Tips to Minimize Occurrence of Stretch Marks During and After Pregnancy

Stretch marks during and after pregnancy are inevitable. It occurs as a result of the stretching of the skin up to its limits. As the skin tends to stretch to house the growing fetus, the collagen fibers tend to compensate to bring skin together. This is the reason why there are white streaks around the mother’s tummy. This does not only happen to mothers but to those who have suffered from a drastic change in weight. While this seems to be a big problem to a lot of people, there are actually things that one can do to be able to get rid of the scars it leaves.

One of the secrets in order to hasten the process of healing is hydration. Hydration is important in order to clean the body from toxins that may come interfering with the process of healing. Hydration is also important to keep the tissues intact and not dried out.

Moisturize skin. Moisturizers will help prevent itching and drying caused by the stretching of collagenous material. As the skin is moisturized, it will avoid inflicting harm on the skin brought by stretching. There are creams available in the market that can be bought with prescription or over the counter. But before this, one should consult on a physician in order to find the cream that will suit your needs. Consultation is important in order to get rid of the possible existence of allergies brought by some ingredients comprising the cream.

Diet does not always go out of style. Most of the health problems existing can be controlled with the use of proper diet. Controlling the effects of stretch marks is one. Vegetables and fruits for instance helps the body get the needed amount of nutrients to function. This is a proven fact but it goes with a bonus too. These foods tend to let you have softer and moisturized skin which is great news to combat the effects of drying brought by stretch marks. Once the skin is softer, marks may come limited.

If diet is one of the vital things to consider, exercise goes to follow. Exercise, just like proper diet has never grown out of the spotlight. It has always brought myriad of benefits in the aspect of health. It is also linked with the reduction stretch marks. As one goes with exercise, the skin is tightened and toned. Once this happens, the skin easily comes back to its original form which means reducing the visible marks. This is also beneficial to help the uterus come back to its non-pregnant state after the pregnancy. This does not stop only once you achieve the form you have always wanted. Exercising regularly will help you tone your muscles, strengthening it to resist the effects of tearing.

Load yourself with vitamins. Vitamins specifically A, E and C are perfect for the skin. These vitamins have anti-toxin properties which wash away the toxins brought by the foods, beverages and drugs taken in. Once these toxins are completely washed away, it will reveal healthy skin. Once you have got the skin that is healthy, it will be easy for it to resist the effects of stretch marks and that the effects will be minimized. Even the feeling of itchiness will be controlled as you have the best defenses to achieve such.

Proper diet coupled with exercise should be enough in order to minimize the effects of stretch marks. If you come to observe it, it will just boil down to the idea of living a healthy life. You can never really go wrong over living the healthy life as it tends to direct you to becoming an individual resistant to health problems.

For an expectant mother, there are a lot of things to do to be able to finally get rid of the effects of stretch marks. Yet, for those who have already acquired such, it is never the end. Consult your doctor to know what you can do to get rid of it. You might be prescribed with creams safe enough to use during the pregnancy. All you have got to do is to relay your worries. Having stretch marks during and after pregnancy may come to shake you but these are controllable. And don’t forget to follow special diet, read some helpful recipes.

Naturally, the body reacts to the sudden change in the size of a person. You may think of it as a problem but stretch marks are just the effect of the natural mechanism of the body to resist tearing of skin when it has reached the limit. This is actually an indication that your body is working its functions well enough. But since its appearance is bothersome, you would naturally get rid of it. Living the healthy life would help well enough to combat the not so good effects of this naturally occurring body process.

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Diabetes + Depression = Increased Risk of Death

Review Finds People living with diabetes who also have untreated depression are at increased risk of death, according to a new evidence review in General Hospital Psychiatry.

More than 42,000 patients with type 1 or type 2 diabetes and depression were analyzed in the review. The reviewers discovered that depression was associated with a 1.5 fold increase in the risk of dying. In four of the studies reviewed, co-morbid depression was linked to about a 20 percent higher risk of cardiovascular death for people with diabetes.

Diabetes affects 25.8 million people in the U.S., according to the 2011 National Diabetes Fact Sheet, and about 30 percent of these people also experience symptoms of depression.

"Depression consistently increased the risk of mortality across virtually all studies," said Mijung Park, Ph.D., lead author and assistant professor at the University of Pittsburgh School of Nursing. "We can now postulate that the harmful effect of depression is universal to individuals with diabetes."

Todd Brown, M.D., associate professor of medicine and epidemiology at Johns Hopkins University in Baltimore, said it is very common to see a patient go into a downward spiral when obesity-related co-morbidities, such as diabetes, high blood pressure, obesity and depression converge.

"Obesity can lead to worsening metabolic status that can lead to hopelessness and decreased physical activity, which in turns worsens obesity, and the cycle continues," he explained.

The encouraging news is that depression is a highly treatable condition, said Park. Because depression can make diabetes self-care more difficult and lessen quality of life, she suggested that depression treatment should be included in overall diabetes care strategies.

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Age Matters in Weight Gain: Overweight at Young Age Takes Toll

Being overweight, especially from a young age, appears to lead to a bigger heart later in life, a condition that has been linked to serious heart problems and even death, according to research being presented at the American College of Cardiology's 62nd Annual Scientific Session.

Results of this longitudinal study found that people who carry excess weight over their lifetime are much more likely to have increases in left ventricular mass and relative wall thickness -- both strong and independent predictors of cardiovascular morbidity and mortality. In this instance, timing is indeed everything; the earlier someone becomes overweight, the greater the increase in the heart's mass later in life.

"Being overweight in your 20s can have detrimental effects on the heart 40 years in the future, especially if you keep the weight on over the years," said Arjun K. Ghosh, MBBS, MRCP (U.K.), MSc, clinical research fellow at the International Centre for Circulatory Health of Britain's National Heart and Lung Institute and at the U.K. Medical Research Council's Unit for Lifelong Health and Aging and the study's lead investigator, on behalf of the full study team.

"It's probably the wrong attitude to think 'I know I'm overweight now, but I'll lose the weight later' because the longer you spend overweight, the greater the weight of your heart muscle. And we know from other studies that even if we take away or account for high blood pressure, diabetes or other risk factors for heart disease, somebody with a bigger heart muscle is more likely to have a heart attack, die or have other problems, such as stroke."

