Wellness

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Fasting could provide "enormous potential" in managing or preventing inflammation which is thought to contribute to type 2 diabetes, US researchers have said.

A team from the Mount Sinai hospital report that fasting also improves chronic inflammatory diseases such as cancer, multiple sclerosis and cardiovascular disease.

Fasting has been shown to help lower HbA1c in people with type 2 diabetes, with a study published last month also showing that intermittent fasting could prevent a build-up of fat in the pancreas that could protect against type 2 diabetes.

"Caloric restriction is known to improve inflammatory and autoimmune diseases, but the mechanisms by which reduced caloric intake controls inflammation have been poorly understood," said senior author Dr Miriam Merad, Director of the Precision Immunology Institute at the Icahn School of Medicine at Mount Sinai.

To understand the mechanisms behind fasting more clearly, Dr Merad and colleagues tested the effects of fasting on both human and mouse cells.

They discovered that intermittent fasting kick-started the release of 'monocytes', a collection of pro-inflammatory cells. During fasting periods these cells go into sleep mode and are less inflammatory than the cells that had been fed.

"Monocytes are highly inflammatory immune cells that can cause serious tissue damage, and the population has seen an increasing amount in their blood circulation as a result of eating habits that humans have acquired in recent centuries," explained Dr Merad.

The number of these monocytes was significantly reduced following fasting, which researchers say emphasises the link between high-calorie dietary patterns and inflammatory disease outcomes.

"Considering the broad spectrum of diseases that are caused by chronic inflammation and the increasing number of patients affected by these diseases, there is an enormous potential in investigating the anti-inflammatory effects of fasting," said first author Stefan Jordan, a postdoctoral fellow in the Department of Oncological Sciences at Mount Sinai.

The study findings have been published in the Cell journal.

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First Opinion

Transplanting islet cells can fix brittle diabetes. Why isn’t it available in the U.S.?

By Camillo Ricordi and Anthony Japour

August 27, 2019

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APStock

The term “type 1 diabetes” generally conjures up images of insulin. That makes sense, because insulin is the main treatment for this common disease. But it isn’t a cure. A type of cell transplant that comes close to a cure for some people with type 1 diabetes, a technique pioneered and tested in the United States, is now available in many countries but is still deemed an experimental procedure in the U.S., making it almost impossible to get.

That doesn’t make sense to us.

Type 1 diabetes, which affects 1.25 million American children and adults, and more than 20 million people around the world, is a challenging chronic disease caused by the body’s inability to make insulin. Among its most severe forms is brittle diabetes. People with brittle diabetes frequently experience large swings in blood sugar that can quickly move from too high to too low or vice versa. Severely low blood sugar, called hypoglycemia, can cause sudden and unexpected seizures, coma, heart attacks, and even death.

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Insulin is made by specialized cells in the pancreas called islet cells. Transplanting these cells from a donated pancreas to an individual with brittle diabetes can restore the recipient’s ability to naturally produce insulin. The procedure has a record of effectiveness. A Phase 3 clinical trial sponsored by the National Institutes of Health, for which one of us (C.R.) was an investigator, showed that such transplants worked in 80% to 90% of the patients treated in eight centers in North America. The procedure virtually eliminated the risk of life-threatening hypoglycemia one and two years after the transplant. As with other types of transplant, the recipient must take anti-rejection drugs.

Related:

One-quarter of people with diabetes in the U.S. are rationing their insulin

Individuals with brittle diabetes in Canada, Europe, Asia, and Australia can receive islet cell transplants, much the same way that individuals who need new hearts or livers can receive transplants. Islet cell transplants are even performed in China and Iran, whose doctors came to the U.S. to learn the technique and carried it back home. So why is this successful procedure, which can vastly improve the lives of those living with brittle diabetes, available in the U.S. only after a convoluted process that is often impossible to complete?

If a patient needed a pancreas transplant (which would include islet cells), he or she would be registered on the national organ transplant list and, once a pancreas became available, would receive the transplant, which is generally paid for by insurance.

But for a less-invasive islet cell transplant, an institution that wants to perform the procedure must file an investigational new drug application with the Food and Drug Administration, a very challenging process — and also figure out how to pay for the transplant.

That’s due to the way the FDA interprets the code of federal regulations; specifically the criteria of minimal manipulation of human cells, tissues, and cellular and tissue-based products.

