it was the equivalent of men getting cancer in their seventies or eighties rather than their fifties.

But the study showed going on a permanent low-calorie diet did not have the same powerful effect.

Scientists think occasional rationing may ward off cancer by constantly adjusting the balance of certain fat hormones.

High levels of leptin, a hormone released by fat cells, have been found to stimulate cancer cell growth, while high levels of another hormone, called adinopectin, appear to have a protective effect.

The latest findings, published in the journal Prostate, suggest frequent rationing cuts leptin levels and boosts those of adinopectin.

Several other studies have suggested limiting calories could be crucial to good health and a longer life.

In 2004, experts at Harvard Medical School in Boston, found women who regularly rationed their food were half as likely to get breast cancer as those who always ate until they were full.

More recently, researchers studying daughters of women caught in the Dutch famine of 1944-45 found they were more fertile and had a higher number of pregnancies than those born to mothers with better food supplies.

In Australia, meanwhile, scientists have recently embarked on a clinical trial to see if depriving cancer patients of food for a couple of days before chemotherapy treatment can protect the body against its toxic effects."

Individuals With ADHD Inattention Subtype More Likely to Quit Smoking

Individuals With ADHD Inattention Subtype More Likely to Quit Smoking:

Investigators at Columbia Medical Center, in New York, found individuals with ADHD who have the subtype of the disorder characterized by inattention alone are more likely to benefit from combination therapy with bupropion and nicotine patches than their counterparts who have ADHD with elevated symptoms of hyperactivity and impulsivity, with or without inattention.

Greater understanding of the divergent associations that exist between the different kinds of ADHD have important public-health consequences for smoking cessation and decreased tobacco-related mortality in this population, principal investigator Lirio S. Covey, PhD, said in a statement.

The study is published in the December issue of Nicotine & Tobacco Research.

As shown in previous research, as a group, smokers with ADHD had greater difficulty quitting than smokers without ADHD. However, the researchers showed for the first time that individuals with the inattention subtype of ADHD derived the same benefit from an 8-week smoking-cessation program as smokers without ADHD.

'Finding that smokers with the inattention subtype of ADHD benefit from bupropion and nicotine-patch treatment is encouraging news,' Dr. Covey told Medscape Psychiatry."

Wednesday, December 03, 2008

Too Much Commitment May Be Unhealthy For Relationships, Professor Says

Too Much Commitment May Be Unhealthy For Relationships, Professor Says:

"Romantic relationships establish special bonds between partners. Oftentimes, passionate rapport leads to permanent partnerships, and ultimately, the start of families.

Sometimes, however, one or both partners place too much emotional weight on their relationship. As a result, men or women may tend to evaluate their self-worth solely based on the outcomes of their romantic interactions. This is what psychologists term as relationship-contingent self-esteem (RCSE), and, according to University of Houston researcher Chip Knee, it's an unhealthy factor in romantic relationships.

"Individuals with high levels of RCSE are very committed to their relationships, but they also find themselves at risk to become devastated when something goes wrong -- even a relatively minor event," said Knee, UH assistant professor of psychology and director of the university's Interpersonal Relations and Motivation Research Group. "An overwhelming amount of the wrong kind of commitment can actually undermine a relationship."

Knee added that RCSE can trigger depression and anxieties during even the most minor or common relationship-based incidents, such as miscommunication, short spats over noncritical matters or a critique of one's personality or appearance.

It also factors into one or more partners developing manic, obsessive (or needy) behaviors with regard to love.

RCSE might place one at risk for serious mood changes after break-ups, divorce or threats to one's relationship. Identifying it during the early stages of a relationship can prevent such negative outcomes or help partners recognize that they are incompatible."

Waking up Teens -- Scientists Show Blue Light Can Help Reset Sleep Cycle

Waking up Teens -- Scientists Show Blue Light Can Help Reset Sleep Cycle:

"Teenagers' morning drowsiness is often caused by out-of-tune body clocks, in a condition known as 'delayed sleep phase syndrome.' Scientists now say that timing exposure to blue light -- avoiding it during the first two hours of being wake, then getting a good dose of it -- can help restore the sleep cycle, so teens feel sleepy earlier at night and are more awake in the morning."

Antioxidants Are Unlikely To Prevent Aging, Study Suggests


Antioxidants Are Unlikely To Prevent Aging, Study Suggests



Diets and beauty products which claim to have anti-oxidant properties are unlikely to prevent aging, according to research funded by the Wellcome Trust. Researchers at the Institute of Healthy aging at UCL (University College London) say this is because a key fifty year old theory about the causes of aging is wrong.

[...]

In 1956, Denham Harman proposed the theory that aging is caused by an accumulation of molecular damage caused by "oxidative stress", the action of reactive forms of oxygen, such as superoxide, on cells. This theory has dominated the field of aging research for over fifty years. But now, a study published online today in the journal Genes & Development suggests that this theory is probably incorrect and that superoxide is not a major cause of aging.

"The fact is that we don't understand much about the fundamental mechanisms of aging," says Dr David Gems from UCL. "The free radical theory of aging has filled a knowledge vacuum for over fifty years now, but it just doesn't stand up to the evidence."

Dr Gems and colleagues at the Institute of Healthy aging studied the action of key genes involved in removing superoxide from the bodies of the nematode worm C. elegans, a commonly-used model for research into aging. By manipulating these genes, they were able to control the worm's ability to "mop up" surplus superoxide and limit potential damage caused by oxidation.

Contrary to the result predicted by the free radical theory of aging, the researchers found that the lifespan of the worm was relatively unaffected by its ability to tackle the surplus superoxide. The findings, combined with similar recent findings from the University of Texas using mice, imply that this theory is incorrect.

"One of the hallmarks of aging is the accumulation of molecular damage, but what causes this damage?" says Dr Gems. "It's clear that if superoxide is involved, it only plays a small part in the story. Oxidative damage is clearly not a universal, major driver of the aging process. Other factors, such as chemical reactions involving sugars in our body, clearly play a role."

Dr Gems believes the study suggests that anti-aging products which claim to have anti-oxidant properties are unlikely to have any effect.

"A healthy, balanced diet is very important for reducing the risk of developing many diseases associated with old age, such as cancer, diabetes and osteoporosis," he says. "But there is no clear evidence that dietary antioxidants can slow or prevent aging. There is even less evidence to support the claims of most anti-aging products."