Researchers tracked the body mass index (BMI) of 1,653 men and women at different points in their lives to examine the effects of being overweight on the structure of the heart. BMI is a simple measure of the body's fat using a calculation of weight to height. People who were considered overweight, with a BMI of 25 to 29.9, or obese, with a BMI of 30 or above, had the heaviest hearts. Dr. Ghosh said few, if any, studies have been able to look at this question over such a long duration. He and his team drew from 44 years of data. Strikingly, the heart was 7 percent heavier for those who were overweight beginning in their 20s compared to those who only became overweight in their 60s.

"Our findings add to the wealth of evidence that obesity and being overweight from a young age is not good and provide yet another reason why we need to focus on preventing obesity and promoting a healthy lifestyle," he said. "Being overweight is a significant risk factor for heart disease, and worldwide, people seem to be becoming overweight at younger and younger ages."

Dr. Ghosh said previous research demonstrates that it is difficult to go back to and maintain a normal weight once someone has become overweight. As such, prevention of becoming overweight in the first place should be the aim. This is especially relevant amid the growing obesity epidemic, even among children. One in three school-aged children in North America are now overweight and this upward trend shows no signs of slowing, which means more children are entering adulthood carrying excess weight.

Individuals included in this study are participants in the Medical Research Council National Survey of Health and Development (or the 1946 British birth cohort), which is the longest running birth cohort study in the United Kingdom. Between ages 60 and 64, participants underwent echocardiography, an ultrasound of the heart, to allow researchers to measure the size of the heart muscle and their BMI was calculated. BMI and other cardiovascular risk factors had previously been measured at 20, 26, 36, 43 and 53 years of age. Higher BMI from 20 years onward was associated with increased heart muscle mass, with those with higher BMIs at each time point having heavier hearts at age 60-64 years of age. These associations remain after researchers adjusted for related risk factors, e.g., high blood pressure, diabetes and sex.

Two previous analyses of cardiac health indicators in the same study cohort revealed that people with diabetes are at greater risk of heart problems the longer they had diabetes and that a sharp spike in blood pressure during midlife, not just crossing a certain threshold, such as becoming hypertensive, can increase a person's risk of heart disease later in life. Both were presented at ACC.12.

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Depressed Stroke Survivors May Face Triple the Risk of Death

People who are depressed after a stroke may have a tripled risk of dying early and four times the risk of death from stroke than people who have not experienced a stroke or depression, according to a study released January 12 that will be presented at the American Academy of Neurology's 65th Annual Meeting in San Diego, March 16 to 23, 2013.

"Up to one in three people who have a stroke develop depression," said study author Amytis Towfighi, MD, with the Keck School of Medicine of the University of Southern California and Rancho Los Amigos National Rehabilitation Center in Los Angeles, and a member of the American Academy of Neurology. "This is something family members can help watch for that could potentially save their loved one."

Towfighi noted that similar associations have been found regarding depression and heart attack, but less is known about the association between stroke, depression and death.

The research included 10,550 people between the ages of 25 and 74 followed for 21 years. Of those, 73 had a stroke but did not develop depression, 48 had stroke and depression, 8,138 did not have a stroke or depression and 2,291 did not have a stroke but had depression.

After considering factors such as age, gender, race, education, income level and marital status, the risk of dying from any cause was three times higher in individuals who had stroke and depression compared to those who had not had a stroke and were not depressed. The risk of dying from stroke was four times higher among those who had a stroke and were depressed compared to people who had not had a stroke and were not depressed.

"Our research highlights the importance of screening for and treating depression in people who have experienced a stroke," said Towfighi. "Given how common depression is after stroke, and the potential consequences of having depression, looking for signs and symptoms and addressing them may be key."

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'Switch' Critical to Wound Healing Identified

Scientists from A*A*STAR's Institute of Medical Biology (IMB) have identified a molecular "switch" that controls the migration of skin cells necessary for wounds to close and heal. This is especially significant for diabetics and other patients who suffer from chronic wounds, wounds that do not heal or take years to do so, which are vulnerable to infections and could lead to amputations. This switch mechanism may hold the key to developing therapeutics that will reduce or prevent chronic wounds.

The scientists discovered that a tiny "micro-RNA" molecule, called miR-198, controls several different processes that help wound healing, by keeping them switched off in healthy skin. When skin is wounded, the manufacture of miR-198 quickly stops and the levels of miR-198 drop, switching on many wound healing processes.

In the non-healing wounds of diabetics, miR-198 does not disappear and wound healing remains blocked. This therefore identifies miR-198 as a potential diagnostic biomarker for non-healing wounds.

These findings were recently published in the journal Nature. The research leading to this discovery was carried out in collaboration with A*STAR's Bioinformatics Institute (BII), National University Hospital (NUH), Singapore and Jnana Sanjeevini Diabetes Center, Bangalore, India.

Importance of this discovery

Chronic wounds in patients with diabetes are a major global health burden and the most common cause of lower extremity amputations. In Singapore, diabetes is the fifth most common medical condition diagnosed and one in nine people aged 18 to 69 has diabetes. Unfortunately, chronic wounds are currently poorly understood and insufficiently treated. Chronic wounds also tend to affect the elderly and disabled patients, especially those confined to a wheelchair or bed-bound.

Dr. Prabha Sampath said, "Moving forward, we hope to translate this research into improved patient outcomes. We can now build on this research, to see how we can modulate the defective switch in chronic wounds by targeting miR-198 and its interacting molecules, to develop new strategies for treating chronic wounds."

Professor Birgitte Lane, Executive Director of IMB, said, "This switch appears to be an entirely new regulatory component in wound healing, and probably a very important one. Poor wound healing is a major healthcare burden, and this discovery is particularly timely in the face of aging populations and the sharp global rise in diabetes. The finding gives us a platform from which to develop therapies that could significantly reduce chronic wounds and improve healthcare."

