Category: Health


Guinness World Records

A 32-year-old woman is attempting to become the heaviest woman ever, but her nearest competitor, a woman who holds the record of “World’s Fattest Mom,” is having a hard time letting go of her heavyweight claim to fame, even as she says she’sgoing on a diet.

Susanne Eman, a 728-pound woman in Casa Grande, Ariz., is attempting to get into Guinness World Records as the “World’s Heaviest Woman,” and hopes to reach her goal by the time she’s 41. The 2012 edition of the book will be released later this month.

The last woman to hold the title, 1,200-pound Rosalie Bradford, died in 2006.

“The category is currently open,” a Guinness representative told HuffPost Weird News. “We’ve got several claims that we’re researching, and we may have a new title holder very soon.”

Eman has told reporters that she wants to shatter the record by packing on 1,600 pounds. Her ultimate goal: weighing in at one ton.

One of Eman’s high profile rivals, Donna Simpson, of Akron, Ohio, holds the Guinness record for heaviest woman ever to bear children. She won the title by weighing a whopping 532 pounds when she gave birth to her daughter, Jacqueline, in February 2007 — an event that required 30 doctors.

Simpson just announced to the world via HuffPost Weird News that she’s decided to go on a diet, but she’s having a hard time letting go of the “prestige” that goes along with the honor of being America‘s heaviest woman — and said she views Eman as an upstart trying to usurp her hard-earned

“She’s Lady Goo Goo to my Lady Gaga,” Simpson laughed, adding that no one in the “feeder” community — a subculture of men who love large women — knows who Eman is.

“If she was a serious gainer, the community would know about her,” Simpson said.

Simpson said she suspects that Eman is in cahoots with her ex-manager and is trying to get publicity in order to compete for her fan base. Even worse: She accuses Eman of trying to take away her “World’s Fattest Mom” title.

“She says she’s surpassed me as the world’s fattest mom, but she doesn’t understand that Guinness gave me the record because I was 532 pounds when I gave birth,” Simpson said. “She wasn’t that large when she gave birth to her kids.”


Simpson also feels Eman is irresponsible for having her teenage kids feed her, as opposed to the adult “feeder/gainer” relationship she had with her former fiance, Philippe Gouamba, with whom she broke up a few weeks ago.

Eman is chowing down on nearly 22,000 calories daily, including six eggs scrambled in butter, a half-pound of bacon, four potatoes, six pieces of buttered toast and a 32-ounce shake — and that’s just for breakfast.

Eman is under an exclusive contract to Barcroft Media, a British-based news agency, and was unavailable to be interviewed. However, a source close to her camp considers Simpson’s comments to be “a load of crap” designed to make Simpson money and get her a reality show.

The source added that while there is a push among the media to get the two into a cat fight, Eman prefers to stay focused on her own career, including a potential appearance on “Dr. Oz,” where she will prove she’s healthy by submitting to a physical.


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A new study suggests smoking, high blood pressure, diabetes and being overweight in middle age may cause brain shrinkage and lead to cognitive problems up to a decade later. The study is published in the August 2, 2011, print issue of Neurology®, the medical journal of the American Academy of Neurology.

“These factors appeared to cause the brain to lose volume, to develop lesions secondary to presumed vascular injury, and also appeared to affect its ability to plan and make decisions as quickly as 10 years later. A different pattern of association was observed for each of the factors,” said study author Charles DeCarli, MD, with the University of California at Davis in Sacramento and a Fellow of the American Academy of Neurology. “Our findings provide evidence that identifying these risk factors early in people of middle age could be useful in screening people for at-risk dementia and encouraging people to make changes to their lifestyle before it’s too late.”

The study involved 1,352 people without dementia from the Framingham Offspring Study with an average age of 54.

Participants had body mass and waist circumference measures taken and were given blood pressure, cholesterol and diabetes tests. They also underwent brain MRI scans over the span of a decade, the first starting about seven years after the initial risk factor exam. Participants with stroke and dementia at baseline were excluded, and between the first and last MRI exams, 19 people had a stroke and two developed dementia.

The study found that people with  developed white matter hyperintensities, or small areas of vascular brain damage, at a faster rate than those with normal  readings and had a more rapid worsening of scores on tests of executive function, or planning and decision making, corresponding to five and eight years of chronological aging respectively.