After islet cells are extracted from a donated pancreas, they need to sit in a culture medium at a temperature between 72 and 75 degrees Fahrenheit for two to three days. This gives the transplant team time to perform quality controls on the cells, and also to prepare the recipient for the transplant.

The FDA has interpreted the brief hiatus for islet cells as going beyond minimal manipulation, a concept based on the premise that processing cells does not alter their relevant biological characteristics. The hibernation process for islet cells does not change the cells’ characteristics or increase their number, both of which occur with the manipulation of advanced stem cell therapies, which reasonably need extra scrutiny.

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The European Medicines Agency has determined that transplanting pancreatic islet cells should just follow the standard rules of organ transplantation, even though the cells require a brief hibernation period. This recommendation is based in part on its view that transplanting a pancreas, with islet cells intact, is an organ transplant, so there is no reason to treat transplantation of just the islet cells as anything different.

Because of the benefits to the thousands of Americans with brittle diabetes, there is a strong incentive to harmonize the FDA’s approach to islet cell transplantation with the EMA’s approach.

More than a decade ago, the United Kingdom’s National Health Service approved islet cell transplantation for type 1 diabetes — an approval based on an extensive review of the evidence generated by clinical trials conducted in the United States. Our federal dollars supported that research, and this treatment ought to be available to U.S. citizens.

Islet cell transplantation is not a panacea for all forms of type 1 diabetes. And transplantation of any organ, including islet cells, requires the use of anti-rejection drugs that can have a range of adverse side effects. That said, individuals with severe brittle diabetes who are fully informed of the risks and benefits should have the ability to access this lifesaving treatment option.

We fully understand the FDA’s efforts to rein in companies marketing unapproved stem cell products that have little or no evidence to support their use and that may put patients at risk. Yet the FDA should stay equally focused on its commitment to approving evidence-based transformative treatments for devastating diseases and conditions, including brittle diabetes.

Camillo Ricordi, M.D., is professor of surgery and medicine and chief of the Division of Cellular Transplantation at the University of Miami Miller School of Medicine, where he has directed the Diabetes Research Institute and Cell Transplant Center since 1996. Anthony Japour, M.D., is a medical director at ICON plc. The views expressed are those of the authors and not those of the University of Miami or ICON.

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from MIT

Living drug factories” may one day replace injections

Startup develops implantable, encased cells that live in the body and secrete insulin and other therapeutics.

Rob Matheson | MIT News Office
May 16, 2018

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Patients with diabetes generally rely on constant injections of insulin to control their disease. But MIT spinout Sigilon Therapeutics is developing an implantable, insulin-producing device that may one day make injections obsolete.

Sigilon recently partnered with pharmaceutical giant Eli Lilly and Company to develop “living drug factories,” made of encapsulated, engineered cells that can be safely implanted in the body, and produce insulin over the course of months or even years. Down the road, cells may also be engineered to secrete other hormones, proteins, and antibodies.

The technology at Sigilon — based on research performed over the last decade at MIT — has led to creation of a device that encases cells and protects them from the patient’s immune system. This can be combined with engineered cells that produce a target therapeutic, such as insulin. The devices are tiny hydrogel beads, about 1 millimeter in diameter, that can be implanted into the patient through minimally invasive procedures.

“This allows us to have ‘living drug factories’ inside our bodies that can deliver therapeutics, at the right amount and in the right location, as needed,” says co-founder and co-inventor Daniel G. Anderson, an associate professor in MIT’s Department of Chemical Engineering, Institute for Medical Engineering and Science, and Koch Institute For Integrative Cancer Research. “The hope is that this living device can be placed in a patient, avoid the need for immune-suppression, and provide long-term therapy.”

Sigilon’s other co-founders and co-inventors are Robert Langer, the David H. Koch Institute Professor at MIT; José Oberholzer, a researcher and surgeon, director of the Charles O. Strickler Transplant Center, and professor of surgery and biomedical engineering at the University of Virginia; Arturo Vegas, a former MIT postdoc and now a professor of chemistry at Boston University; and Omid Veiseh, a former MIT postdoc and now a professor of bioengineering at Rice University.

