High Fructose Death Syrup Causes Low Energy and Fatty Liver

It is a testament to Pavlov and his dogs that the average American is dumb enough to consume 35 pounds of high fructose death syrup every year.  The Corn Refiners Association loves to say that their death syrup is no different than any other sugar.  Two recent studies prove that is not true and also prove that the death syrup uniquely causes fatty liver disease, which is a key marker of metabolic malfunction.  Even the FDA is onto the charade, denying a petition from the Corn Refiners Association to change food labels from “high fructose corn syrup” to innocent sounding “corn sugar.”

The public has a great deal of confusion on this topic because fructose is also the sugar naturally contained in fruit.  The new information helps explain why excess consumption of high fructose corn syrup creates metabolic problems; it turns one’s liver fatty and increases the risk for becoming a “metabolic cripple” when higher levels of fructose intake continue as problems are occurring.

Clearly, the preferred intake of fructose is from fruit (never high levels of fruit juice).  Fruit is a comprehensive nutritional package that also contains flavonoid antioxidants, magnesium, potassium, vitamin C, and fiber – along with a modest amount of fructose.  In comparison, most manufactured products containing large amounts of high fructose corn syrup have little nutritional value. Instead, they contain a branded flavor that is full of addictive chemical stimulants.  The goal for manufacturers is to create brand addiction, resulting in the powerful subconscious urge to consume more of their brand, which leads to massive overconsumption of fructose. 

The interesting thing about fructose is that unlike other sugar molecules it actually requires ATP (energy) to be metabolized.  At the same time the fructose molecule could potentially become energy as it is metabolized, leading to increased ATP synthesis.  When healthy people eat fruit, this happens.  Unfortunately, consuming high fructose corn syrup in excess is like flooding your engine with gas.  Your liver simply conks out.  Energy is actually depleted.  And enzymes are activated that turn on fat buildup in the liver while elevating uric acid to a point that it causes free radical damage and inflammation.  This is a fast path to obesity, fatty liver disease, type 2 diabetes, and cardiovascular disease.

Two studies show the results of high fructose corn syrup intake.  The first is an animal study that analyzed how fructose is metabolized.  It shows that fructose is first acted upon by the fructokinase enzyme, which adds energy (ATP) to the fructose molecule so that it can proceed in metabolism.  As it turns out there are two forms of this enzyme, fructokinase A and C.  Fructokinase A operates around the body and has a low affinity for fructose, meaning that when eaten in moderation this enzyme will slowly and steadily help metabolize the fructose.  Fructokinase C is highly concentrated in the liver and loves fructose.

These researchers showed that if both enzymes were knocked out in mice then they couldn’t develop metabolic syndrome from any amount of fructose metabolism because none of the fructose was metabolized.  Then they showed that mice lacking the A form rapidly developed insulin resistance, fatty liver, and metabolic syndrome.  They went on to show that the A form balances and protects against the potential adverse effects of the C form, but only at moderate intake.  At high intake the A form, which has low affinity for fructose, is no longer able to maintain balance and the C form goes wild.  This study is extremely important as it is the first to show this precise mechanism explaining why high intake of fructose is problematic.

The next study involved human type 2 diabetic patients and their ability to metabolize fructose.  The researchers used less than 15 grams of fructose per day to define low and more than 15 grams per day to define high fructose intake.  Please note that the average American consumes about 42 grams per day to get to 35 pounds a year. 

Diabetic patients who consumed more than 15 grams of fructose had lower stores of liver ATP, meaning liver energy function was compromised as predicted by the above animal study mechanism.  Furthermore, a fructose challenge resulted in further decreased energy production, meaning that the people were metabolic cripples when it now came to the fructose they were consuming in high amounts.  The degree of the fructose metabolism problem predicted fatty liver disease and its severity, as well as higher than normal levels of uric acid, which is highly inflammatory to the liver and general circulation. 

High fructose corn syrup is the fastest way to get large and excess amounts of fructose into your body.  It is clear that this compromises your liver’s energetic function, which will take its toll sooner or later.  The first sign of a problem is weight gain.  If not corrected, liver damage and malfunction follow, locking in metabolic disease.  This is not a pretty picture.

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Curry spice, omega-3 fatty acid preserve walking ability following spinal-cord injury

ScienceDaily (June 26, 2012) — UCLA researchers discovered that a diet enriched with a popular omega-3 fatty acid and an ingredient in curry spice preserved walking ability in rats with spinal-cord injury. Published June 26 in the Journal of Neurosurgery: Spine, the findings suggest that these dietary supplements help repair nerve cells and maintain neurological function after degenerative damage to the neck.