People with diabetes in middle age lost brain volume in the hippocampus (measured indirectly using a surrogate marker) at a faster rate than those without. Smokers lost brain volume overall and in the hippocampus at a faster rate than nonsmokers and were also more likely to have a rapid increase in white matter hyperintensities.

People who were obese at  were more likely to be in the top 25 percent of those with the faster rate of decline in scores on tests of executive function, DeCarli said. People with a high waist-to-hip ratio were more likely to be in the top 25 percent of those with faster decrease in their  volume.

A) A schematic cross-section of a mouse brain showing the distribution of CRHR1 gene activity and the associated neurotransmitter specificity. B) A glutamatergic neuron of the hippocampus. Credit: MPI of PsychiatryControl of fear in the brain decoded

 

 

 

 

When healthy people are faced with threatening situations, they react with a suitable behavioural response and do not descend into a state of either panic or indifference, as is the case, for example, with patients who suffer from anxiety. With the help of genetic studies on mice, scientists from the Max Planck Institute of Psychiatry have discovered two opposing neuronal regulatory circuits for the generation and elimination of fear. Both are controlled by the stress-inducing messenger substance corticotropin-releasing hormone (CRH) and its type 1 receptor (CRHR1). The availability of these factors in neurons that release glutamate in brain areas of the limbic system activates a neuronal network which causes anxiety behaviour. Conversely, in dopamine-releasing neurons in the mid-brain, these factors give rise to behaviour that reduces fear. Because disorders of the stress factors may be observed in many patients with affective illnesses, the scientists suspect that the pathological alteration of the CRHR1-dependent regulatory circuits may be at the root of such emotional maladies.

An organism’s response to stress is one of the key strategies essential to its survival in dealing with environmental factors. A balanced  is of particular importance here and is subject to a highly complex molecular regulation system. Corticotropin-releasing hormone (CRH), which is released in the brain and places the organism in a state of alert, is a central molecular factor of the. In addition to its effect as a hormonal messenger substance, it also controls the activity of neurons through binding to its receptors.

Many patients with  and depression display an altered hormonal stress response and have increased volumes of CRH in the brain. To investigate the underlying pathological processes, the research team working with Jan Deussing at the Max Planck Institute of Psychiatry carried out studies on the system. This enabled them to selectively deactivate an important factor, for example the CRH type 1 receptor, in certain cells, and thus establish the locations where the receptor is normally active and identify its function.

Using immunohistochemical methods and a series of transgenic mouse lines, the researchers succeeded in mapping the gene activity of the type 1 CRH receptor in the mouse brain in detail for the first time. Interestingly, a specific activity pattern emerged in different neuron groups which release different neuronal messenger substances. In regions of the forebrain (cortex, hippocampus, thalamus, septum), CRHR1 is detectable in glutamatergic and GABAergic neurons. As the , these regions are linked and, as the current study shows, trigger fear-inducing behaviour in glutamatergic neurons.

In regions of the midbrain (substantia nigra, ventral tegmental area), CRHR1 arises in dopamine-releasing neurons. The functional examination of the mice gave rise to the fairly sensational discovery that the stress hormone CRH actually reduces fear through its receptors in this part of the brain. These neurons demonstrably trigger the direct release of dopamine in regions of the forebrain and hence cause behaviour that overcomes fear.

The opposing effects of the fear-generating and fear-eliminating effect of the CRH/CRHR1 was demonstrated for the first time by this study and prompted the re-evaluation of the use of CRH-receptor antagonists as anxiolytic and antidepressant drugs. The authors speculate that the over-activity of the CRH system in patients with mood disorders is not general but probably limited to certain regulatory circuits in the brain, thus causing imbalanced emotional behaviour. “The use of CRH-receptor 1 antagonists could be particularly useful in patients in who one of these systems is out of sync,” says research group leader Jan Deussing.

With diabetes, untreated depression can lead to serious eye disease

With diabetes, untreated depression can lead to serious eye disease

 

 

Patients with diabetes who also suffer from depression are more likely to develop a serious complication known as diabetic retinopathy, a disease that damages the eye’s retina, a five-year study 

Diabetic retinopathy occurs when  is not properly managed and is now the leading cause of blindness in patients between 25 and 74 years old, according to the study appearing online in the journal General Hospital Psychiatry.

