Glooko is coming to Android and Google Play

So there is a product on the market called Glooko, which is a revolutionary new device that allows you to connect your Glucose meter to your iPhone and copy all of your test results over to your phone, thus allowing you to email them to your doctor.

 

Well back in 2011 – 2012 I was accepted to be a tester for this new product and wrote a series of articles about it. Since then they have made leaps and bounds with it. You see Glooko use to only be available to iPhone users.

However, I was again chosen to be a beta tester for their new Android App. I must say so far I'm a bit disappointed (so far) with the outcome of the Android version of Glooko. You see unlike the iPhone single sync cord version (left), the Android sync version (right) requires 2 parts. These parts are a square box that plugs into the earphone jack of your phone or mobile device and has a cord that plugs into that, then into your meter. The other thing about the Android version is that it is not powered by the phone or the tester. It requires a large button cell battery, and the unit must be manually turned on in order to begin the sync with your phone.

One thing that I did notice though, was the large database of supported glucose meters the new Android version has. When I tested the iPhone version back in 2011 they had very limited number of supported meters. They now have all the main name brands and a few off brand glucose meters supported. The other thing that I was pleased to see was that unlike the iPhone sync which needed a whole different attachment or meters that had IR (infrared) beaming abilities, it is now built into the Android version.

The other thing that has been improved is the app for both Android and iPhone. The new and improved app allows for better, smoother functioning, making it super simple for even the most tech challenged person to use.

All in all I give the Android Glooko reader 8 out of 10 stars. The only reason I’m scoring it at an 8 is because of the 2 piece system and the fact that it is battery operated and not self powered like its counterpart for the iPhone. Other than that, I am happy that they finally crossed over to the Android market. You can get your own Glooko setup for iPhone here. It is not fully available for Android consumers yet. But keep up to date with them via their Facebook Page, Website, or Twitter, so that you can be the first to know when the consumer version of Glooko for Android is released.

[UPDATE] 10/29/13

It seems as if I was a bit to harsh/hasty on the rating scale of 8 out of 10 stars. At first glance I was off put by the over all appearance of the sync cable being in 2 separate parts and being battery operated. However, it did not dawn on me that the unit having a built in IR might need the additional power that the phone would not be able to give and provide normal functioning battery life for the phone itself. And the fact that there are some meters on the market that are IR compatible that would be unnecessary to have a data cable that was constantly attached. So I am reevaluating it and giving it a 10 out of 10.

I am also pleased to know that your meter data is available across platforms. I was able to pull readings from my iPhone and see them on my Android. So this makes the device even more universal and friendly. That is why Im giving it 10 out of 10. I have also synced my other meters with the App with only a few finger swipes. Unlike other mobile Apps that boost their ‘ease’ of use features. With Glooko its 2 swipes and your new meter is ready to go.

Get your Glooko meter cable here http://www.amazon.com/gp/product/B00F9K7BWQ
Get Glooko for Android here https://play.google.com/store/apps/details?id=com.glooko.logbook
Get Glooko for iPhone here https://itunes.apple.com/us/app/glooko-logbook-diabetes-take/id471942748?mt=8

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ABOUT INSULIN

What is insulin?

Insulin is the internal secretion of the pancreas formed by groups of cells called the islets of Langerhans. It is the hormone needed to enable glucose to enter the cells and provide energy. Insulin is also important in keeping blood glucose levels within the acceptable limits.

Insulin is injected into the body by people with type 1 diabetes in whom the cells that produce insulin have been destroyed. This is the most common form of diabetes in children and young adults, and they depend on insulin for survival. Insulin may also be used by people with type 2 diabetes, where the body needs more insulin than it can produce.

How is insulin prepared?

Since the landmark discovery of insulin by Frederick Banting and Charles Best in 1922, huge steps have been made in research and development regarding its preparation. Early preparations of insulin were purified quite crudely from pancreas tissue extracted from animals - either pigs or cattle. Today, insulin is mostly made biosynthetically by recombinant DNA technology or 'genetic engineering'.

Animal insulin

Until the 1980s, all insulin was extracted from the pancreases of cattle and pigs. The sequence of amino acids (the building blocks that make up the protein) is slightly different in insulin's from the different species. Compared to human insulin, porcine (pork) insulin has one different amino acid and bovine (beef) insulin three different amino acids. These very slight differences do not affect the way in which the insulin works inside the human body. Pork insulin is structurally closer to human insulin than is beef insulin. These days, animal insulin's are made from highly purified pancreas extracts and are marketed as 'natural' insulin's.