Finding the right material

Today, most patients with diabetes will ****** their fingers several times a day to draw blood and test blood-sugar levels. When needed, they’ll inject insulin. It’s an effective treatment but is often dosed incorrectly, leading to uncontrolled blood sugar levels. “Even the most careful, hard-working diabetics have trouble doing it right, so they will often find their blood sugar is too high or too low,” Anderson says.

Another promising treatment, called cell therapy, has been around for decades. In this treatment, a patient receives transplanted human cells that secrete a protein, hormone, or other agent that’s needed to fight a disease or that the patient’s bodies can’t produce. Patients with diabetes, for instance, receive transplanted pancreatic beta cells, from cadavers, which sense blood sugar levels and produce insulin in response.

Some patients using this approach get long-term control of blood-sugar levels, and no longer need to inject insulin, Anderson says. However, these patients have to take immune suppressants, or their immune systems will reject and kill the foreign cells.

In more recent years, researchers have focused on cell encapsulation, surrounding transplanted cells in a thin polymer film to ward off the immune response but still nourish the cells. Such therapies have shown potential to treat cancer, heart failure, hemophilia, glaucoma, and Parkinson’s disease, among other diseases and conditions. But, so far, no treatments have made it to market.

In the mid-2000s, Julia Greenstein of the Juvenile Diabetes Research Foundation (JDRF) reached out to the MIT team for help developing new technological approaches toward islet cell encapsulation. This collaboration resulted in funding from JDRF and the Leona M. and Harry B. Helmsley Charitable Trust to MIT and Children’s Hospital Boston, to develop commercially viable cell-encapsulation technology for diabetes.

The issue was identifying the right material that protected cells but made them, essentially, invisible to the immune system. Most materials placed in the body lead to scar tissue accumulation, a process called “fibrosis.” When medical devices are covered in scar tissue, for instance, they become isolated from the body, which can block transfer of insulin and cause encapsulated cells to die.

The answer was to chemically modify alginate, a polysaccharide that lines the cell walls of brown algae. When combined with water, alginate can also be made into a gel that can safely encapsulate cells without limiting function. However, the researchers had to ensure the coating would not cause fibrosis. To do so, they attached different molecules to the alginate’s polymer chain, chemically modifying the structure hundreds of times until they found a version that didn’t provoke an immune response.

The end result: “A hydrogel that keeps cells alive and is permeable so that sugar and nutrients can come in and insulin can come out, but still blocks cellular elements of the immune system, like T cells, which can destroy the therapeutic cells inside,” Anderson says.

In three studies, published in Nature Materials in 2015 and in Nature Medicine and Nature Biotechnology in 2016, the researchers implanted cells encapsulated in their hydrogel into animals. They found the cells immediately produced therapeutic amounts of insulin in response to blood sugar levels and kept blood sugar under control over the course of a six-month study. They also found that small capsules of the hydrogel implanted in the subjects, which didn’t contain engineered cells, prevented fibrosis.

“There had been a growing collection of scientific work, taking different approaches to this problem,” Anderson says. “The key challenge was finding materials that avoid scar tissue formation.”

Just the beginning

Langer and Anderson launched Sigilon to commercialize the technology by setting up Sigilon headquarters in Cambridge, Massachusetts, with more than $23 million in venture capital.

In early April, Sigilon partnered with Lilly, a worldwide leader in diabetes care, to use Sigilon’s encapsulation technology, called Afibromer, to develop a treatment for type 1 diabetes. Under the agreement, Sigilon will receive an upfront payment of $63 million, an equity investment, and more than $400 million in milestone payments to take the Afibromer devices containing stem-cell-derived pancreatic beta cells through clinical trials.

But that’s just the beginning, Anderson says. “Lilly is a major player in diabetes treatment, and we will take this forward [to treat diabetes],” he says. “But we see this as technology that can be used for many applications.”

Sigilon is working on various other applications, including “sense and respond” therapies, where cells sense biological signals and respond with precise dosage of a target therapeutic. Engineered cells could, for instance, secrete proteins to treat lysosomal storage diseases, where patients lack enzymes to break down lipids or carbohydrates; treat hemophilia with hormone release; or respond to inflammatory mediators with anti-inflammatory proteins.

In the future, Sigilon’s polymer could also be modified as a coating for implanted medical devices, such as coronary stents or insulin pumps. “Wires and shunts and pumps all have problems with scar tissue formation,” Anderson says. “The more we connect things with the body, the more important it will be to have materials that can avoid fibrosis.”