“Our study controlled for obesity, smoking, sedentary lifestyle and HbA1c levels, and still found that  was associated with an increased risk of retinopathy,” said co-author Wayne Katon, M.D.

HbA1c is a blood test that measures a person’s average blood sugar levels over several months.

Katon is the director of health services and psychiatric epidemiology at the University of Washington Medical School, in Seattle. He and his colleagues studied 2,359 patients with diabetes enrolled in the Pathways Epidemiologic Study and assessed their levels of depression using the Patient Health Questionnaire-9 (PHQ-9), a self-reported survey of depression symptoms.

Over the five-year follow-up period, 22.9 percent of the patients who had PHQ-9 scores that ranked as “major depression” developed , compared with 19.7 percent of the patients without depression. With a five-point increase on the PHQ-9 score, patients’ risk of having diabetic retinopathy increased by up to 15 percent.

“Our findings suggested that psychobiologic changes associated with depression such as increased cortisol levels and activity of blood-clotting factors may be linked to the development of retinopathy,” Katon said.

“There is no question that the burden of depression among patients with diabetes is very high and that depression is a risk factor for worse outcomes in patients with diabetes, as was seen in this study,” said Todd Brown, M.D., an assistant professor of medicine at the division of endocrinology and metabolism at Johns Hopkins University.

He added that multiple explanations might account for these findings—some related to biological changes and some due to behavioral social issues, such as decreased physical activity and poorer utilization of health care.

“The big question with all of this is whether identifying and treating depression in patients with diabetes will change clinical outcomes,” Brown said. “And currently, there are no universal recommendations for depression screening among patients with diabetes.”

Many Americans suffer from diabetes and hypertension and, according to a study by researchers at the University of Michigan Kellogg Eye Center, these individuals may have an increased risk of developing open-angle glaucoma (OAG).

 

Joshua D. Stein, M.D., M.S., a glaucoma specialist at Kellogg, led a research team that recently reviewed billing records of more than 2 million people aged 40 and older who were enrolled in a managed care network in the United States and who visited an eye care provider one or more times from 2001 to 2007. The researchers found that people with  alone had a 35 percent increased risk of developing OAG and those with hypertension alone had a 17 percent increased risk. For people with both diabetes and hypertension, there was a 48 percent increased risk of developing OAG, the most common form of glaucoma in the country.

The study focused on the possible associations between various components of—a collection of conditions that includes obesity, hypertension, diabetes, and hyperlipidemia (high cholesterol and high triglyceride levels)—that affects one fifth of the U.S. population. The Kellogg researchers also examined how each component increased or decreased the risk of glaucoma.

While the researchers found that diabetes and hypertension increased the risk of OAG, the study showed that hyperlipidemia actually reduced by 5 percent the risk for developing the disease. Further research is under way to evaluate whether it is the hyperlipidemia itself, the medications used to treat the condition, or both that reduces the risk of glaucoma. Findings from this research may eventually lead to novel treatments for glaucoma.

“Patients who have diabetes and hypertension are already known to be at elevated risk for eye conditions like diabetic retinopathy, a condition that harms the blood vessels in the retina,” says Dr. Stein. “This study and others suggest that, for these patients, an increased likelihood of glaucoma is also a concern.”

Glaucoma is a leading cause of irreversible blindness worldwide. In the United States, more than 2.2 million individuals have this disease. And, as the U.S. population ages, glaucoma diagnoses are expected to increase. Because OAG symptoms usually don’t surface until the disease has progressed, understanding the risks associated with OAG—elevated intraocular pressure, positive family history of glaucoma, increased age and non-white race—will help physicians identify which patients would benefit most from screening and monitoring.

“This study reinforces the importance of regular eye examinations for patients at increased risk of , including those with diabetes and ,” says Dr. Stein. ”

Researchers at the Joslin Diabetes Center have shown that an enzyme found in the mitochondria of cells is decreased in the skeletal muscle of those with diabetes, a finding that could lead to the development of drugs to boost the activity of this enzyme in an effort to fight the disease.

A paper in published online today in the , showed that the enzyme, Sirt3, is decreased in the skeletal muscle of humans and animals with  by at least half, compared to those without diabetes and that this may contribute to development of , one of the earliest manifestations of the disease. Sirt3 is found in the , the power producers of cells that convert energy into usable forms.