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"Normal aging often narrows the spinal canal, putting pressure on the spinal cord and injuring tissue," explained principal investigator Dr. Langston Holly, associate professor of neurosurgery at the David Geffen School of Medicine at UCLA. "While surgery can relieve the pressure and prevent further injury, it can't repair damage to the cells and nerve fibers. We wanted to explore whether dietary supplementation could help the spinal cord heal itself."

The UCLA team studied two groups of rats with a condition that simulated cervical myelopathy -- a progressive disorder that often occurs in people with spine-weakening conditions like rheumatoid arthritis and osteoporosis. Cervical myelopathy can lead to disabling neurological symptoms, such as difficulty walking, neck and arm pain, hand numbness and weakness of the limbs. It's the most common cause of spine-related walking problems in people over 55.

The first group of animals was fed rat chow that replicated a Western diet high in saturated fats and sugar. The second group consumed a standard diet supplemented with docosahexaenoic acid, or DHA, and curcumin, a compound in turmeric, an Indian curry spice. A third set of rats received a standard rat diet and served as a control group.

Why these supplements? DHA is an omega-3 fatty acid shown to repair damage to cell membranes. Curcumin is a strong antioxidant that previous studies have linked to tissue repair. Both reduce inflammation.

"The brain and spinal cord work together, and years of research demonstrate that supplements like DHA and curcumin can positively influence the brain," said coauthor Fernando Gomez-Pinilla, professor of neurosurgery. "We suspected that what works in the brain may also work in the spinal cord. When we were unable to find good data to support our hypothesis, we decided to study it ourselves."

The researchers recorded a baseline of the rats walking and re-examined the animals' gait on a weekly basis. As early as three weeks, the rats eating the Western diet demonstrated measurable walking problems that worsened as the study progressed. Rats fed a diet enriched with DHA and curcumin walked significantly better than the first group even six weeks after the study's start.

Next, the scientists examined the rats' spinal cords to evaluate how diet affected their injury on a molecular level. The researchers measured levels of three markers respectively linked to cell-membrane damage, neural repair and cellular communication.

The rats that ate the Western diet showed higher levels of the marker linked to cell-membrane damage. In contrast, the DHA and curcumin appeared to offset the injury's effect in the second group, which displayed equivalent marker levels to the control group.

Levels of the markers linked to neural repair and cellular communication were significantly lower in the rats raised on the Western diet. Again, levels in the animals fed the supplemented diet appeared similar to those of the control group.

"DHA and curcumin appear to invoke several molecular mechanisms that preserved neurological function in the rats," said Gomez-Pinilla. "This is an exciting first step toward understanding the role that diet plays in protecting the body from degenerative disease."

"Our findings suggest that diet can help minimize disease-related changes and repair damage to the spinal cord," said Holly. "We next want to look at other mechanisms involved in the cascade of events leading up to chronic spinal-cord injury. Our goal is to identify which stages will respond best to medical intervention and identify effective steps for slowing the disease process."

Holly's and Gomez-Pinilla's coauthors included Dr. Donald Blaskiewicz, Aiguo Wu, Cameron Feng and Zhe Ying, all of UCLA. Their research was supported by grants from the National Institutes of Health (RO1 NS056413) and the Craig H. Neilsen Foundation.

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Pictures of Fatty, Sugary Foods May Spur Cravings

HealthDay – 31 mins ago WEDNESDAY, June 27 (HealthDay News) -- Looking at pictures of hamburgers, cupcakes and other high-calorie edibles can trigger cravings for fattening foods, especially if you're drinking something sweet at the time, according to a new study.

Researchers from the University of Southern California found that drinking a sugary beverage while viewing these foods activates appetite and reward centers in the brain, which could play a role in obesity.

"Studies have shown that advertisements featuring food make us think of eating, but our research looked at how the brain responds to food cues and how that increases hunger and desire for certain foods," said the study's principal investigator, Kathleen Page, assistant professor of clinical medicine at the university's Keck School of Medicine, in a university news release.

"This stimulation of the brain's reward areas may contribute to overeating and obesity, and has important public health implications," said Page.

In conducting the study, the researchers measured the brain responses of 13 obese, Hispanic females, aged 15 to 25 years, as they looked at both high-calorie and low-calorie foods.

Using functional magnetic resonance imaging (fMRI), the women's brains were scanned twice as they viewed images of foods such as hamburgers, cookies, cakes, fruits and vegetables.