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A scientist from City of Hope, an institution with expertise in both diabetes and cancer, will present research on why diabetes patients have an increased risk of developing some forms of cancer.
DUARTE, Calif. — Higher-than-normal blood sugar levels are linked to heightened DNA damage that is fixed less often, which could explain why people with diabetes have an increased risk of developing cancer, according to ongoing research led by City of Hope.
Genomic instability can cause and promote the progression of cancer, said John Termini, Ph.D., professor in the Department of Molecular Medicine at City of Hope, a world-renowned independent research and treatment center for cancer, diabetes and other life-threatening diseases. 
“As the incidence of diabetes continues to rise, the cancer rate will likely increase as well,” Termini said. “In an ironic twist of fate, some cancer treatments increase the risk of diabetes, which in turn increases the risk of cancer. The destructive machine feeds itself. That’s why City of Hope – best known for its leading-edge cancer therapies – has also taken on the challenge of finding a cure for diabetes.”
The diabetes and cancer link has been discussed in scientific circles for years; however, researchers are still searching for the disease-causing catalyst. We may be one step closer to finding it. Termini will present his ongoing research at the American Chemical Society (ACS) Fall 2019 National Meeting & Exposition on Aug. 25. He will be in Gallery 1 at the Omni San Diego Hotel at 10:35 a.m. He will elaborate on early findings at an ACS press conference on Aug. 26 at 3 p.m. (mezzanine level of the San Diego Convention Center, room 14B).
The link between diabetes and certain cancers may be due, in part, to shared risk factors such as aging, obesity, increased inflammation, dietary choices and inactive lifestyles. People with type 2 diabetes (the most common form) are 2.5 times more likely to develop liver or pancreatic cancer. They also run a higher-than-normal risk of developing colon, bladder and breast cancer. Diabetic women with breast cancer have a higher mortality rate than women with breast cancer alone. 
Conversely, some forms of chemotherapy induce insulin resistance, bringing on diabetic symptoms. Immunotherapy, one of the most exciting advances in cancer treatment, may bring on the less common type 1 diabetes, which is essentially an autoimmune disorder. With immunotherapy, the body’s immune system is “unleashed,” and it may attack critical insulin-producing cells in the pancreas.
Termini and his colleagues showed, in tissue culture and diabetic mouse models, that elevated glucose increased the presence of DNA adducts – chemical modifications of the DNA. Specifically, they found that a DNA adduct called N2-(1-carboxyethyl)-2′-deoxyguanosine, or CEdG, occurred more frequently in diabetic models than in normal cells or mice. Moreover, high glucose levels increased DNA strand breaks and interfered with DNA repair, which is required for removal of CEdG. The result is genome instability that could cause cancer.
Recently, Termini and colleagues completed a clinical study that measured the levels of CEdG and its RNA counterpart (CEG) in people with type 2 diabetes. People with diabetes had significantly higher levels of both CEdG and CEG than people without the disease.
The scientists identified two proteins that appear to be involved: transcription factor HIF1α and signaling protein mTORC1, both of which are less active in people with diabetes. HIF1α activates several genes involved in the repair process. The scientists found that if they stabilized HIF1α in a high-glucose environment, they increased DNA repair and reduce DNA damage. mTORC1 controls HIF1α, so if mTORC1 is stimulated, then HIF1α is stimulated, Termini said.
In theory, a medication that lowers blood sugar levels in diabetics could also potentially fight cancer by “starving” malignant cells to death. Evidence exists showing that diabetics who take metformin, the No. 1 drug for treating type 2 diabetes, may be less likely to develop cancer. Moreover, if they contract cancer, they are significantly less likely to die from it.
“Metformin helps lower blood glucose levels and stimulates DNA repair,” Termini said. “We’re looking to test metformin in combination with drugs that specifically stabilize HIF1α or enhance mTORC1 signaling in diabetic animal models.”
These studies were supported by the National Institutes of Health. The ACS is the world’s largest scientific society. This year’s ACS National Meeting & Exposition from Aug. 25-29 in San Diego features more than 9,500 presentations on a wide range of science topics.
City of Hope, with support from The Wanek Family Project for Type 1 Diabetes, is committed to designing highly effective treatments, preventions and cures for patients coping with type 1 diabetes. Building on the pivotal breakthroughs made in precision medicine over the past few years, City of Hope experts are creating powerful new approaches to treating type 1 diabetes — approaches that will move beyond just managing the disease to curing it.
###
About City of Hope
City of Hope is an independent research and treatment center for cancer, diabetes and other life-threatening diseases. Designated as one of only 49 comprehensive cancer centers, the highest recognition bestowed by the National Cancer Institute, City of Hope is also a founding member of the National Comprehensive Cancer Network, with research and treatment protocols that advance care throughout the world. City of Hope’s main campus is in Duarte, California, just northeast of Los Angeles, with additional locations throughout Southern California. It is ranked as one of “America’s Best Hospitals” in cancer by U.S. News & World Report. Founded in 1913, City of Hope is a pioneer in the fields of bone marrow transplantation, diabetes and numerous breakthrough cancer drugs based on technology developed at the institution. For more information about City of Hope, follow us on Facebook, Twitter, YouTube or Instagram. 
Media Contact
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Intermittent fasting could help treat inflammation