“Ours is perhaps the first study to understand what is going wrong in the mitochondria of those with diabetes,” said senior author C. Ronald Kahn, M.D., Head of the Joslin Section on Integrative Physiology and Metabolism and the Mary K. Iacocca Professor of Medicine at Harvard Medical School. “Many studies have shown that the mitochondria don’t work well in those with diabetes. This points to a cause of why they don’t work well.”

Dr. Kahn said the study sought to look at how decreased Sirt3 levels might affect the metabolism of cells, particularly how it could affect  in cells. “We know that one of the hallmarks of early diabetes is insulin resistance in muscle, but we didn’t know what caused it,” he said.

He said the study showed that when Sirt3 levels are low, as they are in the case of diabetes, the mitochondria of the cells are not as efficient in as they should be.

When the mitochondria become inefficient, they generate what are known as reactive  (ROS), chemically reactive molecules containing oxygen, which create insulin resistance in the muscles, he said.

“This is the first time this has been shown,” Dr. Kahn said.

The goal for the future will be to find ways to restore levels of Sirt3 or increase the activity of the existing Sirt3, perhaps with a drug, in a bid to improve insulin resistance in the muscle and improve muscle metabolism, he said.

“It is a new target,” he said.

Dr. Kahn noted that this study is one of the first demonstrations of a single defect that could affect mitochondrial metabolism and insulin signaling in the muscle.

“In further studies we will try to understand what proteins Sirt3 acts on,” he said.

He noted that one of the earliest hallmarks of diabetes is insulin resistance in the. As a result, a drug to boost Sirt3 levels could be useful in the treatment of prediabetes or in those newly diagnosed with the disease, he said.

“Agents which increase Sirt3 activity could, therefore, potentially reverse at least some of the adverse effects of type 2 diabetes,” the paper concludes.

Co-authors included Enxuan Jing, lead author, as well as Brice Emanuelli, Jeremie Boucher and Kevin Lee, all of Joslin; Matthew D. Hirschey and Eric M. Verdin, both of Gladstone Institute of Virology and Immunology and the University of California, San Francisco; and David Lombard, formerly of the Department of Genetics at Harvard Medical School and currently at the Department of Pathology and Institute of Gerontology at the University of Michigan.

Dr. Verdin noted that by “uncovering the multi-faceted role of SIRT3, we are laying important groundwork to better combat this widespread disease at the cellular level.”

Provided by Joslin Diabetes Center

A new study by Harvard School of Public Health (HSPH) researchers finds a strong association between the consumption of red meat—particularly when the meat is processed—and an increased risk of type 2 diabetes. The study also shows that replacing red meat with healthier proteins, such as low-fat dairy, nuts, or whole grains, can significantly lower the risk.

The study, led by An Pan, research fellow in the HSPH Department of Nutrition, will be published online in the American Journal of Clinical Nutrition on August 10, 2011 and will appear in the October print edition.

Pan, senior author Frank Hu, professor of nutrition and epidemiology at HSPH, and colleagues analyzed questionnaire responses from 37,083 men followed for 20 years in the Health Professionals Follow-Up Study; 79,570 women followed for 28 years in the Nurses’ Health Study I; and 87,504 women followed for 14 years in the Nurses’ Health Study II. They also conducted an updated meta-analysis, combining data from their new study with data from existing studies that included a total of 442,101 participants, 28,228 of whom developed type 2 diabetes during the study. After adjusting for age, body mass index (BMI), and other lifestyle and dietary risk factors, the researchers found that a daily 100-gram serving of unprocessed  (about the size of a deck of cards) was associated with a 19% increased risk of type 2 diabetes. They also found that one daily serving of half that quantity of processed meat—50 grams (for example, one hot dog or sausage or two slices of bacon)—was associated with a 51% increased risk.

“Clearly, the results from this study have huge public health implications given the rising type 2 diabetes epidemic and increasing  of red meats worldwide,” said Hu. “The good news is that such troubling risk factors can be offset by swapping red meat for a healthier protein.”

The researchers found that, for an individual who eats one daily serving of red meat, substituting one serving of nuts per day was associated with a 21% lower risk of type 2 diabetes; substituting low-fat dairy, a 17% lower risk; and substituting whole grains, a 23% lower risk.

