High-fructose corn syrup is the primary source of calories in the United States. In addition to containing mercury, a known carcinogen, cancer cells actually feed on high-fructose corn syrup after it is metabolized by the liver. A new study, published in the Expert Opinion on Therapeutic Targets, examined the link between refined sugar and cancer. The results add further evidence to the reports of many health experts and scientific studies that have drawn the connection between excess sugar consumption and the development of cancer.

The researchers highlighted the numerous ways in which fructose directly contributes to cancer risk and other health problems, including:

• DNA damage
• Inflammation
• Altered cellular metabolism
• Increased production of free radicals

According to Lewis Cantley, director of the Cancer Center at Beth Israel Deaconess Medical Center at Harvard Medical School, as much as 80 percent of all cancers are “driven by either mutations or environmental factors that work to enhance or mimic the effect of insulin on the incipient tumor cells.”

 Importantly, fructose and glucose metabolism are quite different … These findings show that cancer cells can readily metabolize fructose to increase proliferation.

What is even more concerning is that the scientists conducting the research used pancreatic cancer cells, widely considered to be the most deadly form of cancer. The discovery was monumental because not only did the researchers prove that tumor cells feed on sugar (glucose), but the tumor cells used fructose for cell division in order to speed up the growth and spread of the cancer. Fructose consumption actually led to a massive increase in tumor cell growth and proliferation way beyond that of glucose.

This cancer-feeding fructose is what the majority of Americans are consuming on a daily basis, to the point where high-fructose corn syrup is their number one source of calories. Even children are consuming excessive amounts of sugar in juice boxes, candy, and even ‘healthy’ sports beverages. The amount is so extreme that the average American consumes around 150 grams of sugar each day; whereas, many experts believe that the number should be around 15 grams per day or lower to prevent cancer.

The ubiquitous nature of fructose is so apparent in the food supply that it can be found in one form or another in 5 of the top 10 sources of calories in America, according to a USDA report. As cancer rates continue to explode, it is vital that dietary changes are made involving the emission of fructose from the global food supply. Natural sweeteners like Stevia contain 0 calories, and have been found to prevent and reverse diseases like diabetes. It is time we revolutionize the food supply and utilize natural sweeteners as tools to reduce cancer and obesity rates worldwide, naturally.

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Stevia is a favorable alternative to sugar for many health-conscious individuals, but new research has indicated that it may also help to prevent and reverse diabetes.  Examining the effects of Stevia leaf extract on diabetic rats, the extract was administered orally for 10 days. Amazingly, the treatment led to a reduced blood glucose level, without producing hypoglycemia.

The rats also were found to have lost body weight, showing the natural fat loss effects of Stevia.

The abstract of the study states:

Treatment of diabetes with sulfonylurea drugs (glibenclamide) causes hypoglycemia followed by greater reduction in body weight, which are the most worrisome effects of these drugs. Stevia extract was found to [have] … a revitalizing effect on β-cells of pancreas.

For the first time, scientists have transformed skin cells into functional nerve cells.

“A major goal in regenerative medicine is the facile generation of human neurons for cell replacement therapeutics or disease modeling,” the leader of the study and colleagues wrote in the Aug. 4 online issue of Cell

Medpage today reports:

The battle over the ethics of stem cell use in research led to a search for alternative sources of pluripotent cells — those that can differentiate into any type of cell.

One such technique involves genetic programming of skin cells into an intermediate pluripotent state, from which the cells can subsequently be converted to neuronal cells.

However, the process of transforming fibroblasts into this intermediate pluripotent state is inefficient, with only 1% of cells being converted, and the intermediate state itself is associated with DNA alterations and tumorigenesis.

So Abeliovich’s group sought to skip the intermediate step and transform the cells directly.

Once they determined that the fibroblasts had been converted to a neuronal phenotype through expression of genetic markers, they performed electrophysiologic testing and found that the transformed cells demonstrated the sodium, calcium, and potassium channel activity typical of neuronal cells.

The neuronal cells also exhibited resting membrane potentials of −67 mV to −32 mV, which is also characteristic.

The researchers next transplanted labeled human-derived neuronal cells into the brains of embryonic mice, and demonstrated the integration of the neural cells into the murine neural circuitry by immunostaining using an antibody to a human neural cell adhesion molecule.