An FSTL1-miR-198 molecular 'see-saw' switch

The information necessary to expressmicroRNA-198 (miR-198) and follistatin-like 1 (FSTL1) protein are found in a single "message" produced by the cell. However, miR-198 and FSTL1 protein cannot be produced at the same time -- it can only be one or the other. These two molecules also have opposite roles: miR-198 (found in unwounded skin) inhibits skin cell migration and wound healing, whereas FSTL1 protein (expressed after injury) promotes skin cell migration and wound healing. A regulatory switch dictates their expression, and hence controls the "see-saw" between inactive resting skin cells and the cell migration necessary for wound healing.

Dr. Sampath and her team showed that healthy unwounded skin contained high levels of miR-198 but no FSTL1 protein. They demonstrated that these high levels of miR-198 prevent skin cell migration by suppressing several genes, such as PLAU, LAMC2 and DIAPH1, which are needed for different aspects of the wound healing process. However upon injury, miR-198 is switched off in the wound by a signal from transforming growth factor β1 (TGF-β1). This allows FSTL1 to now be made instead, and the skin migration genes to be unblocked, promoting migration of skin cells into the wound area to drive skin wound healing.

The scientists further examined skin samples of chronic non-healing ulcer wounds from patients with diabetes mellitus. They observed that, unlike healthy skin that had been injured, there remained high levels of miR-198 (inhibiting skin cell migration and wound healing) and an absence of FSTL1 protein (promoting skin cell migration upon wounding), indicating that this "switch" is defective in chronic wounds.

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Mice With Mitochondrial Mutation Live Longer, Have Less Fat

If findings of a new study in mice are any indication, it might be possible to fine-tune cellular powerhouses called mitochondria, tweaking one aspect to increase insulin sensitivity, reduce body and fat mass, and even extend life. Exploiting this target could one day lead to novel treatments for type 2 diabetes - an endocrine system disease that affects 8 percent of the U.S. population. The research also points to promising new avenues of investigation in the biology of aging.
The study, reported in The FASEB Journalby authors from the School of Medicine at the UT Health Science Center San Antonio and the university's Barshop Institute for Longevity and Aging Studies, found that diminished activity of a protein complex involved in mitochondrial function was associated with healthy changes in the mice. The median life span of this strain of mice is 20 percent longer.

Paradoxical
"This is an unexpected finding because you would think that something that decreases mitochondrial function would have a damaging effect, but instead we saw an increase in life span and beneficial metabolic effects," said lead author Deepa Sathyaseelan, Ph.D., research assistant professor of cellular and structural biology in the School of Medicine.
"The most important thing we noticed is reduced body weight and decreased fat mass in the mice," Dr. Sathyaseelan said. "We found that this decreased fat mass is due to increased fat utilization."
Fat utilization
Mitochondria produce an energy source called ATP that is necessary for the functions of life, everything from breathing to thinking. Additionally the cellular powerhouses are a major site of fat utilization, said study senior author Holly Van Remmen, Ph.D., professor of cellular and structural biology. Fat is an endocrine organ that performs many functions, and having it in the correct proportions is important for the body. Too much or too little fat is harmful.
The scientists also observed that mice with the mutation, in contrast to control animals, make greater numbers of new mitochondria. This is important because cells are constantly remodeling themselves, including mitochondrial overhaul.
Age-related
Mitochondrial dysfunction occurs with age and is associated with many age-related diseases such as type 2 diabetes, heart disease and cancer. Dr. Sathyaseelan said the study "opens the door to new clues about how mitochondrial function might modulate insulin sensitivity," representing an important step for diabetes research.
Type 2 diabetes involves abnormalities with insulin, a hormone secreted by beta cells in the pancreas. Insulin helps the body store and use sugar from food, but in type 2 diabetes the body is insulin resistant, that is, it inefficiently responds to the hormone. With time the beta cells in diabetic patients start to die, resulting in less insulin to handle the demands. Levels of the hormone become progressively lower and sugar levels are increased progressively, damaging blood vessels and organs.
Understanding longevity
"I would also like to point out that these mice live longer," Dr. Van Remmen said. "For us they are very important from an aging standpoint. We want to understand how these animals can have added longevity, yet have a 60 percent reduction in a protein complex involved in mitochondrial function."
Dr. Sathyaseelan noted that life extension in association with decrease of the complex's activity is seen across species, including roundworms and flies. Shane Rea, Ph.D., assistant professor of physiology at the Barshop Institute, is one of the first to make this discovery in the worms.
The Barshop Institute team obtained the study mice from an Italian institute where studies are ongoing. Dr. Sathyaseelan recently received a two-year, $140,000 grant from the American Heart Association to understand how mitochondrial dysfunction is related to insulin sensitivity.

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'Brewing' New Medicines?

Researchers employing a century-old observational technique have determined the precise configuration of humulones, substances derived from hops that give beer its distinctive flavor.
That might not sound like a big deal to the average brewmaster, but the findings overturn results reported in scientific literature in the last 40 years and could lead to new pharmaceuticals to treat diabetes, some types of cancer and other maladies.
"Now that we have the right results, what happens to the bitter hops in the beer-brewing process makes a lot more sense," said Werner Kaminsky, a University of Washington research associate professor of chemistry.
Kaminsky is the lead author of a paper describing the findings, published this month in the journal Angewandte Chemie International Edition.
There is documentation that beer and its bittering acids, in moderation, have beneficial effects on diabetes, some forms of cancer, inflammation and perhaps even weight loss.