Human insulin

Human insulin is not prepared from human pancreas tissue. Rather than being extracted from human pancreases, commercially available human insulin is manufactured through recombinant DNA technology, in which the gene for making human insulin is transferred into simple cells such as bacteria or baker’s yeast. The insulin made by those cells is identical to insulin made by the human pancreas. Unlike animal insulin's, recombinant DNA human insulin's can be made in unlimited supply, since they do not depend on the supply of bovine and porcine pancreases.
Analogue insulin
Analogues are altered molecular versions of a natural substance (in this case insulin). They have been used in many therapies where hormone treatment is needed. The natural hormone is changed slightly, by rearranging the position of amino acids within the molecule (rather like changing the position of beads on a necklace). The insulin molecule is modified so as to give it a more desirable activity profile, thereby making it more convenient to use. These molecularly engineered hormones more closely mimic normal insulin secretion than do traditional insulin's.

Types of Insulin
Manufactured insulin comes in several types that differ in the way in which they act inside the body. Each type differs in three ways:

• Onset: the length of time after injection that the insulin begins to work
• Peak: the length of time after injection that the insulin takes to reach its maximum effectiveness
• Duration: the length of time that the insulin remains effective

The four basic types of insulin and their respective onset, peak and duration are as follows:

• Rapid-acting: begins to work after 15 minutes, peaks in 30 to 90 minutes, and has a duration of three to four hours.
• Short-acting: begins to work in 30 to 60 minutes, peaks in two to three hours, and has a duration of three to six hours.
• Intermediate-acting: begins to work in 90 minutes to six hours, peaks in four to 14 hours, and has a duration of up to 24 hours.
• Long-acting: begins to work in six to 14 hours and remains effective for 24 to 36 hours.

Many people with diabetes use combinations of theses different types of insulin to better control and manage their condition.
Sources: Diabetes Insight (www.diabetes-insight.info); Diabetes UK (www.diabetes.org.uk); Juvenile Diabetes Research Foundation (www.jdrf.org) Insulin use in the world
Insulin is currently underutilized in developing countries as shown in the table.
Source: King H. Insulin: availability, affordability, and harmonization. WHO Drug 1998: 4: 219-223.
Some 65% of people with diabetes live in developing countries and account for only 30% of the world's total insulin usage each year. This is in sharp contrast to the industrialized world that has 35% of the world's diabetic population but account for about 70% of the world's total insulin usage each year.
This difference cannot be entirely due to the low incidence and prevalence of type 1 in the developing countries. Moreover, only a small percentage of people with type 2 diabetes in developing countries may require insulin for survival. The consequences are that in some parts of Africa many people with type 1 diabetes under the age of 15 can expect to live for just one year after diagnosis1.

 

ORIGINAL POST FROM http://www.idf.org/about-insulin-0

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Health Website that actually is…Healthy

I have always come across sites that boaster that they have excellent articles about heath, beauty and the like. But I found one that isn’t just a bunch of fluff and hot air. Behealthy24.com is one of the best sites that I have ever come across! They are on Online Magazine or E-zine that has informative articles, and research that is provided to you in a way that makes you truly understand what they are trying to say.

Most times when it comes to health and beauty you are bombarded with tons of information that makes it hard to really understand what it is that you are reading, but with behealthy24 its provided to you in a familiar format that is a easy and convenient read.
What first brought me to this site is that I was researching Diabetics and Skin Tags and Mole removal click here found an article about it (link) and then found other internal links to information about Skin Tags which provided me with information about them that I never knew.

I have bookmarked the site and started following them on Twitter and Facebook just so that I can keep up with their informative articles and helpful tips and tricks resource.

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Get the all new Hello Cupcake It's Me Android App FREE

Get the all new Hello Cupcake It's Me
Android App FREE

or download it from here
http://www.appsgeyser.com/377965
or download the APK Click Here

I am very excited to offer this App to all of my readers. I hope this issues in a new era of communication between me, you, and the blog.
If you have any questions, comments, suggestions, or concerns, please contact me.

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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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What is yours?

What is your favorite Sinful indulgent...? Mine has got to be ice cream or doughnuts *drools* like if I knew that my blood sugar wasn’t going to be 9,012 after eating them I would go freakin crazy on a box of raspberry or lemon jelly filled doughnuts, or a several whole cartons of ‘Death by Chocolatete” ice cream.

So what is yours? Everyone has at least one or two, and you don’t have to be diabetic to answer. My fav food has got to be pizza, my fav fast food has got to be McDonalds and Jack in the Box…

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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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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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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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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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Link Between Vitamin D Deficiency And Type 1 Diabetes