Fri, 23 Aug 2019
Jack Woodfield





Intermittent fasting could help treat inflammation
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Fasting could provide "enormous potential" in managing or preventing inflammation which is thought to contribute to type 2 diabetes, US researchers have said. 

A team from the Mount Sinai hospital report that fasting also improves chronic inflammatory diseases such as cancer, multiple sclerosis and cardiovascular disease. 

Fasting has been shown to help lower HbA1c in people with type 2 diabetes, with a study published last month also showing that intermittent fasting could prevent a build-up of fat in the pancreas that could protect against type 2 diabetes. 

"Caloric restriction is known to improve inflammatory and autoimmune diseases, but the mechanisms by which reduced caloric intake controls inflammation have been poorly understood," said senior author Dr Miriam Merad, Director of the Precision Immunology Institute at the Icahn School of Medicine at Mount Sinai.

To understand the mechanisms behind fasting more clearly, Dr Merad and colleagues tested the effects of fasting on both human and mouse cells. 

They discovered that intermittent fasting kick-started the release of 'monocytes', a collection of pro-inflammatory cells. During fasting periods these cells go into sleep mode and are less inflammatory than the cells that had been fed. 

"Monocytes are highly inflammatory immune cells that can cause serious tissue damage, and the population has seen an increasing amount in their blood circulation as a result of eating habits that humans have acquired in recent centuries," explained Dr Merad.

The number of these monocytes was significantly reduced following fasting, which researchers say emphasises the link between high-calorie dietary patterns and inflammatory disease outcomes. 

"Considering the broad spectrum of diseases that are caused by chronic inflammation and the increasing number of patients affected by these diseases, there is an enormous potential in investigating the anti-inflammatory effects of fasting," said first author Stefan Jordan, a postdoctoral fellow in the Department of Oncological Sciences at Mount Sinai.

The study findings have been published in the Cell journal.

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Gene Plays Role in Early-Onset Heart Disease and Diabetes
When heart disease affects people under age 50, it’s considered “early onset” and experts believe there’s a genetic link. Yale investigators have found that a particular gene is common to families with multiple members who either have early-onset heart disease or who are at risk for it.
The gene, CELA2A, was discovered at Yale by Arya Mani, M.D., professor of medicine and of genetics, and his colleagues. It produces a protein that regulates other proteins in the pancreas. For this new study, Mani and his co-authors examined individuals in families with early-onset heart disease, and learned that the protein plays a more significant role than previously thought, he said.
The researchers studied 30 cases of families with early-onset heart disease, performing whole genome analyses on close relatives and extended family members. They found a common mutation in the CELA2A gene that blocks its function. They also showed that the gene’s encoded protein circulates outside the pancreas, in the blood, where it affects clotting as well as insulin levels.
In further experiments they demonstrated that in humans the level of this protein rises in parallel with insulin after each meal. Subsequently they showed that insulin levels rose in hypoglycemic mice after the animals were given the CELA2A protein.
These findings show that the gene is a hidden link for diverse risk factors that often occur together in a medical condition known as metabolic syndrome, said the researchers. The clustering of these risk factors — including high blood pressure, high blood sugar, obesity, and abnormal cholesterol — dramatically raises the risk of heart disease and diabetes.
Mani and his colleagues think that many other pancreatic enzymes circulate in the blood and potentially have biological functions. He noted that for decades, scientists studied these circulating enzymes to understand the state of organ damage but never considered them as functional enzymes that could contribute to systemic disease.
With this insight, he said, scientists have a target for new therapies to potentially treat a variety of chronic illnesses, from heart disease and hypertension to insulin resistance, an underlying factor in type 2 diabetes. 
The study was published by Nature Genetics.