Kaminsky used a process called X-ray crystallography to figure out the exact structure of those acids, humulone molecules and some of their derivatives, produced from hops in the brewing process. That structure is important to researchers looking for ways to incorporate those substances, and their health effects, into new pharmaceuticals.
Humulone molecules are rearranged during the brewing process to contain a ring with five carbon atoms instead of six. At the end of the process two side groups are formed that can be configured in four different ways - both groups can be above the ring or below, or they can be on opposite sides.
Which of the forms the molecule takes determines its "handedness," Kaminsky said, and that is important for understanding how a particular humulone will react with another substance. If they are paired correctly, they will fit together like a nut and bolt.
If paired incorrectly, they might not fit together at all or it could be like placing a right hand into a left-handed glove. That could produce disastrous results in pharmaceuticals.
Kaminsky cited thalidomide, which has a number of safe uses but was famously used to treatmorning sickness in pregnant women in the late 1950s and early 1960s before it was discovered to cause birth defects. Molecule "handedness" in one form of the drug was responsible for the birth defects, while the orientation of molecules in another form did not appear to have the negative effects.
To determine the configuration of humulones formed in the brewing process, coauthors Jan Urban, Clinton Dahlberg and Brian Carroll of KinDex Therapeutics, a Seattle pharmaceutical firm that funded the research, recovered acids from the brewing process and purified them.
They converted the humulones to salt crystals and sent them to Kaminsky, who used X-ray crystallography - a technique developed in the early 20th century - to determine the exact configuration of the molecules.
"Now that we know which hand belongs to which molecule, we can determine which molecule goes to which bitterness taste in beer," Kaminsky said.
The authors point out that while "excessive beer consumption cannot be recommended to propagate good health, isolated humulones and their derivatives can be prescribed with documented health benefits."
Some of the compounds have been shown to affect specific illnesses, Kaminsky said, while some with a slight difference in the arrangement of carbon atoms have been ineffective.
The new research sets the stage for finding which of those humulones might be useful in new compounds to be used as medical treatments.

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Risk Of Type 2 Diabetes Increased By Binge Drinking By Causing Insulin Resistance

Binge drinking causes insulin resistance, which increases the risk of Type 2 diabetes, according to the results of an animal study led by researchers at the Diabetes Obesity and Metabolism Institute at the Icahn School of Medicine at Mount Sinai. The authors further discovered that alcohol disrupts insulin-receptor signaling by causing inflammation in the hypothalamus area of the brain.

The results are published in the journal Science Translational Medicine.
"Insulin resistance has emerged as a key metabolic defect leading to Type 2 diabetes and coronary artery disease (CAD)," said Christoph Buettner, MD, PhD, senior author of the study and Associate Professor of Medicine (Endocrinology, Diabetes and Bone Disease). "Someone who regularly binge drinks even once a week, over many years, may remain in an insulin resistant state for an extended period of time, potentially years," said Dr. Buettner.
In this study, researchers treated rats with alcohol for three consecutive days to simulate human binge drinking.

A control group received the same amount of calories. Once alcohol was no longer detectable in blood, glucose metabolism was studied through either glucose-tolerance tests or through controlled-insulin infusions. The rats treated with alcohol were found to have higher concentrations of plasma insulin than the control group, suggesting that insulin resistance may have been the cause of the impaired glucose tolerance.
High plasma insulin levels are a major component of the metabolic syndrome, a group of risk factors that occur together and increase the risk for Type 2 diabetes, coronary artery disease, and stroke.

"Previously it was unclear whether binge drinking was associated with an increased risk for diabetes, since a person who binge drinks may also tend to binge eat, or at least eat too much. Our data show for the first time that binge drinking induces insulin resistance directly and can occur independent of differences in caloric intake," said Claudia Lindtner, MD, first author of the study and an Associate Researcher of Medicine, Endocrinology, Diabetes and Bone Disease at the Icahn School of Medicine.

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Do Gender And Ethnicity Alter Childhood Risk For Metabolic Syndrome?

Metabolic syndrome is more likely to affect children who are obese than overweight or non-overweight and who have other characteristics associated with the disorder, such as high blood pressure or insulin resistance. A new comprehensive and systematic review of the medical literature on metabolic syndrome in children that probed deeper to evaluate the risk associated with gender, ethnicity, and geography was published in Metabolic Syndrome and Related Disorders, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available on the Metabolic Syndrome and Related Disorders website.

Amanda Friend, MBChB, Leone Craig, PhD, and Steve Turner, MD, University of Aberdeen, Scotland, assessed data from 85 studies and reported their findings in the article "The Prevalence of Metabolic Syndrome in Children: A Systematic Review of the Literature." Overall, the prevalence of metabolic syndrome increased substantially when comparing groups of overweight or obese children to whole populations of youths.

The authors found significant differences in metabolic syndrome prevalence for boys versus girls and for older compared to younger children. Some evidence suggested that there may also be an association between ethnicity and region of the world where a child lives and the prevalence of metabolic syndrome - a possible link that warrants further study.
"The authors should be lauded for their comprehensive and careful review of a group that has been largely ignored, which is children," says Ishwarlal (Kenny) Jialal, MD, PhD, Editor-in-Chief of the Journal and Director of the Laboratory for Atherosclerosis and Metabolic Research and Professor of Internal Medicine at the University of California, Davis Medical Center (Sacramento). "They clearly show that increasing age, male sex, and adiposity are risk factors for metabolic syndrome in children. They also emphasize the need for future studies to confirm the reported increased prevalence in certain ethnic groups."

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Joslin Scientists Find First Human IPSC From Patients With Maturity Onset Diabetes Of The Young

Joslin scientists report the first generation of human induced pluripotent stem cells from patients with an uncommon form of diabetes, maturity onset diabetes of the young (MODY). These cells offer a powerful resource for studying the role of genetic factors in the development of MODY and testing potential treatments. The findings appear in the Journal of Biological Chemistry.

Human induced pluripotent stem cells (hiPSCs) are adult cells that have been genetically reprogrammed to exhibit the characteristics of embryonic stem cells, including the ability to differentiate into specialized cell types. The generation of hiPSCs, which was first reported in 2006, was a major scientific breakthrough with the potential to increase understanding of many diseases and aid in drug development.

Maturity onset diabetes of the young (MODY) is a form of diabetes that mainly affects individuals age 25 or younger and accounts for about 1 to 5 percent of all diabetes cases in the United States. Unlike type 1 and type 2 diabetes, which are polygenic and result from alterations in genetic and environmental factors, MODY is a monogenic disease that results from mutations in a single gene. To date, eight types of MODY and eleven MODY genes have been identified. Some types of MODY produce only mild symptoms and are often treated solely with oral diabetic medications.

Joslin Diabetes Center is one of a limited number of research institutes with the capability to generate hiPSCs from patients with diabetes. The cells used to produce the hiPSCs were obtained from patients with five different types of MODY at Joslin Diabetes Center and Haukeland University Hospital, Bergen, Norway. The MODY-hiPSCs are morphologically, molecularly and functionally indistinguishable from human pluripotent stem cells (hPSCs).