So avoiding carbs and sugar is the key to longer life, NOT stocking up on antioxidant vitamins or vegetables

Tuesday, December 02, 2008

Fasting intermittently reduces cell proliferation, a marker for cancer risk, s...( Berkeley -- An apple a day keeps the do...)

Fasting intermittently reduces cell proliferation, a marker for cancer risk,


Berkeley -- An apple a day keeps the doctor away, but could eating an apple every other day be better?

A new study by researchers at the University of California, Berkeley, raises such a possibility. It shows that healthy mice given only 5 percent fewer calories than mice allowed to eat freely experienced a significant reduction in cell proliferation in several tissues, considered an indicator for cancer risk. The key was that the mice eating 5 percent fewer calories were fed intermittently, or three days a week.

What is encouraging about the findings is that the reduction in cell proliferation from that intermittent feeding regimen was only slightly less than that of a more severe 33 percent reduction in calories. Until now, scientists have been certain only of a link between a more substantial calorie reduction and a reduction in the rate of cell proliferation.

The results of the study are scheduled to appear in the May 2005 issue of the American Journal of Physiology-Endocrinology and Metabolism, but are now available online.

"Cell proliferation is really the key to the modern epidemic of cancer," said Marc Hellerstein, professor of human nutrition in the Department of Nutritional Sciences and Toxicology at UC Berkeley's College of Natural Resources. Hellerstein is principal investigator of the study.

Wednesday, November 26, 2008

Estrogenic Stimulation of Hypothalamic-Limbic System Metabolism in Ageing Diabetic C57BL/KsJ Mice

Estrogenic Stimulation of Hypothalamic-Limbic System Metabolism in Ageing Diabetic C57BL/KsJ Mice:

"The therapeutic influences of estrogen treatment on age- and diabetes-related declines in regional brain glucose utilization (RBGU) rates were evaluated in 8- to 20-week-old female C57BL/KsJ normal ( /?) and diabetic (db/db) mice.

[...]

A gradual decline in the basal rate of brain glucose utilization was observed in all control (oil- and E-treated) groups between 8 and 20 weeks. Expression of the hyperglycemic-obese diabetes syndrome in db/db mice resulted in a significant reduction in regional brain glucose utilization RBGU rates between 8 and 20 weeks relative to control values.

[...]

These data demonstrate that the normal development-related decline in regional brain carbohydrate metabolism is accelerated by the diabetes syndrome, and that Estrogen therapy can modulate the syndrome-associated suppression of glucose utilization in steroid-sensitive CNS loci. These data suggest that the depressive influences of the diabetes syndrome on brain carbohydrate utilization rates may be therapeutically modified in recognized CNS regions possessing steroid-sequestering, metabolically responsive neurons."

I'm not as interested in the estrogen part, but rather this is further proof that the brain's failure to use carbohydrate effectively can be made worse by diabetes(carbohydrate consumption)

Tuesday, November 25, 2008

Behaviour in Fronto-temporal dementia and Semantic dementia

Behaviour in Fronto-temporal dementia and Semantic dementia

FTD - The frontal lobes

The frontal lobes develop later in maturity. They help to control incoming information from the environment, and to guide our actions and behaviour (see diagram). When the frontal lobes don’t work as they should, the system of control begins to break down. This can affect behaviour in a number of ways.

Planning and foresight
People with FTD may lose the ability to plan future actions and anticipate the consequences of their actions. This lack of planning may lead to the following behaviours:

* Inertia, apathy, lack of motivation – people with damage to the frontal lobes can become less proactive
* Purposeless activity, impulsivity – sometimes people act quickly without thinking things through
* Neglect of self care and personal responsibilities – lack of motivation to carry out simple tasks
* Behaviour governed by immediate wants – lack of foresight may result in inappropriate judgements about things such as money or eating

So, inability to anticipate the consequences of actions may lead to poor judgement and decision-making.

Organisation
Frontal lobe dysfunction may also result in disorganised behaviour. FTD sufferers may fail to complete tasks, or may attempt to carry out activities in a rather unusual manner. Even a simple task such as making a cup of tea might present problems, as there are several components involved, and the order in which they are carried out affects the outcome. Difficulties occur because the frontal lobes play an important role in our ability to sequence and organise our thoughts and actions.

Attention
People with FTD may also have impaired attention. It may be difficult to engage them in tasks and they may fail to complete activities because they are easily distracted by something else.

Checking
As mentioned earlier, there can be a loss of motivation and subsequent failure to anticipate the consequences of actions. People with FTD may have little insight into the effects of their behaviour and fail to ‘check’ their conduct. Thus, they may make numerous mistakes, and may be oblivious to their errors.

Abstraction
People with FTD may demonstrate ‘concrete’ or literal thinking. For example, a figure of speech such as ‘too many cooks spoil the broth’ might be interpreted literally as having something to do with cooking. The frontal lobes play an important part in our ability to understand abstract concepts, meaning that people with FTD may interpret things differently, often with reference to their own personal experience. Thus, they may appear self-centred, with little interest in others’ viewpoints.

Flexibility
A common symptom is a loss of flexibility in behaviour. The frontal lobes are very important in allowing us to adapt our behaviour according to the situation. People with FTD often lose this ability, and become quite rigid in their thinking. They may be unable to adjust their actions in unfamiliar situations, and thus behave inappropriately. Also, they may ‘perseverate’ (do/say the same thing over and over again). This is because their brain fails to tell them that the action/information is no longer relevant to the current situation.

Emotions and social behaviour
The frontal lobes are not only important in cognition. They also play a key role in our emotions. Often, one of the most difficult factors that carers encounter is their relatives’ loss of feeling towards them and their family. People who may have once been very affectionate towards their loved ones may become ‘cold’ in manner. There may be a loss of sympathy and empathy, and people may no longer respond appropriately to situations. In contrast to this picture of a ‘loss’ of emotion, it is also common for people with FTD to show inappropriate demonstration of emotion. People may become ‘disinhibited’ and tactless, for example they may laugh loudly or tell jokes at a funeral. They are typically unembarrassed by their behaviour, and lack insight into the effect it has on others.

Sensory information
People with FTD are able to feel normally, but it is our experience that sometimes their responses to stimuli are abnormal. For example, there may be no response to painful stimuli such as scalding hot water. The reason for this behaviour is yet to be clarified, but it is possible that there may be a relationship with impaired attention. There is evidence to suggest that how we behave is governed by attention, for example, a runner focussed on winning a race may complete the circuit without feeling the pain of a sprained ankle, simply because they are not attending to it. Impaired attention may therefore influence FTD sufferers’ reactions to stimuli.

