A place for all diabetics to meet, to support each other during their hard times, to discover that everyone of them has a healthy, happy and a wonderful life ahead.

If you are alive with Diabetes today, its because there are people who love you and want you to live along with them and care for you. And it is because of yourself too that you are living because you like yourself and you want to live this wonderful life successfully too.

Now face the reality, all you have to do is alter your lifestyle in a healthy manner, change your diet to  healthy but still tasty and predict the future complications and work towards them from now that is from this very second. consult doctor if needed, get a strategic plan.

Don't  forget that every process takes time. Be patient but active. have frequent fitness workouts , LAUGH

Sit back and relax, meditate in the  mornings. But don't forget to live your life to the top.


For further inspiration 
you can talk to me at
vaishnavinulureddi@gmail.com


Make your life special!!!!

Diabetes Facts

Rising Prevalence of Diabetes

An estimated 366 million people, corresponding to 8.3% of the world's adult population, lived with diabetes in 2011. The number is expected to grow to 552 million by 2030, corresponding to 7.8% of the adult population¹

While the global prevalence of diabetes is 8.3%, the prevalence varies from 10.7% in North America and the Caribbean to 4.5% in the African region.¹ However, the African region is expected to experience the highest increase¹

80% of the current cases of diabetes occur in low- and middle income countries.⁴ With an estimated 90 million people living with diabetes, China has the world's largest diabetes population, followed by India with 61.3 million¹

Diabetes is one of the major causes of premature illness and death worldwide.² Non-communicable diseases including diabetes account for 60% of all deaths worldwide³

The largest age group currently affected by diabetes is between 40-59 years¹

Bringing long term glucose levels down by a single point reduces the risk of blindness and kidney failure by 37%⁴

Diabetes Diagnosis and Treatment

Many people in developing countries with type 1 diabetes die before they are diagnosed or soon after diagnosis due to inadequate access to diabetes treatment⁵

In developing countries, less than half of people with diabetes are diagnosed. Without timely diagnoses and adequate treatment, complications and morbidity from diabetes rise exponentially⁶

Type 2 diabetes can remain undetected for many years and the diagnosis is often made from associated complications¹

The number of deaths attributable to diabetes in 2011 was approximately 4.6 million, equivalent to one death every seven seconds. The highest number of deaths due to diabetes is in India, China, United States of America, and the Russian Federation¹

Type 2 diabetes is responsible for 85-95% of all diabetes in high-income countries and may account for an even higher percentage in low- and middle-income countries¹

Up to 60% or more of type 2 diabetes is preventable by changing diet, increasing physical activity, and improving the living environment. Yet, without effective prevention and control programmes, the incidence of diabetes is likely to continue rising globally⁷

Insulin is vital for the survival of people with type 1 diabetes and often ultimately required by people with type 2 diabetes. Even though insulin's indispensible nature is recognised by its inclusion in the WHO's Essential Medicines List, insulin is still not available on an uninterrupted basis in many parts of the developing world⁸

In the Africa region, 78% of people with diabetes are undiagnosed¹

Bringing long term glucose levels down by a single point reduces the risk of amputations by 43%⁹

A person requiring insulin for survival in Mozambique will live an average of 12 months⁸

A person requiring insulin for survival in Zambia will live an average of 11 years⁸

A person requiring insulin for survival in Mali will live an average of 30 months⁸

Diabetes Costs – A Burden for Families and Society

The financial burden borne by people with diabetes and their families as a result of their disease depends on their economic status and the social insurance policies of their countries. In the poorest countries, people with diabetes and their families bear almost the whole cost of the medical care they can afford¹

In Latin America, families pay 40-60% of medical care expenditures from their own pockets. In Mozambique, diabetes care for one person requires 75% of the per capita income, in Mali it amounts to 61%, Vietnam is 51%, and Zambia 21%^1,9

Estimated global healthcare expenditures to treat diabetes and prevent complications totaled at least US dollars (USD) 465 billion in 2011. By 2030, this number is projected to exceed some USD 595 billion. An estimated average of USD 1,274 per person with diabetes was spent globally on treating and managing the disease in 2011

Besides excess healthcare expenditure, diabetes also imposes large economic burdens in the form of lost productivity and foregone economic growth. The largest economic burden is the monetary value associated with disability and loss of life as a result of the disease itself and its related complications¹⁰

The World Health Organization (WHO) predicted net losses in national income from diabetes and cardiovascular disease of International Dollars (ID) 557.7 billion in China, ID 303.2 billion in the Russian Federation, ID 336.6 billion in India, ID 49.2 billion in Brazil, and ID 2.5 billion in Tanzania (2005 ID), between 2005 and 2015. International Dollars (ID) correct for differences in purchasing power¹⁰

80% of people in developing countries pay directly for some or all of their own diabetes medication¹⁰

Diabetes and Changes in Society

More than 50 countries worldwide have a formalised "National Diabetes Programme"¹¹

From  changingdiabetesbarometer.com

Do You Meditate?