As a monogenic disease, MODY provides "a valuable opportunity to directly study in more detail the genetic mechanisms underlying the disease and not be influenced by other factors, such as insulin resistance," says senior author Rohit N. Kulkarni, M.D., Ph.D., a Principal Investigator in the Section on Islet Cell and Regenerative Biology at Joslin and Associate Professor of Medicine at Harvard Medical School.
The scientists will first induce the MODY-hiPSCs to differentiate towards beta cells and in the process learn more about the potential blocks in their ability to differentiate. Using the iPSC-derived beta cells, they plan to study how MODY genes regulate the insulin secretory function. "Generating hiPSCs is an important step forward because we cannot obtain beta cells from living patients. These cells will allow us to do many experiments that otherwise would not be possible," says Dr. Kulkarni.

The scientists also plan to explore ways to correct the genetic defect and use the beta cells derived from the "repaired" hiPSCs to test various treatments. "If we find medications that improve beta cell function, we can go back to the clinic and use them to treat patients," says Dr. Kulkarni. "It will allow us to tailor treatments to a patient's unique characteristics and provide personalized medicine to diabetes patients."

 

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Type 3 Diabetes.....Alzheimer's?

Just in case you need another reason to cut back on junk food, it now turns out that Alzheimer’s could well be a form of diet-induced diabetes. That’s the bad news.

The good news is that laying off soda, doughnuts, processed meats and fries could allow you to keep your mind intact until your body fails you. We used to think there were two types of diabetes: the type you’re born with (Type 1) and the type you “get.” That’s called Type 2, and was called “adult onset” until it started ravaging kids. Type 2 is brought about by a combination of factors, including overeating, American-style.

The idea that Alzheimer’s might be Type 3 diabetes has been around since 2005, but the connection between poor diet and Alzheimer’s is becoming more convincing, as summarized in a cover story in New Scientist entitled “Food for Thought: What You Eat May Be Killing Your Brain.” (The graphic — a chocolate brain with a huge piece missing — is creepy. But for the record: chocolate is not the enemy.)

The studies [1] are increasingly persuasive, and unsurprising when you understand the role of insulin in the body. So, a brief lesson. We all need insulin: in non-diabetics, it’s released to help cells take in the blood sugar (glucose) they need for energy. But the cells can hold only so much; excess sugar is first stored as glycogen, and — when there’s enough of that — as fat. (Blood sugar doesn’t come only from sugar, but from carbohydrates of all kinds; easily digested carbohydrates flood the bloodstream with sugar.)

Insulin not only keeps the blood vessels that supply the brain healthy, it also encourages the brain’s neurons to absorb glucose, and allows those neurons to change and become stronger. Low insulin levels in the brain mean reduced brain function. Type 1 diabetes, in which the immune system destroys insulin-producing cells in the pancreas, accounts for about 10 percent of all cases.

Type 2 diabetes is chronic or environmental, and it’s especially prevalent in populations that overconsume hyperprocessed foods, like ours. It’s tragically, increasingly common — about a third of Americans have diabetes or pre-diabetes — and treatable but incurable. It causes your cells to fail to retrieve glucose from the blood, either because your pancreas isn’t producing enough insulin or the body’s cells ignore that insulin. (That’s “insulin resistance”; stand by.)

Put as simply as possible (in case your eyes glaze over as quickly as mine when it comes to high school biology), insulin “calls” your cells, asking them to take glucose from the bloodstream: “Yoo-hoo. Pick this stuff up!” When the insulin calls altogether too often — as it does when you drink sugar-sweetened beverages and repeatedly eat junk food — the cells are overwhelmed, and say, “Leave me alone.” They become resistant. This makes the insulin even more insistent and, to make matters worse, all those elevated insulin levels are bad for your blood vessels.

Diabetes causes complications too numerous to mention, but they include heart disease, which remains our No. 1 killer. And when the cells in your brain become insulin-resistant, you start to lose memory and become disoriented. You even might lose aspects of your personality. In short, it appears, you develop Alzheimer’s. A neuropathologist named Alois Alzheimer noticed, over a century ago, that an odd form of protein was taking the place of normal brain cells.

How those beta amyloid plaques (as they’re called) get there has been a mystery. What’s becoming clear, however, is that a lack of insulin — or insulin resistance — not only impairs cognition but seems to be implicated in the formation of those plaques. Suzanne de la Monte, a neuropathologist at Brown University, has been working on these phenomena in humans and rats. When she blocked the path of insulin to rats’ brains, their neurons deteriorated, they became physically disoriented and their brains showed all the signs of Alzheimer’s.

The fact that Alzheimer’s can be associated with low levels of insulin in the brain is the reason why increasing numbers of researchers have taken to calling it Type 3 diabetes, or diabetes of the brain.[2] Let’s connect the dots: We know that the American diet is a fast track not only to obesity but to Type 2 diabetes and other preventable, non-communicable diseases, which now account for more deaths worldwide than all other causes combined.

We also already know that people with diabetes are at least twice as likely to get Alzheimer’s, and that obesity alone increases the risk of impaired brain function. What’s new is the thought that while diabetes doesn’t “cause” Alzheimer’s, they have the same root: an over consumption of those “foods” that mess with insulin’s many roles. (Genetics have an effect on susceptibility, as they appear to with all environmental diseases.)

“Sugar is clearly implicated,” says Dr. de la Monte, “but there could be other factors as well, including nitrates in food.” If the rate of Alzheimer’s rises in lockstep with Type 2 diabetes, which has nearly tripled in the United States in the last 40 years, we will shortly see a devastatingly high percentage of our population with not only failing bodies but brains.

Even for the lucky ones this is terrible news, because 5.4 million Americans (nearly 2 percent, for those keeping score at home) have the disease, the care for which — along with other dementias — will cost around $200 billion this year. Gee. That’s more than the $150 billion we’ve been saying we spend annually on obesity-related illnesses. So the financial cost of the obesity pandemic just more than doubled.