Eating behaviours
It is common for people with FTD to demonstrate odd eating habits. There is often a preference for sweet foods, such as biscuits and chocolate. People may become gluttonous, eating everything that is put in front of them (sometimes including food on others’ plates). This relates to a lack of ability to inhibit behaviour, and also a tendency to respond indiscriminately to environmental stimuli (this is called ‘utilisation behaviour’). In addition, people with FTD may even seek out food, and also may ‘cram’ food into their mouths instead of chewing and swallowing one item at a time. This may relate to problems in sequencing, or may reflect a ‘repetitive’ behaviour as discussed below.

Repetitive behaviours
It is very common for people with FTD to show repetitive behaviours and mannerisms such as humming the same tune, or repeating the same phrases or words. People often develop repetitive routines and rituals, and it is common for carers to report behaviours such as pacing, wandering, and hoarding.

The role of emotion in decision-making: Evidence from neurological patients with orbitofrontal damage

The role of emotion in decision-making: Evidence
from neurological patients with orbitofrontal damage


Most theories of choice assume that decisions derive from an assessment of the future outcomes of various options and alternatives
through some type of cost-benefit analyses. The influence of emotions on decision-making is largely ignored. The studies of
decision-making in neurological patients who can no longer process emotional information normally suggest that people make
judgments not only by evaluating the consequences and their probability of occurring, but also and even sometimes primarily at a
gut or emotional level. Lesions of the ventromedial (which includes the orbitofrontal) sector of the prefrontal cortex interfere with
the normal processing of ‘‘somatic’’ or emotional signals, while sparing most basic cognitive functions. Such damage leads to
impairments in the decision-making process, which seriously compromise the quality of decisions in daily life.

[...]

OK, so here they focused on decision making in frontal lobe impaired subjects. They make the point that in real life, you don't always know what the results of your actions will be, so you have to estimate. They had subjects choose from two decks of cards: cards with a modest, but fairly certain, payoff, and another deck which was a losing deck, but with some big payoffs spread inside. Normal people tended towards the sure thing, while frontal lobe impaired patients chose from the risky deck. They tied this in to emotions, by studying skin response to view emotional responses. They found that both groups of patients felt emotions when they won or lost, but that normal patients felt emotions before picking, especially from the risky deck. Impaired patients seemed blind to this, and just made their choices and THEN felt the emotion. They also show that different halves of the brain focus on negative or positive rewards. So depending on the damaged lobe, right or left, the subject might be totally focused on positive rewards, ignoring negative consequences, or totally focused on negative rewards, ignoring the positive. Either way leads to impaired decision making skills. Authors are also trying to point out the role emotion plays in decision making, especially when results are uncertain, as they are in most scenarios in real life.

Cigarette smoking exacerbates alcohol-induced brain damage

Cigarette smoking exacerbates alcohol-induced brain damage

Heavy alcohol consumption is known to cause brain damage. A new imaging study has compared 24, one-week-abstinent alcoholics (14 smokers, 10 nonsmokers) in treatment with 26 light-drinking "controls" (7 smokers, 19 nonsmokers), and found that cigarette smoking can both exacerbate alcohol-induced damage as well as independently cause brain damage. The damage is most prominent in the frontal lobes (important in planning, decision-making, and multi-tasking among other functions). Independent of alcohol consumption, cigarette smoking also had adverse effects on brain regions involved in fine and gross motor functions and balance and coordination. Roughly 80% of alcohol-dependent individuals report smoking regularly.

Orbitofrontal Cortex and Social Behavior: Integrating Self-monitoring and Emotion-Cognition Interactions -- Beer et al. 18 (6): 871 -- The Journal of Cognitive Neuroscience

Orbitofrontal Cortex and Social Behavior: Integrating Self-monitoring and Emotion-Cognition Interactions -- Beer et al. 18 (6): 871 -- The Journal of Cognitive Neuroscience

The role of the orbitofrontal cortex in social behavior remains a puzzle. Various theories of the social functions of the orbitofrontal cortex focus on the role of this area in either emotional processing or its involvement in online monitoring of behavior (i.e., self-monitoring). The present research attempts to integrate these two theories by examining whether improving the self-monitoring of patients with orbitofrontal damage is associated with the generation of emotions needed to guide interpersonal behavior. Patients with orbitofrontal damage, patients with lateral prefrontal damage, and healthy controls took part in an interpersonal task. After completing the task, participants' self-monitoring was increased by showing them a videotape of their task performance. In comparison to healthy controls and patients with lateral prefrontal damage, orbitofrontal damage was associated with objectively inappropriate social behavior. Although patients with orbitofrontal damage were aware of social norms of intimacy, they were unaware that their task performance violated these norms. The embarrassment typically associated with inappropriate social behavior was elicited in these patients only after their self-monitoring increased from viewing their videotaped performance. These findings suggest that damage to the orbitofrontal cortex impairs self-insight that may preclude the generation of helpful emotional information. The results highlight the role of the orbitofrontal cortex in the interplay of self-monitoring and emotional processing and suggest avenues for neurorehabilitation of patients with social deficits subsequent to orbitofrontal damage.

Again, frontal lobe malfunction is associated with ADD, diabetes, alzheimers, brain damage, etc. Problems with organization and interpersonal relations can be effected. Here, they use videotaping to show the subject how they behaved, and the subject is finally able to identify that their behavior was inappropriate. Self monitoring is impaired in frontal lobe disorders like ADD.

Molecular Switch in Brain May End Smokers’ Cravings - Health News - Health.com

Molecular Switch in Brain May End Smokers’ Cravings - Health News - Health.com

Blocking a neuropeptide receptor in the brain may be one way to quickly lessen the desire for a cigarette, a new study suggests.

Hypocretin-1, or Orexin A, a short chain of amino acids found in nerve tissue, appears to initiate a series of closely linked biochemical reactions that makes lab rats crave nicotine, the addictive chemical in tobacco, according to researchers at the Scripps Florida research institute in Jupiter.

If duplicated in humans, the finding could be lead to new smoking-cessation treatments, the researchers said.

“Blocking hypocretin-1 receptors not only decreased the motivation to continue nicotine use in rats, it also abolished the stimulatory effects of nicotine on their brain reward circuitries,” study leader Paul Kenny, a scientist at Scripps Florida, explained in a news release issued by the institute. “This suggests that hypocretin-1 may play a major role in driving tobacco use in smokers to want more nicotine. If we can find a way to effectively block this receptor, it could mean a novel way to help break people’s addiction to tobacco.”