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Extra virgin olive oil is one of the few foods that health experts seem to unanimously praise. In fact, the list of benefits is so extensive that olive oil is widely considered to be a superfood. It’s thought to fend off Alzheimer’s disease and cut your risk of diabetes, heart disease and stroke. It’s also packed with antioxidants and good, healthy fats.

Now, new research published in the journal PLOS One suggests that extra virgin olive oil just might have the power to kill off cancer cells — and some types of olive oil may actually protect the body against cancer better than others.

sigridgombert via Getty Images

We talked to experts to figure out if extra virgin olive oil really can prevent cancer and what type we should be stocking in our kitchen cabinets.

Here’s what you should know:

The cancer-fighting power in olive oil mainly relies on one ingredient.

fcafotodigital via Getty Images

Top view of an olive oil bottle and a little glass bowl filled with green olives on rustic wood table. Two olives with leaves are at the top-right while a bowl filled with olive oil is at the center-top beside the two olives. An olive tree branch is at the left-top corner. A wooden spoon with three olives comes from the right. Predominant colors are gold, green and brown. DSRL studio photo taken with Canon EOS 5D Mk II and Canon EF 100mm f/2.8L Macro IS USM

This isn’t the first study to find that extra virgin olive oil might have cancer-killing properties. Previous evidence suggests that certain olive oils can lower your odds of developing cancer, all thanks to an ingredient called oleocanthal — an antimicrobial, antioxidant and anti-inflammatory compound naturally found in high-quality, nonrefined olive oils.

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This new PLOS One study not only reinforced these claims, but also found that extra virgin olive oils rich in oleocanthal are much more protective against cancer than those with only a little bit of oleocanthal. Where extra virgin olive oils seem to zap away cancer cells, non-extra virgin olive oils don’t appear to have any effect on cancer cells.

In other words, because of oleocanthal, extra virgin olive oil can help (key word being help) prevent a range of health conditions and suppress melanoma, breast, liver, and colon cancer cells, according to the researchers.

There are some limitations with this study.

Before you rush off to the grocery store and buy olive oil in bulk, there are a few things you should know. First, while it’s obviously exciting that olive oil could potentially nix cancer cells, it’s way too soon to conclude that olive oil can treat or cure cancer in people based off the research.

“You’re not taking a medication, you’re just eating olive oil, so I’m not going to be trying to give you some advice like ... once you have been diagnosed with cancer, go have olive oil,” explained Vasilis Vasiliou, chair of the department of environmental health sciences at Yale Cancer Center.

Additionally, the new study was conducted in animals — specifically mice — not humans. More research is needed to better understand how well oleocanthal works in humans, not just mice, before we can recommend olive oil as a cancer treatment, Vasilou explained. Still, these findings add to the growing body of evidence that oleocanthal can destroy cancer cells in some capacity, and it’s definitely worth exploring if it can be used to help treat cancer in people.

Bottom line: Olive oil is incredibly beneficial — but make sure you’re getting the right kind.

Michael Moeller / EyeEm via Getty Images

All things considered, it is important to include olive oil in your diet. However, if you want to reap the all the health benefits, you’ll need to invest in the higher-quality stuff. The cheaper, overly processed products aren’t going to do you much good.

“Olive oil comes from olives. Anytime we take a whole food and degrade it, process it, pack it, transport it, stabilize it, etc., we are changing its original form,” said Sharon Zarabi, a nutritionist at Lenox Hill Hospital in New York. Creating capsules, supplements and oils from the olive’s natural form affects our metabolism and how our bodies process it, she added.

To reap the most benefits, always buy extra virgin olive oil, which usually goes for anywhere from $20 to $150 a bottle. Most higher-quality olive oils that contain potential cancer-fighting powers will have a strong, pungent — even peppery — taste.

“When you eat olive oil that has high content [of oleocanthal], you get a little burning in your throat. You may think that this is a bad quality, but that’s the opposite — it’s the [oleocanthal],” Vasilou said.