More than 115 million new cases of Alzheimer’s are projected around the world in the next 40 years, and the cost is expected to rise to more than a trillion of today’s dollars. (Why bother to count? $350 billion is bad enough.) The link between diet and dementia negates our notion of Alzheimer’s as a condition that befalls us by chance. Adopting a sane diet, a diet contrary to the standard American diet (which I like to refer to as SAD), would appear to give you a far better shot at avoiding diabetes
in all of its forms, along with its dreaded complications.

There are, as usual, arguments to be made for enlisting government help in that struggle, but for now, put down that soda!

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Red Wine Could Mask Testosterone Levels, Experts Warn

Red wine could give athletes and players a boost in the sports arena by increasing the amount of performance-enhancing hormone testosterone in their bodies, according to researchers from London's Kingston University.

However not only could the beverage help them to trophy success, it could also allow them to beat anti-doping tests. A team led by Professor Declan Naughton, from the University's School of Life Sciences, found that red wine might reduce the amount of testosterone excreted by the body, which could distort the findings of drug tests taken from urine samples.

Testosterone is a naturally-occurring steroid hormone present in both men and women. It can increase muscle mass, boost stamina and speed up recovery. Sportspeople, however, are prohibited from taking it, or a synthetic version of it, to try to gain a competitive edge.

Although red wine is not a banned substance away from the sports field, Professor Naughton's team has referred its findings to the World Anti-Doping Agency because of the newly-discovered side effect of potential change to the amount of testosterone in the body.

"Previous research has shown the effect over-the-counter anti-inflammatory drugs can have on enzymes," Professor Naughton explained. "Since many of these drugs are derived from plants, we decided to look at the effect particular foods and beverages can have on enzymes involved in testosterone excretion. We chose green tea and then red wine because both have a huge variety of natural molecules and we wanted to see if they affected the amount of testosterone excreted in urine."

The team found that a compound in red wine, known as quercetin, partially blocked the action of an enzyme called UGT2B17, which looks for testosterone and then sends a message to the kidneys to excrete it.

Professor Naughton stressed that the research had so far been conducted in test tube experiments and had yet to be trialled on humans. "A full clinical study would be needed to determine the effects on people but, if the same results were found, it would confirm that compounds in red wine can reduce the amount of testosterone in urine and give a boost to testosterone levels," he explained.

The effect of red wine on an individual would vary because of factors such as weight, fitness, health and diet, making it hard to estimate how much was needed to improve performance, Professor Naughton said.

Teetotallers are not exempt from the effects. In fact, the alcohol content of red wine has very little impact because non-alcoholic molecules are responsible for inhibiting testosterone excretion.

The team also found the results were the same for red wine extract in supplement form. The active compounds such as quercetin are found in many foodstuffs as well as supplements.

The findings have been published in leading international journal Nutrition. The research follows an earlier study from Professor Naughton's team which showed that green and white tea could also inhibit testosterone excretion.

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Most-Used Diabetes Drug Works in Different Way Than Previously Thought

A team, led by senior author Morris J. Birnbaum, MD, PhD, the Willard and Rhoda Ware Professor of Medicine, with the Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, found that the diabetes drug metformin works in a different way than previously understood. Their research in mice found that metformin suppresses the liver hormone glucagon's ability to generate an important signaling molecule, pointing to new drug targets. The findings were published online this week in Nature.

For fifty years, one of the few classes of therapeutics effective in reducing the overactive glucose production associated with diabetes has been the biguanides, which includes metformin, the most frequently prescribed drug for type 2 diabetes. The inability of insulin to keep liver glucose output in check is a major factor in the high blood sugar of type 2 diabetes and other diseases of insulin resistance.

"Overall, metformin lowers blood glucose by decreasing liver production of glucose," says Birnbaum. "But we didn't really know how the drug accomplished that."

Imperfectly Understood

Despite metformin's success, its mechanism of action remained imperfectly understood. About a decade ago, researchers suggested that metformin reduces glucose synthesis by activating the enzyme AMPK. But this understanding was challenged by genetic experiments in 2010 by collaborators on the present Nature study. Coauthors Marc Foretz and Benoit Viollet from Inserm, CNRS, and Université Paris Descartes, Paris, found that the livers of mice without AMPK still responded to metformin, indicating that blood glucose levels were being controlled outside of the AMPK pathway.

Taking another look at how glucose is regulated normally, the team knew that when there is no food intake and glucose decreases, glucagon is secreted from the pancreas to signal the liver to produce glucose. They then asked if metformin works by stopping the glucagon cascade.

The Nature study describes a novel mechanism by which metformin antagonizes the action of glucagon, thus reducing fasting glucose levels. The team showed that metformin leads to the accumulation of AMP in mice, which inhibits an enzyme called adenylate cyclase, thereby reducing levels of cyclic AMP and protein kinase activity, eventually blocking glucagon-dependent glucose output from liver cells.

From this new understanding of metformin's action, Birnbaum and colleagues surmise that adenylate cyclase could be a new drug target by mimicking the way in which it is inhibited by metformin. This strategy would bypass metformin's affect on a cell's mitochondria to make energy, and possibility avoid the adverse side effects experienced by many people who take metformin, perhaps even working for those patients resistant to metformin.

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Treatment For Gastrointestinal Conditions May Be Improved By Targeting Neurotransmitter

Selective targeting of the neurotransmitter that differentially affects brain cells that control the two distinct functions of the pancreas may allow for new medication therapies for conditions like diabetes, dyspepsia and gastro-esophageal reflux, according to Penn State College of Medicine researchers.
"This study differs from what's been reported