Very interesting. Hypocretin or Orexin A deficits are the cause of narcolepsy. This compound activates the Hypothalamus, increasing mood, activity, attention, etc. Low Orexin levels make one sleepy, unmotivated, depressed, etc. Glucose lowers Orexin levels, and may even cause the body to destroy Orexin in the brain, causing narcolepsy. Smoking also seems to damage the body through manipulating insulin and glucose levels. People with ADD are more likely to smoke. It could be that they are self medicating due to low orexin levels. This is why my blog is called "it's all connected". I also think it's interesting that they want to create a med to block orexin, to help smokers stop. Woudn't this compound also cause the low arousal and motivation associated with narcolepsy and ADD? You won't want to smoke, or do much of anything else for that matter. Why not enhance orexin a with a low carb, ketogenic diet and exercise instead? Or just get enough sleep? I guess the idea is that no one will do that, and besides, there's no money in it for big pharm.

Sugar feeds cancer

Drug/diet synergy for managing malignant astrocytoma in mice: 2-deoxy-D-glucose and the restricted ketogenic diet. - 7thSpace Interactive

Astrocytomas are largely dependent on glycolysis to satisfy their bioenergetic requirements for growth and survival. Therapies that target glycolysis can potentially manage astrocytoma growth and progression.

Dietary restriction of the high fat/low carbohydrate ketogenic diet (KD-R) reduces glycolysis and is effective in managing experimental mouse and human astrocytomas

[...]

The results suggest that management of malignant astrocytoma with restricted ketogenic diets could be enhanced when combined with drugs that inhibit glycolysis.

Monday, November 24, 2008

Fasting intermittently reduces cell proliferation, a marker for cancer risk, s...( Berkeley -- An apple a day keeps the do...)

Fasting intermittently reduces cell proliferation, a marker for cancer risk, s...( Berkeley -- An apple a day keeps the do...)

A new study by researchers at the University of California, Berkeley, raises such a possibility. It shows that healthy mice given only 5 percent fewer calories than mice allowed to eat freely experienced a significant reduction in cell proliferation in several tissues, considered an indicator for cancer risk. The key was that the mice eating 5 percent fewer calories were fed intermittently, or three days a week.

What is encouraging about the findings is that the reduction in cell proliferation from that intermittent feeding regimen was only slightly less than that of a more severe 33 percent reduction in calories. Until now, scientists have been certain only of a link between a more substantial calorie reduction and a reduction in the rate of cell proliferation.

Saturday, November 22, 2008

Bottoms Up: Individualists More Likely To Be Problem Drinkers

Bottoms Up: Individualists More Likely To Be Problem Drinkers

ScienceDaily (Nov. 21, 2008) — What makes residents of certain states or countries more likely to consume more alcohol? According to a new study in the Journal of Consumer Research, high levels of individualism lead to more problem drinking.

"We looked at the extent to which consumer levels of individualism (vs. collectivism) were related to their beer and problem alcohol consumption," write authors Yinlong Zhang and L.J. Shrum (both University of Texas-San Antonio).

"We found that the higher a region scored on valuing individualism, the greater their beer and alcohol consumption, and this was true even when taking into account the effects of other variables such as income, climate, gender, and religion."

[...]

The researchers found that people with more interdependent mindsets were less likely to over-consume when they were with peers. "The results suggest that people with collectivistic cultural orientations tend to be more motivated to regulate impulsive consumption tendencies than those with individualistic cultural orientations, which in turn makes them less likely to engage in beer or alcohol consumption," the authors conclude.

Calorie Restriction And Exercise Show Breast Cancer Prevention Differences In Postmenopausal Women

Calorie Restriction And Exercise Show Breast Cancer Prevention Differences In Postmenopausal Women

Epidemiological data has suggested that inducing a so-called "negative energy balance" (where less energy is taken in than expended) through eating a low-calorie diet or increasing exercise levels, decreases the postmenopausal breast cancer risk associated with obesity. Although the mechanism responsible for these anti-obesity strategies was unknown, scientists have suspected hormone alteration plays a critical role. Increased fat tissue is known to be associated with alterations in adipokines, proteins secreted by fat tissue that help modify appetite and insulin resistance. For example, increased levels of leptin and decreased levels of adiponectin have been associated with breast cancer risk.

[...]

The calorie-restricted mice and the exercised mice showed no significant difference in percentage of body fat, but both groups had significantly less body fat than the sedentary mice that were fed at will.

In addition, blood levels of leptin, a hormone that plays a role in fat metabolism, were significantly reduced in the calorie-restricted and exercised mice compared to the controls. The calorie-restricted mice also displayed increased blood levels of adiponectin, a hormone produced in fat tissue that regulates some metabolic processes, compared to the exercised mice.

Some of the cell signaling pathways regulated by these hormones converge at mTOR, Nogueira explains. She and her colleagues found that the key proteins found downstream of mTOR activation were less active in both the calorie-restricted and exercised mice compared to the controls.

"These data suggest that although exercise can act on similar pathways as caloric restriction, caloric restriction possesses a more global effect on cell signaling and, therefore, may produce a more potent anti-cancer effect," Nogueira said.

Type 2 diabetes may slow mental processing speed | Health | Reuters

Type 2 diabetes may slow mental processing speed | Health | Reuters

Diabetes may slow brain processing

Some studies have linked diabetes and cognitive dysfunction, but a new study suggests that mental processing speed may be the brain function most severely affected by diabetes. Researchers looked at data from the AGES Reykjavik Study and found that people who had been diagnosed with diabetes were slower to process information than people who didn’t have diabetes. People with undiagnosed diabetes had similar problems, but those with pre-diabetes had mental functioning similar to people without diabetes. Both memory and “executive function or the ability to plan and multitask, were comparable in people with and without diabetes, though people who’d had diabetes more than 15 years also had impaired executive function, according to the report in the American Journal of Epidemiology.

Monday, November 17, 2008

Want To Know What Is In Fast Food, Lots Of Corn! : ChattahBox

Want To Know What Is In Fast Food, Lots Of Corn! : ChattahBox:

"Washington (ChattahBox) - According to a new study, a key ingredient in fast food is apparently corn!

The study focused on three main fast food chains in Boston, Baltimore, Denver, San Francisco, Detroit, as well as Los Angeles.

The study was led by A. Hope Jahren from the University of Hawaii, along with colleague Rebecca Kraft, and found the key ingredient to be corn.