Finally, “as proof of principle” for the use of these transformed neuronal cells in human neurodegenerative disease, they cultured fibroblast cells from patients with familial Alzheimer’s disease carrying mutations in the presenilin (PSEN)-1 or -2 genes.

These two genes encode for proteins involved in the γ-secretase enzyme system through which amyloid precursor protein is cleaved to Aβ.

The neuropathology of Alzheimer’s disease is characterized by the presence of plaques consisting of fragments of this amyloid precursor protein, with an increased ratio of Aβ42 fragments to Aβ40 fragments, the researchers explained.

This “amyloid hypothesis” of Alzheimer’s disease “proposes that modified cleavage of [amyloid precursor protein] by β-secretase and γ-secretase leads to the generation of a pathogenic Aβ42 fragment,” they wrote.

In these cell cultures from familial Alzheimer’s patients, the researchers observed a marked increase in the Aβ42/Aβ40 ratio compared with cultures from unaffected individuals (P<0.001).

Combining all the cell lines from Alzheimer’s patients found a significant and amplified increase in the Aβ42/Aβ40 ratio (P<1 ×10⁻⁹).

In comparison, the Aβ42/Aβ40 ratio in cell lines from unaffected individuals was not increased (P>0.05).

These in vitro findings were “consistent with patient brain pathology,” in Alzheimer’s patients, they observed.

The results of these experiments in which fibroblasts can be directly transformed into neuronal cells should provide researchers with an opportunity for in vitro exploration of other abnormalities associated with Alzheimer’s disease, such as in synaptic function.

And future murine experiments can focus on actually testing the therapeutic effects of integration of the induced human neuronal cells, Abeliovich and colleagues predicted.

They noted that a limitation of their work is that thus far they have only analyzed two of the PSEN mutations, and that there are many others that could yield further information.

Researchers at the MIT-Harvard Division of Health Sciences and Technology (HST) found a way to encapsulate living cells and arrange them into 3-D structures.

The living cells are formed into cubes, and stacked on top of each other like building blocks. The blocks of cells are kept together by a gel-like substance. The process has been named “micromasonry,” as it is similar to practice of masonry.

Before the new technique was discovered, scientists were unsuccessful in getting the cells to grow in 3-D shapes. The cells that grew in lab dishes ultimately ended up in flat layers, contrary to what the scientists had hoped for. While the technique makes it possible to create 3-D artificial tissue, it is a challenging task. To obtain single cells that are necessary to the process, scientists must use enzymes to break the original tissue apart. These enzymes digest the extracellular material, which is responsible for holding the cells together.

Jennifer Elisseeff, associate professor of biomedical engineering at Johns Hopkins University, praised the tiny cell blocks. “They’re very elegant and have a lot of flexibility in how you grow them,” she said.
After this process is complete, it is very difficult to assemble the free cells into a 3-d structure that is similar to the composition of the natural tissue. Scientists have been successful in building simple tissues. Such simple tissues include cartilage, skin, and bladder using biodegradable foam scaffolds.

Ali Khademhosseini, assistant professor of HST, says that such methods do not yield tissues with the same complexity as normal tissues. “You don’t get tissues with the same complexity as normal tissues,” he says.

Other researchers have developed a technique called organ printing to assemble 3-D tissues, but it requires machinery that is not often used. This makes the building blocks technique stand out, as it does not require special equipment.

“You can reproduce this in any lab,” former HST postdoctoral associate Javier Gomez Fernandez.

The new technique allows for artificial tissue to be created without expensive technology, signifying the possibility of artificial tissue being assembled abundantly.

“The short-term next step is really looking at different cell types and the viability of tissue growth,” says Jennifer Elisseeff, associate professor of biomedical engineering at Johns Hopkins University.

The researchers hope to discover the uses of different polymers that may be able to replace PEG (Polyethylene glycol), a popular polyether compound used in medicine. The researchers are looking for a polymer that may offer more control over cell placement.

Sources:

Geoffrey M. Spinks, Seon Jeong Kim et al. Tough Supersoft Sponge Fibers with Tunable Stiffness from a DNA Self-Assembly Technique. Angewandte Chemie International Edition, DOI: 10.1002/anie.200804788