A study led by researchers from the University of California, San Diego School of Medicine has found a correlation between vitamin D3 serum levels and subsequent incidence of Type 1 diabetes. The six-year study of blood levels of nearly 2,000 individuals suggests a preventive role for vitamin D3 in this disease. The research appears the December issue of Diabetologia, a publication of the European Association for the Study of Diabetes (EASD).
"Previous studies proposed the existence of an association between vitamin D deficiency and risk of and Type 1 diabetes, but this is the first time that the theory has been tested in a way that provides the dose-response relationship," said Cedric Garland, DrPH, FACE, professor in UCSD's Department of Family and Preventive Medicine.
This study used samples from millions of blood serum specimens frozen by the Department of Defense Serum Registry for disease surveillance. The researchers thawed and analyzed 1000 samples of serum from healthy people who later developed type 1 diabetes and 1000 healthy controls whose blood was drawn on or near the same date but who did not develop type 1 diabetes. By comparing the serum concentrations of the predominant circulating form of vitamin D - 25-hydroxyvitamin D (25(OH)D) - investigators were able to determine the optimal serum level needed to lower an individual's risk of developing type 1 diabetes.
Based mainly on results of this study, Garland estimates that the level of 25(OH)D needed to prevent half the cases of type 1 diabetes is 50 ng/ml. A consensus of all available data indicates no known risk associated with this dosage.
"While there are a few conditions that influence vitamin D metabolism, for most people, 4000 IU per day of vitamin D3 will be needed to achieve the effective levels," Garland suggested. He urges interested patients to ask their health care provider to measure their serum 25(OH)D before increasing vitamin D3 intake.
"This beneficial effect is present at these intakes only for vitamin D3," cautioned Garland. "Reliance should not be placed on different forms of vitamin D and mega doses should be avoided, as most of the benefits for prevention of disease are for doses less than 10,000 IU/day."

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Electronic Medical Records

Living in the digital age has brought around new technologies that revolutionize the health care industry. In a day and age where you can keep the contents of your entire computer on something the size of a stick of gum, doctors and healthcare professionals are now pushing for their patients to carry thumb-drives with Electronic Medical Records on it. I know being a Diabetic I carry a thumb-drive with all my medical information on it so that way if I have a medical emergency, doctors and emergency response teams will have my whole history right there at their fingertips. Electronic medical Records Software is typically easy to use and there are companies that will even maintain these records for you. One such company that provides these services is Optimus ERM they offer:

ADT and Resident Information

The Electronic Chart (eChart)

Point-of-Care (POC) Documentation

Automated MDS

Integrated Electronic Heath Records

Fully Integrated Billing and Financial System

Electronic Control Center (eCC)—Management Dashboard

CPOE Physician Order Module

eMAR and eTAR (Electronic Medication Administration Records and Electronic Treatment Administration Records)

Pharmacy and Lab Interfaces

Physician Full Clinical Module

Complete Support for Integrated CCRC Campuses

Full Therapy (Rehab) Module that is Integrated with Resident Clinical Records

I strongly urge everyone to at least get one and update it with your current records and place one in a safety deposit box or on your keychain, you never know when it will save your life.

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Diet Enriched With Arginine And Proline May Speed Wound Healing In Diabetes

Chronic wounds such as foot ulcers are a common problem for diabetics and are the cause of more than 80 percent of the lower leg amputations in these patients. There is currently no effective way to improve healing of these types of wounds, but new research offers hope.
French researchers found that diabetic rats on a high protein diet with arginine and proline - specific molecules found in protein - showed better wound healing over rats fed either standard or high protein food without arginine and proline supplementation.
The article is entitled "Arginine plus proline supplementation elicits metabolic adaptation that favors wound healing in diabetic rats." It appears in the online edition of the American Journal of Physiology - Regulatory, Integrative and Comparative Physiology published by the American Physiological Society.
Methodology
Researchers divided 18 rats into three groups that were either fed a standard diet, a high-protein diet, or a high protein diet supplemented with arginine and proline (ARG+PRO). On the first day of the experiment, each rat was given an incision, under which a sponge was placed in order to collect wound-healing fluid. To assess skin regrowth and healing, researchers also removed two full-thickness sections of skin from the rats' backs each day from day 1 until day 5, when the experiment ended.
At the end of the experiment, the rats' blood was analyzed for blood sugar, insulin, and amino acid concentrations. The wounds on their backs were examined for skin regrowth and development of new blood vessels. And, finally, macrophages were collected from the sponges and analyzed for indications of cytokine stimulation and pro-inflammatory activity.
Results
Rats on both high protein diets had better nitrogen balance than those on the standard diet. However, the wounds of the rats on the ARG+PRO diet showed more new blood vessel growth on day 5. New blood vessel growth is an essential part of wound healing as the blood vessels supply nutrition and oxygen to growing tissue.
Furthermore, the macrophages in the ARG+PRO group showed less cytokine stimulation and pro-inflammatory activity than the other groups. This indicates a better environment for promoting wound healing, as inflammation slows the healing process.
The researchers did not find a difference in skin regrowth between groups, but their findings may be limited because of the small number of rats in the study. Additionally, researchers did not measure markers of collagen deposition in the wound, and the study cannot confirm the beneficial effect of arginine on collagen deposition and wound breaking strength reported in previous research.
Importance of the Findings
This study suggests that arginine and proline supplementation could offer new hope for effective treatment in diabetic patients with chronic wounds. This is a promising new area of research where there are no existing effective treatments for these patients.