Using a special technique to analyze the food, they found high levels of both carbon and nitrogen, which means corn
.
The corn is able to fatten the cattle in a very short period of time.

This could explain why fast food causes obesity at such a high rate.

Their findings have been published in the Proceedings of the National Academy of Sciences."

Tuesday, November 11, 2008

Metabolic Syndrome and Psychiatric ... - Google Book Search

Metabolic Syndrome and Psychiatric ... - Google Book Search

Major depression

It has long been known that a disproportionately large percentage of patients with diabetes also suffer major depression. The prevalence of major depression in diabetics, regardless of whether their diabetes is type 1 or type 2, is roughly 3 times that seen in the general population. However, the likelihood of depression is often increased in individuals dealing with serious and potentially disabling illnesses. Plus, the significance of the high prevalence of depression in diabetics, and whether it reflects some interaction between the two seemingly disparate conditions has not been entirely clear.

Over recent years it has become apparent that there is a relationship between major depression and metabolic syndrome, which is frequently the precursor of diabetes type 2. Men and women with depression are more likely than those without depression to develop metabolic syndrome. People with depression often have the abdominal obesity, insulin resistance, hypertension, hyperlipidemia, and elevated fasting glucose levels that characterize the syndrome. There is also a strong relationship between depression and insulin resistance. Insulin resistance, a cardinal feature of metabolic syndrome, is four times more likely to occur in depressed individuals. Although Major depression is associated with metabolic syndrome, it is not clear how the two are related. Does depression cause the metabolic syndrome, or do the biochemical changes of metabolic syndrome lead to depression?

Evidence suggests that depression can set the stage for later development of metabolic syndrome. Women who complain of depression, anxiety, and anger are more likely than women without those psychological characteristics to develop metabolic syndrome in subsequent years. Path analyses have shown statistically that the progression from depression to poor health habits to metabolic syndrome is the most likely course of events when depression and metabolic syndrome coexist.

One explanation for how depression might lead to metabolic syndrome is that depression fosters unhealthy lifestyles. Patients with depression often smoke. They are inactive and eat poorly. Although many patients with major depression have poor appetites, some sufferers crave sweets and indulge in "comfort foods" packed with high glycemic index carbohydrates. This is particularly the case in so-called atypical depression. Despite its name, atypical depression may actually be a common form of depression in women. Comorbidity of depression, obesity, and metabolic syndrome occurs more often in women than in men.

Overeating, smoking, drinking, inactivity, and carbohydrate craving are at least partially responsible for the tendency of people with depression to develop metabolic syndrome. However, even when these unhealthy habits are statistically removed from the equation, there is an unexpectedly high incidence of metabolic syndrome among sufferers of major depression. It is possible that some of the same, underlying physiological abnormalities contribute to both major depression and metabolic syndrome.

Insulin resistance and major depression

The insulin resistance of metabolic syndrome may play a role in major depression. Although insulin dramatically affects the way muscle and fat cells take up and metabolize glucose, neuroscientists have come to believe that it had no significant effect on the brains utilization of glucose. However, insulin has subtle, yet potentially important effects on the way the brain uses glucose.

Insulin is actively transported into the brain, and insulin receptors are found in a variety of important areas of the brain. The amount of insulin in the brain is affected by changes in serum insulin levels. Insulin levels in cerebrospinal fluid increase during acute episodes of hyperinsulemia. In chronic hyperinsulinemia, such as occurs in metabolic syndrome, insulin levels in cerebrospinal fluid can decrease. This is likely due to down regulation of the activity of the insulin transport system into the brain. When insulin is reduced to levels below those generally seen during the fasting state in humans, the brain uses less glucose. It is the older areas of the brain, such as the cerebellum and brainstem, that have the highest density of insulin receptors. However, it is the cerebral cortex, where the higher functions of mind reside, that is most strongly affected by the depletion of insulin.

The insulin resistance that defines metabolic syndrome is most clearly seen in muscle, adipose tissue, and liver. Although changes in insulin levels can clearly affect brain activity, there has been a question as to whether the insulin resistance seen in peripheral tissue also occurs in the brain tissue of patients with metabolic syndrome. Recent studies with human subjects have shown that this is the case. When glucose and insulin levels are controlled by clamping techniques, insulin resistant subjects show less cortical excitation than insulin sensitive subject to the same serum levels of insulin. The degree of insulin's affect on cortical activity is in positive correlation with insulin sensitivity as measured by the ability of insulin to stimulate glucose uptake in peripheral tissues. The ability of a specific level of serum insulin to enhance glucose metabolism in the cerebral cortex is also diminished in subjects with peripheral insulin resistance. This resistance to insulin is most apparent in the prefrontal cortex and other areas of the brain involved in motivation and reward.

Perhaps the most compelling evidence of brain tissue becoming resistant to insulin comes from a study in which the response to insulin was evaluated ex viVo using slices of brain removed from hamsters made insulin resistant by feeding them a fructose enriched diet. Direct administration of insulin into brain tissue was less effective in generating insulin induced long-term inhibition in sections from insulin resistant animals than in those for control animals. Existing data do suggest that decreases in insulin activity in the brain, due either to insulin resistance in brain tissue or decreases in the ability of insulin to reach the brain, could play a significant role in the development of major depression.

Consistent with insulin resistance causing depression are findings that chromium, an essential mineral known to enhance the effects of insulin, can help relieve depression. Chromium has been used successfully for treatment of both depression and dysthymia. The latter is a mild but persistent form of depression. Interestingly, the type of depression that may best be helped by chromium is atypical depression. This is the form of depression were commonly seen in women, that is characterized by a depressed mood, lack of motivation, low sex drive, carbohydrate craving, and sleeping too much. The strongest effects of chromium were in countering carbohydrate craving, increased appetite, and decreased sex drive.

Lithium is a medication that has long been used to treat bipolar and affective disorder. It is also used to augment the effects of antidepressants in treatment resistant depression. Lithium mimics several of the effects of insulin in the brain. Both lithium and insulin inhibits the passivity of the increasingly important enzyme, glycogen synthase kinase 3. Moreover, both lithium and insulin stimulates the effects of the enzymes phosphatidylinositol-3-kinase and protein kinase B. it is not known to what degree the benefits of lithium are due to mimicking the effects of insulin. Neither is it known if lithium has any special benefit for patients that suffer both depression and metabolic syndrome or diabetes type 2. Omega-3 deity assets, which have been found to improve some symptoms of both major depression and metabolic syndrome have also been found to enhance the activity of phosphatidylinositol 3 kinase.