After seeing all of the images, they were asked to rate their hunger as well as their desire for sweet or savory foods.

Halfway through the scans, the women drank 50 grams of glucose, which is similar to drinking a can of sugary soda. In a separate instance, they drank 50 grams of fructose. Glucose and fructose are found in table sugar and high-fructose corn syrup.

"We hypothesized that the reward areas in the women's brains would be activated when they were looking at high-calorie foods, and that did happen," said Page. "What we didn't expect was that consuming the glucose and fructose would increase their hunger and desire for savory foods."

The researchers pointed out that fructose resulted in more intense cravings and hunger among the women than glucose.

"Our bodies are made to eat food and store energy, and in prehistoric days, it behooved us to eat a lot of high-calorie foods because we didn't know when the next meal was coming," Page said.

"But now we have much more access to food, and this research indicates added sweeteners might be affecting our desire for it," she added in the news release.

The researchers said they limited the study to Hispanic women because research has indicated women are more sensitive to food cues, and the Hispanic community has a high incidence of obesity and type 2 diabetes.

More studies are needed to explore whether these cravings are due to obesity or genetics, the authors noted.

The study was presented Tuesday at the Endocrine Society's annual meeting in Houston. Data and conclusions of research presented at meetings should be considered preliminary until published in a peer-reviewed medical journal.

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The U.S. National Library of Medicine provides tips on how to tame food cravings.

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Fatty acid found in fish prevents age-related vision loss, study suggests

ScienceDaily (May 30, 2012) — An omega-3 fatty acid found in fish, known as DHA, prevented age-related vision loss in lab tests, according to recent medical research from the University of Alberta.

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Yves Sauvé, a researcher in the Faculty of Medicine & Dentistry, and his team discovered that lab models fed DHA did not accumulate a toxic molecule at the back of the eyes. The toxin normally builds up in the retina with age and causes vision loss.

"This discovery could result in a very broad therapeutic use," says Sauvé, whose work was recently published in the peer-reviewed journal Investigative Ophthalmology & Visual Science.

"In normal aging, this toxin increases twofold as we age. But in lab tests, there was no increase in this toxin whatsoever. This has never been demonstrated before -- that supplementing the diet with DHA could make this kind of difference."

The team recently started another study, looking at people who have age-related macular degeneration, a condition that results in loss of central vision and is the main cause of blindness in people over the age of 50. The researchers will look for DNA markers in the blood of study participants. The team wants to determine whether participants with certain genetic markers will respond better to increasing amounts of DHA in their diet, and if so, why.

Sauvé is a researcher in the departments of ophthalmology and physiology at the U of A.

Various organizations funded the research; the primary funder was the Canadian Institutes of Health Research.

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Soy protein alleviates symptoms of fatty liver disease, study suggests

ScienceDaily (Apr. 22, 2012) — University of Illinois researchers have shown how soy protein could significantly reduce fat accumulation and triglycerides in the livers of obese patients by partially restoring the function of a key signaling pathway in the organ.

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Hong Chen, an assistant professor of food science and human nutrition at the University of Illinois, presented her team's findings on April 22, at the annual meeting of the American Society for Biochemistry and Molecular Biology, held in conjunction with the Experimental Biology 2012 meeting in San Diego.

"Almost a third of American adults have fatty liver disease, many of them without symptoms," Chen explained. "Obesity is a key risk factor for this condition, which can lead to liver failure."

Fat is metabolized in the liver, and in those who are obese the transport of fat to adipose tissue can slow down to the point at which the liver becomes a dumping ground for excess fat, she said.

"When fat accumulates in an organ that's not supposed to store fat -- like the liver, that organ's vital function can be dangerously compromised," she noted.

Eating soy protein, from such sources as tofu and yogurt, appears to alleviate some of the stress on fatty livers, Chen said. For her study, Chen compared fat accumulation in the livers of lean and obese rats, which were assigned to either a diet containing casein, a milk-based protein, or a diet containing soy protein, for 17 weeks after weaning.

While diet had no effect on the liver profiles of lean animals, the obese rats that were fed soy showed a 20 percent reduction in triglycerides and overall fat accumulation in the liver, leading Chen to believe that soy protein could be used to alleviate the symptoms of fatty liver disease.

Furthermore, the scientists discovered that soy protein isolate partially restored the Wnt/β-catenin signaling pathway, a crucial player in fat metabolism. "In many obese persons, there's a sort of traffic problem, and when more fat can make its way out of the liver, there is less pressure on that organ," Chen said.

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