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Free Kindle Fire Books

Hey everyone at the time of making this post these books are free for Kindle you don’t have to have a Kindle Fire you can download the free reading app for your computer. Here are the books.

Diabetes: Learn About Type 1 and Type 2 Diabetes (Diabetics Handy Guide to Diabetes)

 

 

The Complete Diabetic Diet: Small Changes Big Results - How a Special Diabetic Diet Can Help You in Prevention, Management and Reversal of Diabetes

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FREE Engraved Medical ID

Get a FREE Engraved Medical ID personalized with your name and medical information. If you have No medical conditions or allergies you can engrave your emergency contact information instead. Shipping is Free and No Credit Card is needed.

Click Here to Claim

You can choose from 3 different designs Stainless Steel Classic Bracelet with Curb Chain, Stainless Steel Dog Tag Blue on Bead Chain or Stainless Steel Small Silicone FlexBracelet.

One complimentary medical ID per address. Offer while supplies last.

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Free Diabetic Wrist Band

Get a Free Diabetes Awareness Bracelet Band + Free Shipping. November is Diabetes Awareness Month and American ID will be offering a free silicone bracelet band all month long. You can choose the color you would like black or white. Limit one per customer.

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Self-Application Of Electrical Stimulation At Acupressure Points May Relieve Stomach Woes For Diabetics

Diabetic patients who suffer from a common complication of diabetes called gastroparesis may find that chronic electrical stimulation (ES) at specific acupuncture points could relieve gastroparesis symptoms such as nausea, vomiting, early satiety, abdominal fullness, upper abdominal pain and bloating, according to study results unveiled at the American College of Gastroenterology's (ACG) 77th Annual Scientific meeting in Las Vegas.
The study, "Chronic Electrical Stimulation at Acupuncture Points Improves Dyspeptic Symptoms," used a watch-sized digital microstimulator that was specially developed for this project to assess the effects of ongoing electrical stimulation at acupuncture points on gastroparesis symptoms in diabetic patients with refractory gastroparesis. Despite medical therapy, these patients have not found relief for their symptoms and experience frequent physician and emergency room visits or hospitalizations because often they are unable to eat or keep food down and maintain proper nutrition, according to lead investigator Jiande Chen, Ph.D., of the University of Texas Medical Branch. "These are very severe symptoms and could be life-threatening as the treatment options for these patients are very limited and there are no effective medications," said Dr. Chen who noted that the device looks and works like the microstimualtors used to alleviate motion sickness that are already on the market.
Diabetes is a lifelong disease in which there are high levels of sugar in the blood. High blood glucose causes chemical changes in nerves and damages the blood vessels that carry oxygen and nutrients to the nerves. Gastroparesis is a type of nerve damage affecting the vagus nerve which controls the movement of food through the digestive tract. Ten to fifteen percent of the 25.8 million Americans living with diabetes have gastroparesis. This condition can worsen diabetes by making it more difficult to manage blood glucose levels because a delay in gastric emptying can cause a spike in glucose levels when the food finally enters the small intestine, according to the American Diabetes Association.
The device used for this blind cross-over design study on 26 diabetic patients with gastroparesis (18 completed the study) was worn either on the wrist or the leg with four-week ES and four-week sham ES in a randomized order. Electrical stimulation was performed via surface ECG electrodes placed at acupoints PC6 and ST36 using pulse trains. Sham-ES was performed using same parameters via non-acupoints. The PC6 acupuncture point is located on the wrist about 2 1/2 fingers up from the wrist crease on the inside of the forearm, while ST36 is located on the front of the leg, one hand width (four fingers) below the kneecap, on the outside, in the depression between the shinbone and the leg muscle.
Patients were asked to self-apply ES/Sham ES for two hours after each lunch and dinner and the electrogastrogram (EGG) and ECG were recorded at the beginning and end of each 4-week treatment.
According to investigators, 4-week ES not sham-ES "significantly improved" 5 of 9 gastroparesis symptoms: nausea by 29.7 percent; vomiting by 39.3 percent; abdominal fullness by 21.4 percent, bloating by 20.6 percent and retching by 31.1 percent. ES also resulted in a trend of increased vagal activity after eating.
"With all five symptoms significantly improving between 20 and 40 percent, this home-based, non-invasive electrostimulation therapy is feasible and effective in treating gastroparesis symptoms and possible mechanisms involving central, gastric and autonomic functions require further study, " said Dr. Chen. "Although this is a small study, the results are noteworthy because the side-effects and the cost are low." Dr. Chen added that the device is not yet on the market.

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