Based on these results, the researchers advise that consumption of processed red meat—like hot dogs, bacon, sausage, and deli meats, which generally have high levels of sodium and nitrites—should be minimized and unprocessed red meat should be reduced. If possible, they add, red meat should be replaced with healthier choices, such as nuts, whole grains, low-fat dairy products, fish, or beans.

Worldwide, diabetes has reached epidemic levels, affecting nearly 350 million adults. In the U.S. alone, more than 11% of adults over age 20—25.6 million people—have the disease, according to the Centers for Disease Control and Prevention. Most have type 2 diabetes, which is primarily linked to obesity, physical inactivity, and an unhealthy diet.

Previous studies have indicated that eating processed red meats increases the risk of developing type 2 diabetes. Risks from unprocessed meats have been less clear. For instance, in 2010, HSPH researchers found no clear evidence of an association between eating unprocessed meats and increased risk for either coronary heart disease or type 2 diabetes, but that study was based on smaller samples than the current study, and the researchers recommended further study of unprocessed meats. Another HSPH study in 2010 linked eating red meat with an increased risk of heart disease—which is strongly linked to diabetes—but did not distinguish between processed and unprocessed red meats.

This new study—the largest of its kind in terms of sample size and follow-up years—finds that both unprocessed and processed meats pose a type 2 diabetes risk, thus helping to clarify the issue. In addition, this study is among the first to estimate the risk reduction associated with substituting healthier protein choices for red meat.

“Our study clearly shows that eating both unprocessed and processed red meat—particularly processed—is associated with an increased risk of type 2 diabetes,” said Pan. He noted that the 2010 U.S. dietary guidelines continue to lump red meat together with fish, poultry, eggs, nuts, seeds, beans, and soy products in the “protein foods” group. But since red meat appears to have significant negative health effects— of , cardiovascular disease, and even total mortality, as suggested by several recent studies—Pan suggested the guidelines should distinguish red meat from healthier protein sources and promote the latter instead.

More information: “Red Meat Consumption and Risk of Type 2 Diabetes: 3 Cohorts of U.S. Adults and an Updated Meta-Analysis,” An Pan, Qi Sun, Adam M. Bernstein, Matthias B. Schulze, JoAnn E. Manson, Walter C. Willett, and Frank B. Hu, American Journal of Clinical Nutrition, online August 10, 2011.

 

79 million American adults have prediabetes and will likely develop diabetes later in life, according to the Centers for Disease Control and Prevention. As the number of people diagnosed with diabetes continues to grow, researchers are focusing on discovering why the prevalence of the disease is increasing. John Thyfault, an assistant professor in MU’s departments of Nutrition and Exercise Physiology and Internal Medicine, has found that ceasing regular physical activity impairs glycemic control (control of blood sugar levels), suggesting that inactivity may play a key role in the development of type 2 diabetes.

“We now have evidence that physical activity is an important part of the daily maintenance of ,” Thyfault said. “Even in the short term, reducing daily activity and ceasing regular exercise causes acute changes in the body associated with diabetes that can occur before weight gain and the development of obesity.”

Thyfault studied the relationship between low levels of physical activity and elevated levels of postprandial glucose (PPG), or the spikes in blood sugar that occur after a meal. PPG is a risk factor for the development of type 2 diabetes and has been associated with increased incidences of cardiovascular disease and death. Thyfault found that when healthy individuals reduced their physical activity by about half for three days, their PPG responses to meals doubled.

“A single bout of moderate exercise can improve the way the body maintains (blood ) and reduce PPG, but becoming inactive for a short period of time quickly disrupts glucose homeostasis,” Thyfault said. “This study shows that physical activity directly impacts health issues that are preventable.”

In the study, Thyfault monitored the activity levels and diets of healthy and moderately active young adults. Participants then reduced their physical activity by 50 percent for three days while replicating the diet they consumed when they were active. Continuous glucose monitors worn by the subjects during the period of inactivity revealed significantly increased levels of PPG. Spikes in blood glucose after meals can indicate increased risks for type 2 diabetes and cardiovascular disease.