HowStuffWorks "How Nicotine Works"

HowStuffWorks "How Nicotine Works"

Effects of Nicotine

Nicotine changes how your brain and your body function. The net results are somewhat of a paradox: Nicotine can both invigorate and relax a smoker, depending on how much and how often they smoke. This biphasic effect is not uncommon. Although the actions of nicotine and ethanol in the body are quite different, you also see dose-dependent effects when you drink alcoholic beverages. Your first drink may loosen your inhibitions and fire you up, but after several drinks, you're usually pretty sedate.

Nicotine and the Body
Nicotine initially causes a rapid release of adrenaline, the "fight-or-flight" hormone. If you've ever jumped in fright at a scary movie or rushed around the office trying to finish a project by your deadline, you may be familiar with adrenaline's effects:

* Rapid heartbeat
* Increased blood pressure
* Rapid, shallow breathing

Adrenaline also tells your body to dump some of its glucose stores into your blood. This makes sense if you remind yourself that the "fight-or-flight" response is meant to help you either defend yourself from a hungry predator or hightail it out of a dangerous situation -- running or brawling both require plenty of energy to fuel your muscles. (For more information, see How Exercise Works.)

Nicotine itself may also block the release of the hormone insulin. Insulin tells your cells to take up excess glucose from your blood. This means that nicotine makes people somewhat hyperglycemic, having more sugar than usual in their blood. Some people think that nicotine also curbs their appetite so that they eat less. This hyperglycemia could be one explanation why: Their bodies and brain may see the excess sugar and down-regulate the hormones and other signals that are perceived as hunger.

Nicotine may also increase your basal metabolic rate slightly. This means that you burn more calories than you usually would when you are just sitting around. (For more information on metabolism, see How Calories Work.) However, losing weight by smoking doesn't give you any of the health benefits that you'd get if you were losing weight by exercising -- it actually does the opposite! Over the long haul, nicotine can increase the level of the "bad" cholesterol, LDL, that damages your arteries. This makes it more likely that you could have a heart attack or a stroke.

Insulin's Brain Impact Links Drugs And Diabetes

Insulin's Brain Impact Links Drugs And Diabetes

Insulin, long known as an important regulator of blood glucose levels, now has a newly appreciated role in the brain.

Vanderbilt University Medical Center researchers, working with colleagues in Texas, have found that insulin levels affect the brain's dopamine systems, which are involved in drug addiction and many neuropsychiatric conditions.

In addition to suggesting potential new targets for treating drug abuse, the findings raise questions as to whether improper control of insulin levels -- as in diabetes -- may impact risk for attention deficit hyperactivity disorder (ADHD) or influence the effectiveness of current ADHD medications.

The antidepressant properties of the ketogenic diet

The antidepressant properties of the ketogenic diet .

Biological Psychiatry , Volume 56 , Issue 12 , Pages 981 - 983

P . Murphy , S . Likhodii , K . Nylen , W . Burnham

Elsevier Article Locator


Background

The ketogenic diet is used to treat epilepsy refractory to anticonvulsant medication. Individuals with epilepsy often have behavioral problems and deficits in attention and cognitive functioning. The ketogenic diet has been found to effect improvements in these domains. It has also been suggested that the ketogenic diet may act as a mood stabilizer.
Methods

The present research used the Porsolt test, an animal model of depression, to determine whether the ketogenic diet has antidepressant properties. Porsolt test scores of rats on the ketogenic diet were compared with those of rats on a control diet.
Results

The rats on the ketogenic diet spent less time immobile, suggesting that rats on the ketogenic diet, like rats treated with antidepressants, are less likely to exhibit “behavioral despair.”
Conclusions

It is concluded that the ketogenic diet may have antidepressant properties.

Monday, November 10, 2008

Insulin Resistance and Executive Dysfunction in Older Persons

Wiley InterScience :: JOURNALS :: Journal of the American Geriatrics Society

ABSTRACT

Objectives: To evaluate the association between insulin resistance (IR) and executive dysfunction in a large, population-based study of older persons without diabetes mellitus (DM) or dementia.

[...]

Measurements: Anthropometric measurements; plasma fasting levels of glucose, insulin, cholesterol (total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol), and insulin-like growth factor-1 (IGF-1); homeostasis model assessment (HOMA) to estimate degree of IR; Trail Making Test (TMT) A; TMT-B; TMT-B minus TMT-A (DIFF B–A); and Mini-Mental State Examination (MMSE).

Results: IR (HOMA) was associated with longer TMT-B (correlation coefficient (r)=0.11; P=.006) and DIFF B–A times (r=0.10; P=.022). Subjects in the upper tertile of IR were older and had longer TMT-B and DIFF B–A than participants in the lowest tertile. After adjusting for age, sex, and years of formal education, IR was significantly correlated with TMT-A, TMT-B, and DIFF B–A. After adjusting for age, sex, education, body mass index, waist:hip girth ratio, HDL-C, triglycerides, IGF-1, hypertension, drug intake, and physical activity, the results did not significantly change. After introducing MMSE score into the model, IR continued to be an independent determinant of TMT-A (β=11.005; P=.021), TMT-B (β=28.379; P<.001), and DIFF B–A (β=17.374; P=.011).

Conclusion: IR is independently associated with frontal cortex function evidenced by poor TMT times in older persons without DM or dementia.

Diabetes and executive dysfunction go hand in hand. Executive dysfunction is a hallmark of ADD.

Erectile Dysfunction Linked To Smoking

Erectile Dysfunction Linked To Smoking

Men who smoke cigarettes run an increased risk of experiencing erectile dysfunction, and the more cigarettes smoked, the greater the risk, according to a study by Tulane University researchers published in the American Journal of Epidemiology.