previously about brain neurons that control the gastrointestinal tract," said R. Alberto Travagli, professor, Department of Neural and Behavioral Sciences, and lead investigator. "It provides further support to the idea that separate nerve pathways regulate the diverse functions of organs along the upper gastrointestinal tract."
The pancreas has two functional parts: one that releases digestive enzymes, and one that releases hormones like insulin and glucagon. The vagus nerve, which originates in the brain, regulates both of these pancreatic functions. This nerve detects chemical and biological changes that occur along the gastrointestinal tract and interprets and integrates these signals before sending appropriate responses back to the organs. In the brain, these signals tell the nerves controlling each specific organ what the proper response is -- for example, digestive processes and insulin release -- according to the signals detected in the GI tract.
Neurotransmitters in the brain and in organs like the pancreas control the nerve networks that receive these signals. Neurotransmitters are chemicals released from nerves that allow them to communicate with each other as well as with organs of the body. One of these neurotransmitters is glutamate, which acts on specific proteins called receptors that are present on the nerve cells. There are different classes and types of receptors that glutamate can act upon; one major class of these receptors is metabotropic glutamate receptors (mGluRs). This class is further divided into three subgroups -- I, II or III -- depending on their location and function on the nerve cells.
"The aim of this study was to investigate how these mGluRs are organized on nerve synapses -- the specialized structures that allow a signal to pass from one cell to another cell," Travagli said. "The second aim of the study was to see whether pancreatic insulin and enzyme secretions are controlled by different types of vagal motoneurons -- the cells of the nervous system that control motor functions of the pancreas through the vagus nerve."
Group II and III mGluRs are present in synapses that can either excite or inhibit the vagal nerve cells that send signals to the pancreas, and different outcomes can be seen depending on which group of mGluRs glutamate acts upon. When glutamate acts upon either group II or group III mGluR, insulin secretion is decreased. Pancreatic enzyme secretion is increased only by activation of group II mGluR by glutamate.
"The data shows mGluRs on brainstem vagal nerve circuits that regulate pancreatic functions are organized in a very specific manner," Travagli said. "This type of separation in their organization may allow for development of selective drugs that target very specific vagal neurocircuits in patients with such conditions as gastrointestinal reflux disorders, functional dyspepsia, gastroparesis and pancreatic exocrine or endocrine dysfunctions."

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Pig That Models Human Diseases Such As Obesity, Diabetes, And Cardiovascular Disease Gets International Attention

A detailed annotation of the genome of T.J. Tabasco, a pig from the University of Illinois South Farms, is the outcome of over 10 years of work by an international consortium. It is expected to speed progress in both biomedical and agricultural research. U of I Vice President for Research Lawrence Schook said that the College of ACES played a crucial role in getting the work started.

Funding that came through ACES allowed Schook and others to put together the Swine Genome Sequencing Consortium, an alliance of university, industry, and government laboratories in the U.S., Europe, and Asia. The USDA committed 10 million dollars to the project. Today the project includes scientists from more than 50 research groups.
Schook said that the project has three main objectives: (1) to serve as a blueprint for understanding evolution and domestication, (2) to advance research on animal production and health, and (3) to explore ways to use the pig in biomedical applications.
The first publication, which just appeared in Nature, focuses on the pig's evolution. Researchers compared the reference genome from T.J. Tabasco with genomes of wild and domestic pigs from Europe and Asia (including archaeological and museum samples), and to human, mouse, dog, horse, and cow genomes.
"The pig is interesting because the wild boar still exists," Schook explained. "We could look at domestication, and we also looked at speciation. From an evolutionary perspective, these Sus species diverge in a very short time."
The researchers traced the domestic pig back to Southeast Asia. From there, it spread across Eurasia. The glaciation period separated the pigs into two groups about one million years ago. Today they are almost sub-species. "However, their chromosome structures have stayed very similar," Schook noted.
Pigs were independently domesticated in western Eurasia and East Asia 10,000 to 15,000 years ago. There is evidence that as the early European settlers moved around, they bred the domesticated females with wild boars.
Pigs in Central and South America are thought to have originated on the Iberian Peninsula. In a paper soon to be published in Heredity, the researchers tracked how these pigs adapted to different climates, altitudes, and diets.
As well as providing insights into how the pig evolved, the genome sequencing provides valuable new tools for animal breeding. One is a DNA test that can identify individual pigs that are less susceptible to certain diseases or have a genetic predisposition to fattening rapidly, eating less, and bearing many offspring.
On the biomedical side, researchers will build on ongoing efforts to use the pig to model human diseases, including lifestyle diseases such as obesity, diabetes, and cardiovascular disease. The sequencing identified 112 genes in pigs that are also responsible for diseases in people, suggesting that pigs could be used for drug testing.
Another direction is to use pigs as a source of organs for humans. Schook mentioned islet cells for diabetics as an example.
"Human transplant of eyelets doesn't work because there's not enough cells in a single pancreas," he explained. "If you could have an animal source, even if they get rejected, they're plentiful."
Clearly, there are a plenitude of exciting possibilities for future research. "For me, the next phase is looking at this concept of epigenomics - of how the environment affects gene expression," Schook said.

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Gene Variations Linked To Higher Risk Of Bipolar Disorder

Scientists from the Florida campus of The Scripps Research Institute (TSRI) have identified small variations in a number of genes that are closely linked to an increased risk of bipolar disorder, a mental illness that affects nearly six million Americans, according to the National Institute of Mental Health.

"Using samples from some 3,400 individuals, we identified several new variants in genes closely associated with bipolar disorder," said Scripps Florida Professor Ron Davis, who led the new study, which was published recently by the journal Translational Psychiatry.
A strong tendency towards bipolar disorder runs in families; children with a parent or sibling who has bipolar disorder are four to six times more likely to develop the illness, according to the National Institute of Mental Health.
While the genetic basis for bipolar disorder is complex and involves multiple genes, it appears to be associated with a biochemical pathway known as cyclic adenosine monophosphate (cAMP) signaling system. The Davis laboratory and others have previously shown that the cAMP signaling plays a critical role in learning and memory processes. The new study focused on this signaling pathway.
"As far as I know, this has not been done before - to query a single signaling pathway," said Davis. "This is a new approach. The idea is if there are variants in one gene in the pathway that are associated with bipolar disorder, it makes sense there would be variants in other genes of the same signaling pathway also associated with the disorder."
The new study examined variations in 29 genes found in the two common types of bipolar disorder - bipolar disorder I (the most common form and the most severe) and bipolar disorder II. Genes from a total of 1,172 individuals with bipolar disorder I; 516 individuals with bipolar disorder II; and 1,728 controls were analyzed.
Several statistically significant associations were noted between bipolar disorder I and variants in the PDE10A gene. Associations were also found between bipolar disorder II and variants in the DISC1 and GNAS genes.
Davis noted that the location of PDE10A gene expression in the striatum, the part of the brain associated with learning and memory, decision making and motivation, makes it especially interesting as a therapeutic target.

