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.

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.


Immunoendocrine Abnormalities in Narcolepsy

Immunoendocrine Abnormalities in Narcolepsy Elsevier Article Locator

Narcolepsy is a sleep disorder emerging in early adulthood on an HLA-related genetic background. Through unresolved pathways, involving the destruction or silencing of specific cells in the lateral hypothalamus, a deficiency of orexin production occurs. An autoimmune process targeting orexin-producing cells may cause acquired orexin deficiency. Abnormalities in cytokine production reported in narcolepsy unspecifically support this idea, but empirical evidence for a causative role of immunopathology is lacking. Orexin deficiency affects neuroendocrine and neurotransmitter systems leading to reduced stability of and/or disturbed transitions between wakefulness, REM, and nonREM sleep. However, narcolepsy is rather a complex neuroendocrine disorder rather than a pure sleep disorder because orexin deficiency induces endocrine and metabolic disturbances such as obesity and diabetes.

Cut the Carbs to Stay Awake | Bastyr Center for Natural Health

Cut the Carbs to Stay Awake | Bastyr Center for Natural Health

Cut the Carbs to Stay Awake

People with narcolepsy, a debilitating nervous-system disorder that causes excessive daytime sleepiness, may benefit from eating a low-carbohydrate diet, according to a study in Neurology (2004;62:2300–02).

People with narcolepsy may have “sleep attacks” that cause them to involuntarily fall asleep during activities. They may also have episodes of paralysis or muscle weakness (such as jaw drop, slurred speech, and buckling of the knees), paralysis while sleeping, and vivid dreams and sounds when they first fall asleep. Symptoms usually start between the ages of 15 and 30 years. While the cause is not fully understood, results of new research suggest that a deficiency of a chemical called hypocretin may be associated with the disease. Hypocretin is a chemical messenger (neurotransmitter) produced in the brain that plays a role in the regulation of sleep and appetite. People with narcolepsy have 85 to 95% fewer hypocretin-producing cells than do people without the disorder. Stimulant medications such as dextroamphetamine (Dexedrine™) and methylphenidate (Ritalin™) are used to decrease sleepiness in people with narcolepsy. Although they provide some benefit, these drugs may cause insomnia, high blood pressure, and headaches. A newer drug called modafinil (Provigil™) increases alertness with fewer side effects than other stimulant medications. Imipramine (Tofranil™) and fluoxetine (Prozac™) are antidepressants used to treat muscle weakness and paralysis, vivid dreams, and sleep paralysis. These medications are helpful for some people, but may be associated with side effects such as anxiety, fatigue, and sexual dysfunction.

Eating carbohydrates is thought to aggravate sleepiness in narcoleptics, though the role of diet in the management of narcolepsy has not been fully investigated. The new study examined the effect of a low-carbohydrate, high-protein, high-fat diet on daytime sleepiness in people with narcolepsy. For eight weeks, the eight participants were instructed to follow the dietary guidelines in the book Dr. Atkins’ New Diet Revolution, which included consuming less than 20 grams of carbohydrates per day. Narcolepsy symptoms were assessed by the participants using self-administered rating scales at the start of the study and at weeks two, four, and eight. Blood pressure and blood fats were measured at the beginning and end of the study.

The total score on the Narcolepsy Symptoms Severity Questionnaire improved by 18% over the eight-week study period. Specifically, the amount of sleepiness, number of sleep attacks, and frequency of sleep paralysis improved significantly. Blood pressure and blood fat levels were not adversely affected by the diet, and only a few minor side effects were experienced, such as headaches and leg cramps.

In addition to its beneficial effect on narcolepsy, the Atkins diet has also recently been found to help some people with epilepsy.