Frontal Lobe Injury

Frontal Lobe Injury

Consequences of Frontal Lobe Injury

The major role of the frontal lobes is the regulation of behavior. They coordinate attention, memory, language, perception, motor functions, and social behavior as we go about our daily living and vocational activities. In short, they put the human machine to work. When function is impaired, all of the other cognitive systems are affected even though they remain individually intact. The frontal lobes have been likened to the pilot of a Boeing 747, without whom millions of dollars worth of highly complex technology would sit idle at the airport. Recognition and appreciation of these deficits is critical to rehabilitation efforts with the closed head injured population. These deficits can be classed generally and include:

* Problems of Starting--This may manifest as decreased spontaneity and initiation. Such individuals seem to lack motivation and may sit silently without apparent interest in or curiosity about surroundings until they are directed to do something.
* Difficulties in Making Mental or Behavioral Shifts--This includes rigidity or perseveration on a single idea or a single action. Individuals with these problems may be able to successfully verbalize solutions to problems, including plans necessary to meet goals successfully, yet be unable to put any plan into effective action.
* Difficulties with Attention--Individuals with frontal lobe deficits are often captured by extraneous aspects of a task. As a result, they may demonstrate behaviors which seem irrelevant, even bizarre, to the observer. Because they may be highly distractible, they often seem to shift focus continually, never arriving at a point which seems purposeful.
* Problems in Stopping--This may manifest as a more general deficit in self monitoring. It may present as impulsivity or a quickness to anger, speaking too loudly, or carrying a joke or sexual innuendo too far.
* Problems with Social Awareness--This category would include deficits in the ability to appreciate the impact one makes on others, sometimes resulting in rude or insensitive behavior or with a general lack of apparent concern about social conventions.
* Deficient Self-Awareness--Defective self-criticism may be associated with a tendency to be self-satisfied, to experience little or no anxiety, and to fail to appreciate the existence and practical implications of deficits (limited insight).
* A Concrete Attitude--Some patients with frontal lobe lesions retain high-level conceptual abilities but demonstrate a day-to-day literal-mindedness and loss of perspective.

Monday, November 03, 2008

more kids taking medication for ADD and diabetes USATODAY.com

USATODAY.com

The number of children who take medication for chronic diseases has jumped dramatically, another troubling sign that many of the youngest Americans are struggling with obesity, doctors say.

The number of children who take pills for type 2 diabetes — the kind that's closely linked to obesity — more than doubled from 2002 to 2005, to a rate of six out of 10,000 children. That suggests that at least 23,000 privately insured children in the USA are now taking diabetes medications, according to authors of the new study in today's Pediatrics.

Doctors also saw big increases in prescriptions for high cholesterol, asthma and attention deficit and hyperactivity. There was smaller growth for drugs for depression and high blood pressure.

"We've got a lot of sick children," says author Emily Cox, senior director of research with Express Scripts, which administers drug benefit programs for private insurance plans. "What we've been seeing in adults, we're also now seeing in kids."

Type 2 diabetes was once known as adult-onset. But Cox says her records show kids as young as 5 being treated with prescription diabetes drugs.

Cox based her study on prescription records of nearly 4 million children a year, ages 5 to 19, covered by Express Scripts. She says her findings may not apply to the 40% of children who are uninsured or covered by government health plans.

Unless these children make major changes — such as eating healthier and exercising more — they could be facing a lifetime of illness, Cox says.

"These are not antibiotics that they take for seven to 10 days," Cox says. "These are drugs that many are taking for the rest of their lives."

Cox couldn't explain one surprising finding: Most of the increase in drugs for diabetes, attention deficit/hyperactivity and depression was seen in girls. The gender gap was most striking in diabetes: While the number of boys taking medication grew by 39%, the number of girls using them climbed by 147%, Cox found.

Wednesday, October 29, 2008

Food Restriction Increases Dopamine Receptors -- Linked to Pleasure -- In Rats

Food Restriction Increases Dopamine Receptors -- Linked to Pleasure -- In Rats:

"A brain-imaging study of genetically obese rats conducted at the U.S. Department of Energy's Brookhaven National Laboratory provides more evidence that dopamine - a brain chemical associated with reward, pleasure, movement, and motivation - plays a role in obesity. The scientists found that genetically obese rats had lower levels of dopamine D2 receptors than lean rats. They also demonstrated that restricting food intake can increase the number of D2 receptors, partially attenuating a normal decline associated with aging.

[...]

It's not clear whether reduced receptor levels are a cause or consequence of obesity: Overeating may chronically reduce receptor levels, which, over the long term, could eventually contribute to obesity. But having genetically low receptor levels may also lead to obesity by predisposing the individual to overeating in an attempt to stimulate a "blunted" reward system. Either way, revving up receptor levels by restricting food intake could enhance the impact of this common strategy for combating obesity."

Tuesday, October 28, 2008

Fructose Sets Table For Weight Gain Without Warning

Fructose Sets Table For Weight Gain Without Warning

he University of Florida researchers hypothesized that a high-fructose diet could lead to leptin resistance, which in turn could lead to exacerbated weight gain in the face of a high-fat, high-calorie diet, a typical diet in industrialized countries. To test their hypothesis, the research team performed a study with two groups of rats. They fed both groups the same diet, with one important exception: one group consumed a lot of fructose while the other received no fructose.

Two groups similar over six months

During these six months, there were no differences in food intake, body weight, and body fat between rats on the high-fructose and the rats on the fructose-free diets. In addition, there was no difference between the two groups in the levels of leptin, glucose, cholesterol or insulin found in their blood. There was only one difference at the end of the six months: The rats on the high-fructose diet had higher levels of triglycerides in their blood.

The researchers next tested the animals to see if they were leptin resistant. They injected all the animals with leptin, to see if they would respond by eating less. Animals whose leptin response is functioning normally will lower their food intake. The researchers discovered that the rats on the high-fructose diet were leptin resistant, that is, they did not lower their food intake when given leptin. The no-fructose animals responded normally to leptin by eating less.

This first six months of the study showed that leptin resistance can develop silently. “Usually, leptin resistance is associated with obesity, but in this case, leptin resistance developed without obesity,” Shapiro said. “This was very surprising.”

Role of diet

Having seen that leptin resistance could develop silently, the researchers next wanted to find out what would happen if they switched the rats to a high-fat, high-calorie diet -- the kind many Americans eat. They found that the animals exposed to the high-fructose diet, the leptin resistant rats, ate more and gained much more weight and fat than the leptin responsive animals on the fructose-free diet. All told, this study showed that leptin resistance can:

* develop by eating a lot of fructose
* develop silently, that is, with very little indication it is happening
* result in weight gain when paired with a high fat, calorie dense diet

Scarpace said the study suggests it is the interaction between consumption of large amounts of fructose-containing foods and eating a high-fat, high-calorie diet that produces the weight gain. “This study may explain how the global increase in fructose consumption is related to the current obesity epidemic,” Shapiro said.

How it happens

Other studies have shown that elevated triglycerides impair the transport of leptin across the blood brain barrier. The researchers hypothesize that the elevation in triglycerides produced by fructose prevented leptin from reaching the brain. If leptin does not reach the brain, the brain will not send out the signal to stop eating.