Another important tip: Buy small bottles of extra virgin olive oil. If olive oil isn’t stored properly or used swiftly, the fats can degrade over time and may actually pose more of a health risk than benefit.

“Degradation of any compound will cause oxidative stress and actually contribute to degenerative disease, doing the complete opposite of what it was intended to treat,” Zarabi said.

Lastly, don’t overdo it. While it may be tempting to center your meals around olive oil based on all its health powers, it’s always best to eat your foods in moderation. Adding high-quality olive oil to an overall healthy diet is the best way to go.

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A molecular "trick" that kept our ancient ancestors from starving may now be contributing to the obesity epidemic, a new study finds.

In starvation times, researchers say, animals were more likely to survive if they could hoard and stretch out their stored energy. Even if an animal secured a rare feast, evolution smiled on the storage of excess fuel as fat, given the likelihood of a quick return to starvation.

"We discovered an anti-starvation mechanism that has become a curse in times of plenty because it sees cellular stress created by overeating as similar to stress created by starvation -- and puts the brakes on our ability to burn fat," says lead study author Ann Marie Schmidt, MD, the Dr. Iven Young Professor of Endocrinology at NYU School of Medicine.

Published online July 16 in Cell Reports, the current study reveals that the natural function of a protein called RAGE on the surface of fat cells is to stop the breakdown of stored fat in the face of stress. Its existence may partly explain why 70 percent of American adults are overweight or obese, according to the American Heart Association (AHA). In March 2017, the AHA announced a grant to help researchers find the elusive "metabolic brake."

The AHA funding followed a 2016 study that found contestants from America's Greatest Loser gained back their lost pounds after the show ended. Why did their metabolisms slam to a halt in the face of weight loss, as if their bodies were bent on returning to obesity?

A Brake on Fat Burning

According to the authors, the most efficient way for evolution to create an anti-starvation mechanism was from ancient systems that helped animals use food for cellular energy and recover from injury. Also wired into these primal mechanisms was the hormone adrenalin, which signals for the conversion of fat into energy as animals run from predators, or into body heat when they get cold.

This convergence -- through the same signaling proteins -- means that RAGE may block "fat burning" called for when we starve, freeze, get injured, panic, or ironically, overeat.

According to the new study and experiments done elsewhere in human tissues, RAGE is turned on by the advanced glycation endproducts (AGEs), which form when blood sugar combines with proteins or fats -- most often in aging, diabetic and obese patients. Other molecules also activate RAGE, such as those released when cells die and spill their contents into intracellular spaces in response to stress.

A disturbing possibility, says Schmidt, is that many proteins and fats have come to activate "the RAGE break" as they warp and stack up (as toxic oligomers) in people that eat more than their ancestors did.

The current study found that removing RAGE from fat cells caused mice to gain up to 75 percent less weight during three months of high-fat feeding, despite equal amounts of food consumption and physical activity, than mice with the RAGE brake on. Transplanting fatty tissue lacking RAGE into normal mice also decreased weight gain as they were fed a high-fat diet.

In both sets of experiments, the deletion of RAGE from fat cells released the braking mechanisms that restrained energy expenditure. Once freed up, energy expenditure rose, contributing to the reduced body weight gain in mice with the fatty diet.

The new study complements the team's discovery of experimental compounds that attach to the "tail" of RAGE. From there, they prevent RAGE from turning down the action of protein kinase A, a key player in the chain reaction that ends with a protein called UCP1 turning fat into body heat.

The research team plans -- once they optimize the design of these "RAGE inhibitors" -- to examine whether the agents can keep bariatric surgery patients, and patients undergoing medical weight loss regimens, from regaining lost weight.

Importantly, RAGE is much more active during metabolic stress (e.g. starving or overeating) than in everyday function, which suggests it can be safely interfered with through drugs, the authors say.

"Because RAGE evolved out of the immune system, blocking it may also reduce the inflammatory signals that contribute to insulin resistance driving diabetes," says Schmidt. "Further, such treatments may lessen the system-wide inflammation linked to risk for atherosclerosis, cancer, and Alzheimer's disease."

Among with Schmidt, study authors in Diabetes Research Program, Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, NYU School of Medicine, were first authors Carmen Hurtado del Pozo and Henry Ruiz, Lakshmi Arivazhagan, Juan Francisco Aranda, Cynthia Shim, Peter Daya, Julia Derk, Michael MacLean, Meilun He, Laura Frye, and Ravichandran Ramasamy.

