A new study has found that fructose may be the insidious ingredient that drives human metabolism toward obesity.
Although it is not the largest source of calories, it leads to the desire to eat fatty foods in larger quantities, which leads to overeating.
The analysis, led by Dr. Richard Johnson of the University of Colorado Anschutz Medical Campus, revealed that the best way to lose weight is to reduce the intake of sugars and carbohydrates together.
“Although all hypotheses acknowledge the importance of limiting ultra-processed foods and ‘junk food,’ it remains unclear whether the focus should be on reducing sugar intake, or high-glycemic carbohydrates,” the research team wrote. Or fats, or polyunsaturated fats, or simply increasing your protein intake.”
Fructose is a type of sugar that can be found naturally in fruits, which is balanced with the vitamins and fiber found in them. But it is also found in sweeteners such as table sugar and corn syrup in much higher quantities. The body can also make fructose from carbohydrates such as glucose and salty foods.
Johnson and his colleagues conducted a comprehensive study of all known contributing factors to obesity, and found that fructose metabolism in the body causes a decrease in a compound called adenosine triphosphate (ATP), which provides energy for cellular processes in the body.
When ATP decreases significantly, this is a signal to your body that you need more energy, which makes you hungry, so you eat. This is what researchers call the fructose survival hypothesis, and it links different theories about the causes of obesity, even ones that seem largely incompatible, such as eating fat versus eating carbohydrates.
“Basically, these theories, which place a series of metabolic and nutritional factors at the center of the obesity epidemic, are all pieces of the puzzle united by a final piece: fructose, which pushes our metabolism into low-energy mode and loses appetite control,” Johnson says. Fatty foods become the main source of calories that lead to weight gain.”
Fructose only mimics a low-energy state by reducing ATP in the body’s cells, even when there is plenty of energy available in the form of stored fat. It essentially prevents the body from utilizing that stored energy.
The results represent an important step in resolving this escalating health crisis.
Publish the research in Obesity .
An experimental treatment fights untreatable brain cancer with a modified herpes virus
An experimental gene therapy using a modified herpes virus has shown promise as a treatment for brain cancer, according to a new study.
A phase 1 study by scientists at Brigham and Women’s Hospital in Boston, Massachusetts, found evidence that the herpes simplex virus can trigger a response in the body that will trigger a person’s immune system to attack brain cancer cells.
The treatment, called CAN-3110, is modified to ensure that healthy cells are not killed as well.
“Unlike other treatments to date, we were able to show that a single time-point administration of CAN-3110 is enough to activate the patient’s immune cells traffic and fight the cancer, and we showed that this correlates with Survival responses.
In fact, brain cancers are difficult to treat, as traditional cancer treatments such as chemotherapy and radiation often cannot rid the body of all types of cancer. Glioblastoma (GBM), one of the most deadly types of cancer, is incurable, with an average of Survival time is about eight months.
In the laboratory, his team designed a tumor-selective biological agent based on the herpes virus. The idea was that this could be injected into glioblastoma patients to “reshape” the glioblastoma to make it less able to evade the patient’s immune cells.
The treatment contains a gene called ICP34.5, which helps the herpes virus cause illness in humans through cold sores or genital herpes.
Scientists believe that this gene is key to triggering a strong enough immune response to brain cancer cells.
In a phase 1 study published in Nature, the team gave 41 patients with recurrent glioblastoma a single dose of CAN-3110.
The main goal of the phase I trials was to ensure that the drug was safe and well-tolerated. However, two patients had a seizure, which was likely related to the drug.
Nearly two-thirds of the participants had antibodies to herpes virus from previous infections. However, the team found that even in patients with existing antibodies, CAN-3110 treatment boosted the immune system’s response to the cancer.
The team measured the enhanced immune response by measuring the level of T cells, a type of immune cell, that increased.
The average survival rate for the group with antibodies was about 14 months, while those who had not previously been exposed to herpes had a survival rate of eight months, which is the average survival rate for glioblastoma.
More studies are needed to determine whether CAN-3110 could be an effective treatment for brain cancer, especially in people who do not have antibodies to herpes, and the team is now working on a study to give patients multiple doses of the treatment over four months.