“The presence of high fructose alters the way leptin works, fooling the brain so that it ignores leptin,” Scarpace said. Consumers should be cautious about what they eat, checking labels to see how much sugar the items contain, Shapiro said.

The researchers hope to perform future studies to find out if leptin resistance can be reversed by removing or reducing the fructose content of the diet.

Brain's 'Sixth Sense' For Calories Discovered

Brains Sixth Sense For Calories Discovered

In analyzing the brains of the sweet-blind mice, the researchers showed that the animals' reward circuitry was switched on by caloric intake, independent of the animals' ability to taste. Those analyses showed that levels of the brain chemical dopamine, known to be central to activating the reward circuitry, increased with caloric intake. Also, electrophysiological studies showed that neurons in the food-reward region, called the nucleus accumbens, were activated by caloric intake, independent of taste.

Insulin levels affect the brain's dopamine systems

Insulin levels affect the brain's dopamine systems

Insulin, long known as an important regulator of blood glucose levels, now has a newly appreciated role in the brain.

Vanderbilt University Medical Center researchers, working with colleagues in Texas, have found that insulin levels affect the brain's dopamine systems, which are involved in drug addiction and many neuropsychiatric conditions.

In addition to suggesting potential new targets for treating drug abuse, the findings raise questions as to whether improper control of insulin levels - as in diabetes - may impact risk for attention deficit hyperactivity disorder (ADHD) or influence the effectiveness of current ADHD medications.

The study, led by Aurelio Galli, Ph.D., in the Center for Molecular Neuroscience and Calum Avison, Ph.D., in the Institute of Imaging Science (VUIIS), appears online this week in the Public Library of Science Biology (PLoS Biology).

[...]

The results are some of the first to link insulin status and dopaminergic brain function and hold several implications for human health and disease.

"This is really the first mechanistic connection in vivo between diabetes and amphetamine action," Galli said. "This offers a completely new perspective on the influence of this disease (diabetes) on brain function, as well as diseases with altered dopamine signaling, such as schizophrenia and ADHD."

The findings suggest that ADHD risk may have an insulin-dependent component and that control of insulin levels and response to the hormone may be an important determinant of amphetamine efficacy in patients with ADHD, Galli noted.

"We have described a novel mechanism by which diabetes may affect brain function."

Monday, October 27, 2008

Is ADHD An Advantage For Nomadic Tribesmen?

Is ADHD An Advantage For Nomadic Tribesmen?:

"A propensity for attention deficit hyperactivity disorder (ADHD) might be beneficial to a group of Kenyan nomads, according to new research. Scientists have shown that an ADHD-associated version of the gene DRD4 is associated with better health in nomadic tribesmen, and yet may cause malnourishment in their settled cousins."

A study led by Dan Eisenberg, an anthropology graduate student from Northwestern University in the US, analyzed the correlates of body mass index (BMI) and height with two genetic polymorphisms in dopamine receptor genes, in particular the 48 base pair (bp) repeat polymorphism in the dopamine receptor D4 (DRD4) gene.

The DRD4 gene codes for a receptor for dopamine, one of the chemical messengers used in the brain. According to Eisenberg "this gene is likely to be involved in impulsivity, reward anticipation and addiction". One version of the DRD4 gene, the '7R allele', is believed to be associated with food craving as well as ADHD. By studying adult men of the Ariaal of Kenya, some of whom still live as nomads while others have recently settled, the research team investigated whether this association would have the same implications in different environments.

While those with the DRD4/7R allele were better nourished in the nomadic population, they were less well-nourished in the settled population. Although the effects of different versions of dopamine genes have already been studied in industrialized countries, very little research has been carried out in non-industrial, subsistence environments like the areas where the Ariaal live, despite the fact that such environments may be more similar to the environments where much of human genetic evolution took place.

Eisenberg explains, "The DRD4/7R allele has been linked to greater food and drug cravings, novelty-seeking, and ADHD symptoms. It is possible that in the nomadic setting, a boy with this allele might be able to more effectively defend livestock against raiders or locate food and water sources, but that the same tendencies might not be as beneficial in settled pursuits such as focusing in school, farming or selling goods".

Monday, October 13, 2008

Failure of magnesium to maintain self-administration in cocaine-naive rats.

Failure of magnesium to maintain self-administration in cocaine-naive rats.:

"Title: Failure of magnesium to maintain self-administration in cocaine-naive rats.
Author: Kantak, K M : Bourg, J F : Lawley, S I
Citation: Pharmacol-Biochem-Behav. 1990 May; 36(1): 9-12


Abstract: Previous research has shown that magnesium interacts with cocaine in such a way that it potentiates its action in a variety of behavioral situations. More recently, it has been demonstrated that magnesium will dose dependently substitute for cocaine self-administration and reduce the intake of cocaine. It is of considerable interest to determine if magnesium would be self-administered in cocaine-naive animals. The results of two experiments demonstrate that magnesium is not self-administered by cocaine-naive rats since although responding for magnesium chloride is above hypertonic saline control levels on day 1 of access, this responding is not maintained on subsequent days, does not occur in a regularly spaced pattern over time, and is not inversely related to dose. Taken together these data indicate that magnesium is a substitute for cocaine that has low abuse potential."

Magnesium Reduces cravings- sweets, heroin and cocaine

I have been reading about magnesium lately! Fascinating stuff. It is low in people with diabetes, ADD, migranes, leg cramps, depression, and more. Low magnesium causes carb cravings. Women having PMS are low in magnesium, and crave chocolate, which is high in magnesium. Lots of calcium drives magnesium out of the body, so balance out your supplements. Coffee, alcohol, stress, diabetes, diuretics and carbs lower magnesium.

Healthnotes Newswire: Magnesium Reduces Opiate Dependency and Cocaine Cravings - Medfinds

Magnesium Reduces Opiate Dependency and Cocaine Cravings

By Darin Ingels, ND

Healthnotes Newswire (August 14, 2003)?People addicted to opiate drugs, such as heroin and morphine, may be able to reduce their use by taking oral magnesium, according to a new study in Journal of Addictive Diseases (2003;22:49?61). Magnesium may also help cocaine addicts experience fewer cravings for the drug, although it is not clear that it reduces cocaine use.
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Mineral deficiencies. In addition to magnesium, deficiencies of the minerals zinc and chromium may contribute to food cravings, too. Simontacchi says that if you find yourself craving carbohydrates, you may be deficient in zinc. Sugar cravings may indicate a chromium deficiency.

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http://en.wikipedia.org/wiki/Hypomagnesemia