Also authors of the study were Randall Friedline, Hye Lim Noh, and Jason Kim from the Program in Molecular Medicine and Division of Endocrinology, Metabolism and Diabetes, Department of Medicine at the University of Massachusetts Medical School; as well as Richard Friedman of the Herbert Irving Comprehensive Cancer Center, and Department of Biomedical Informatics, at the College of Physicians and Surgeons, Columbia University.

This work was supported by United States Public Health Service grants 1R01DK109675, 1PO1HL131481, 5T32HL098129-10, and 1F31AG054129-01; and by the American Diabetes Association grant 1-15-MI-14. The work was also partly funded by research funds of the Diabetes Research Program at NYU, and by the Experimental Pathology Research Laboratory's Cancer Center Support grant (P30CA016087). Additional funding came from the National Mouse Metabolic Phenotyping Center at UMass, which is funded by National Institutes of Health grant 2U2C-DK093000.

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Materials provided by NYU Langone Health / NYU School of Medicine. Note: Content may be edited for style and length.

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Reuters) - AstraZeneca Plc said on Tuesday that the U.S. Food and Drug Administration has granted fast track status for the development of its diabetes drug Farxiga to prevent heart and kidney failure in patients with chronic kidney disease (CKD).

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Farxiga, one of AstraZeneca’s top 10 drugs by sales, is part of the SGLT2-inhibitor class of antidiabetics that cause the kidneys to expel blood sugar from the body through urine.

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In July, U.S. regulators declined to approve Farxiga as a supplement to insulin in adults with type-1 diabetes where insulin alone was not able to control blood sugar levels.

The treatment is already approved in the United States to treat type-2 diabetes, the more common form of the condition.

Farxiga competes with rival diabetes drugs, including Eli Lilly and Boehringer Ingelheim’s Jardiance and Novo Nordisk’s Victoza.

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Targeting the liver with insulin could be the best way to treat type 1 diabetes, US researchers have claimed.

A team from the Vanderbilt University Medical Center set out to investigate whether people with type 1 diabetes experience resistance to the manufactured insulin they take and consider how insulin delivery may affect the risk of complications.

To date, it is widely believed that high levels of glucose leads to greater risk of diabetes-related complications, but lead researcher Dr Justin Gregory, who was diagnosed with type 1 diabetes more than 19 years ago, does not agree.

The assistant professor of Pediatrics at the medical centre said: "There's more to treating type 1 diabetes than just bringing down high blood sugar."

He thought the answer might have more to do with the way insulin is delivered into muscle. In people who do not have diabetes, insulin is produced by the pancreas first before it travels via the liver, halving the amount of the hormone before it is despatched to the muscle.

However, when insulin is injected under the skin in those with diabetes, a key part of that process is bypassed, and the liver is initially missed. 

Dr Gregory said that injecting insulin under the skin meant he had "too much insulin at muscle and not enough at liver—all because I'm putting insulin in the wrong place".

"Restoring that balance is important toward helping people with type 1 diabetes reduce their risk of heart disease," he added.

Dr Gregory's theory with regard to heart disease risk is based on association between insulin resistance and inflammation.

To prove the theory that people with type 1 diabetes have resistance to the insulin they take, the team carried out tests on people with type 1 diabetes and compared the results with people with a different form of diabetes, known as GCK-MODY.

People with GCK-MODY have a genetic condition, affecting the GCK (glucokinase) gene, that affects the pancreas’ sensing of how high blood glucose levels are. This leads to people with GCK-MODY having higher than normal blood glucose levels.

By choosing people with GCK-MODY as a comparison group, the team were able to compare differences in tests with two groups that both had similarly high blood glucose levels.

Both groups had their blood glucose adjusted to the same level, then their insulin levels were compared. The MODY group's insulin levels were deemed in the healthy range, whereas insulin levels among those with type 1 were 2.5 times higher.

Dr Gregory said his study "brings to light the need to develop therapeutic strategies to keep the appropriate balance of insulin between the liver and peripheral insulin-sensitive tissues".

He added: "We need to come up with ways of delivering insulin that replicate that normal balance of insulin."

The findings have been published in the journal Diabetes.