“It is recommended that people take about 10,000 steps each day,” Thyfault said. “Recent evidence shows that most Americans are only taking about half of that, or 5,000 steps a day. This chronic inactivity leads to impaired glucose control and increases the risk of developing diabetes.”

More information: The study, “Lowering Physical Activity Impairs Glycemic Control in Healthy Volunteers,” will be published in Medicine & Science in Sports & Exercise. 

Increased low-grade inflammation in the body resulting from obesity is widely viewed as contributing to type 2 diabetes. Going against this long-held belief, researchers from Children’s Hospital Boston report that two proteins activated by inflammation are actually crucial for maintaining good blood sugar levels – and that boosting the activity of these proteins can normalize blood sugar in severely obese and diabetic mice.

The research, led by Umut Ozcan, MD, in the Division of Endocrinology at Children’s, is reported in the October issue of Nature Medicine, published online September 4.

“This finding is completely contrary to the general dogma in the  field that low-grade inflammation in obesity causes insulin resistance and ,” says Ozcan. “For 20 years, this inflammation has been seen as detrimental, whereas it is actually beneficial.”

Ozcan’s team previously showed that obesity places stress on the endoplasmic reticulum (ER), a structure in the cell where proteins are assembled, folded and dispatched to do jobs for the cell. This so-called “ER stress” impairs the body’s response to insulin in maintaining appropriate blood glucose levels, and is a key link between obesity and type 2 diabetes. Last year, Ozcan and colleagues showed that a  that relieves ER stress, called XBP1s, cannot function in obese mice. Earlier this year, they showed that activating XBP1s artificially in the liver normalized high  in obese, insulin-resistant type 2 diabetic mice (as well as lean, insulin-deficient type 1 diabetic mice).

The new study shows that a second protein triggered by inflammatory signals, p38 MAPK, chemically alters XBP1s, enhancing its activity — and that without these alterations, XBP1s cannot function to maintain normal glucose levels. The study further showed that obese mice have reduced p38 MAPK activity, and that re-activating p38 MAPK in the liver reduced their , increased insulin sensitivity and glucose tolerance, and significantly reduced blood glucose levels.

Together, the findings suggest that either increasing p38 MAPK activity — despite its being an inflammatory signal — or increasing XBP-1 activity by other means could represent new therapeutic options for diabetes.

The study also suggests a new model for understanding type 2 diabetes, in which may interfere with the ability of people’s cells to respond to inflammatory signals. “It may be that inflammatory pathways are not working optimally and there could be a resistance to cytokines which mediates the ,” Ozcan says. “This could be a paradigm shift for the field.”

The researchers also raise a possible down side in using p38 MAPK inhibitors to treat inflammatory diseases such as Crohn’s disease, psoriasis and asthma. “These therapeutic approaches should … be evaluated within the context of our results, and in light of the possibility that inhibition of XBP1s activity also decreases the ability of the cell to cope with the inflammatory conditions,” they write.


 

Bullet Proof Skin

Imagine having a gun fired at you, the bullet whizzing toward you at a super-fast speed. But instead of the bullet piercing your skin and traveling deep inside your body, what if it instead repelled off your skin?

What sounds like a scenario straight out of a superhero movie or a sci-fi novel could eventually become reality. Scientists have created a skin made with goat’s milk packed with spider-silk proteins, according to news reports. Their hope is that they can eventually replace the keratin in human skin — which makes it tough — with the spider-silk proteins.

To make the bullet-proof material, Dutch scientists first engineered goats to produce milk that contains proteins from extra-strong spider silk. Then, using the milk from the goats, they spun a bullet-proof material; a layer of real human skin is then grown around that skin, a process that takes five weeks, the Daily Mail reported.

“Science-fiction? Maybe, but we can get a feeling of what this transhumanistic idea would be like by letting a bulletproof matrix of spidersilk merge with an in vitro human skin,” researcher Jalila Essaidi told the Daily Mail.

Does it work? Well, the skin is only able to stop bullets fired at reduced speeds, TechNewsDaily reported. It was not able to stop a bullet from a .22 caliber rifle shot at a normal speed, which is the required standard for today’s bulletproof vests.

The skin is currently on display at the National Natural History Museum Naturalis in Leiden, Netherlands, until Jan. 8, 2012, TechNewsDaily reported.

More research must be done before this bullet-proof “super skin” can actually be possible to engineer into humans.

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