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Risk Of Diabetes May Be Reduced By Up To 25 Percent By Moderate Coffee Consumption

Drinking three to four cups of coffee per day may help to prevent type 2 diabetes according to research highlighted in a session report published by the Institute for Scientific Information on Coffee (ISIC), a not-for-profit organization devoted to the study and disclosure of science related to coffee and health.
Recent scientific evidence has

consistently linked regular, moderate coffee consumption with a possible reduced risk of developing type 2 diabetes. An update of this research and key findings presented during a session at the 2012 World Congress on Prevention of Diabetes and Its Complications (WCPD) is summarized in the report.
The report outlines the epidemiological evidence linking coffee consumption to diabetes prevention, highlighting research that shows three to four cups of coffee per day is associated with an approximate 25 per cent lower risk of developing type 2 diabetes, compared to consuming none or less than two cups per day. Another study also found an inverse dose dependent response effect with each additional cup of coffee reducing the relative risk by 7-8 per cent.
Whilst these epidemiological studies suggest an association between moderate coffee consumption and reduced risk of developing diabetes, they are unable to infer a causal effect. As such, clinical intervention trails are required to study the effect in a controlled setting. One prospective randomized controlled trial, tested glucose and insulin after an oral glucose tolerance test with 12g decaffeinated coffee, 1g chlorogenic acid, 500 mg trigonelline, or placebo. This study demonstrated that chlorogenic acid, and trigonelline reduced early glucose and insulin responses, and contribute to the putative beneficial effect of coffee.
The report notes that the association between coffee consumption a reduced risk of type 2 diabetes could be seen as counter intuitive, as drinking coffee is often linked to unhealthier habits, such as smoking and low levels of physical activity. Furthermore, studies have illustrated that moderate coffee consumption is not associated with an increased risk of hypertension, stroke or coronary heart disease. Research with patients with CVD has also shown that moderate coffee consumption is inversely associated with risk of heart failure, with a J-shaped relationship.
Finally, the report puts forward some of the key mechanistic theories that underlie the possible relationship between coffee consumption and the reduced risk of diabetes. These included the 'Energy Expenditure Hypothesis', which suggests that the caffeine in coffee stimulates metabolism and increases energy expenditure and the 'Carbohydrate Metabolic Hypothesis', whereby it is thought that coffee components play a key role by influencing the glucose balance within the body. There is also a subset of theories that suggest coffee contains components that may improve insulin sensitivity though mechanisms such as modulating inflammatory pathways, mediating the oxidative stress of cells, hormonal effects or by reducing iron stores.
Dr. Pilar Riobó Serván, Associate Chief of Endocrinology and Nutrition, Jiménez Díaz-Capio Hospital of Madrid and a speaker at the WCPD session concludes the report, commenting: "A dose-dependent inverse association between coffee drinking and total mortality has been demonstrated in general population and it persists among diabetics. Although more research on the effect of coffee in health is yet needed, current information suggests that coffee is not as bad as previously considered!"

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Better Therapies For Cardiovascular Disease May Be Product Of Protein Tug Of War

Two proteins are in a tug of war that determines how much the body makes of superoxide, a highly reactive and potentially destructive product of oxygen that's dramatically elevated in cardiovascular disease, researchers report.
Their finding indicates an antiulcer drug just may help the body reduce excessive levels.
Hsp90 and Hsp70 are both heat shock proteins but appear to have opposite effects on reactive oxygen species production, said Dr. David J.R. Fulton, Interim Director of the Vascular Biology Center at the Medical College of Georgia at Georgia Health Sciences University.
"Our studies show that Hsp90 promotes the activity of Nox enzymes, the source of reactive superoxide and all of the reactive oxygen species that descend from it, while Hsp70 has an opposing action that inhibits Nox," Fulton said.
When researchers gave Hsp90 inhibitors, the binding of Nox enzymes to Hsp90 was reduced, its binding to Hsp70 increased and reactive oxygen species production decreased. The inhibitors also reduced reactive oxygen species production in blood vessels from obese mice, where it contributes to the loss of elasticity and narrowing that are hallmarks of cardiovascular disease. While Hsp90 inhibition was known to suppress inflammation and reduce cardiovascular damage, just how it made these positive changes was unknown.
The yin and yang the researchers found points toward a targeted therapy that should give Hsp70 the edge, said Dr. Feng Chen, postdoctoral fellow. Chen is first author of the study in the American Heart Association journal Arteriosclerosis, Thrombosis and Vascular Biology.
Hsp90 inhibitors are used to treat cancer, which depends on Hsp90 to support rapid cell division. But they also target proteins that help blood vessels relax, such as nitric oxide synthase, so probably are not a good choice in cardiovascular disease. "Cardiovascular disease is a chronic disease, and we want to minimize negative side effects while providing protection," Fulton said.
In this case, a better approach appears to be directly increasing the expression of Hsp70 with a drug such as geranylgeranylacetone, or GGA, an antiulcer drug used in Japan with relatively few side effects, Chen said. When the MCG researchers treated human aortic vascular smooth muscle cells with the drug, for example, Hsp70's binding to Nox increased while Nox's ability to generate superoxide decreased.
Next steps include looking at whether this increased expression of Hsp70 actually translates to healthier blood vessels in a cardiovascular model. "If we can upregulate Hsp70 without affecting nitric oxide synthase, it should," said Fulton, the study's corresponding author.
Hsp70 and 90 are chaperones that guide protein folding in different ways and can influence more than just whether Nox enzymes are stable or degraded. Hsp70 levels are regulated by the molecule heat shock factor, which is bound to and repressed by Hsp90. That's one reason why Hsp90 inhibitors increase Hsp70 levels.
Reactive oxygen species are not all bad, the researchers noted. At normal levels, they aid cell signaling and homeostasis as well as the mounting of an immune response. However, excessive levels associated with chronic inflammation are thought to accelerate cardiovascular disease. "A little bit is good; you want a well-honed immune system to fend of pathogens," Fulton said. "Chronic inflammation is the problem."
The researchers completed their studies in normal and diabetic mice - diabetes increases the risk of cardiovascular disease by at least 50 percent - as well as the saphenous, or major superficial leg veins, of patients with cardiovascular disease.

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