David Spero

Last Monday, I went to my first meditation class. For years, I have heard that meditation reduces stress, increases energy, and improves focus. It might also open the doors to spiritual growth. I’m finally giving it a try.

Perhaps I was inspired by Scott Coulter’s article about living in the moment, on this site last week. So I found a class on Meetup.com.That’s a great site — you just type in the kind of activity or group you’re looking for, and there’s a good chance you will find it not too far away. You have to pay to start your own group, but finding a group and joining it is free.

The class I joined is called Lighten Up Meditation. It’s meditating to music. Surprisingly, it’s not soft, gauzy New Age music. They use rhythmic, up-tempo Celtic music.

The energetic music surprised me, but Lisa, our teacher, explained that meditation is not for relaxing. It’s for focusing. The music reminds you to focus.

Lisa had us focus on one of two places in our bodies. First was the heart (fourth) chakra, which I gather is in the center of the chest. We did that for ten minutes, twice. Then she had us focus on the third eye (sixth) chakra, which is one finger width above the center of the eyebrows.

I don’t know anything about chakras, but Wikipedia says they are “centers of life force… Chakras correspond to…major [connecting points] of arteries, veins and nerves.” They seem sort of like the meridians in acupuncture, points and pathways through which our life energy is supposed to flow.

Unlike most kinds of meditation, in the type used in this class you don’t focus on your breathing, just on the chakra points. I’m not sure if the fourth and sixth chakras are supposed to have special benefits, or if they are just something to focus on. Perhaps I’ll find out more at the next class.

The day after class, I started a practice of meditating 15–20 minutes a day to Celtic music. I’m terrible at it. That’s why I’ve never stayed with it before. My thoughts just pour in. I turn them off for one or two breaths, and then they come right back.

I asked some friends and family about their experience with meditation, and they all said the same things. They tried for a while and gave up because they couldn’t keep the thoughts at bay for more than a few seconds.

But Lisa says that is totally normal. She says I just have to keep practicing. Very gradually, the thoughts will start to take longer breaks. When thoughts do come, it gets easier to let them go. Over time, you can get into deeper and deeper states. When the thoughts (brain chatter) fade, we can focus on other, more healing things.

I sense that this is possible. A few times this week, I was able to sense the world opening up as I focused on my heart, even though the periods only lasted a few seconds. And I must say I felt more relaxed afterward.

Lisa has been meditating for 25 years. She says it has changed her life profoundly, so much so that she teaches these classes for free and even gave out free CDs of meditation music. She says it has brought her to states of ecstasy, joy, and peace, and has brought huge amounts of love into her life.

That’s the kind of thing I was looking for when I came. I’ve become aware lately of people who seem to be able to visit heaven on a regular basis. Some have written books about it, like Jill Bolte Taylor’sMy Stroke of Insight and Eben Alexander’s Proof of Heaven. They got there through brain damage. Now they can visit regularly through meditation or something like it. I’d like to visit, too.

Even if I never get to heaven, there are proven health benefits to meditation. This Huffington Post article reports,

Studies show that meditation is associated with improvement in a variety of psychological areas, including stress, anxiety, addiction, depression, eating disorders and cognitive function, among others. There’s also research to suggest that meditation can reduce blood pressure, pain response, [and] stress hormone levels.

Many hospitals around the world now teach a meditation form calledMindfulness-Based Stress Reduction, because it benefits so many conditions. For 20 minutes a day, even if you can’t achieve Nirvana, it seems like it’s worthwhile.

I’ve committed to giving it one year of daily practice. I would appreciate any advice or experience you can share about meditating. Thanks.

**

My new book, cowritten with Jim Healthy, is out. Diabetes Heroes is about ordinary people reversing their Type 2 diabetes. A lot of inspiring stories like the ones we read here all the time, although the book features people who followed the diet outlined in Stefan Ripich’s30 Day Diabetes Cure. It’s pretty much the same things our readers do.

You can see a very moving video interview with one of the “heroes” here. The video also tells you how to get a free copy of the book.

From  Diabetesselfmanagement.com....

Cocoa May Help Fight Obesity-Related Inflammation

June 12, 2013 — A few cups of hot cocoa may not only fight off the chill of a winter's day, but they could also help obese people better control inflammation-related diseases, such as diabetes, according to Penn State researchers.

Mice that were fed cocoa with a high-fat diet experienced less obesity-related inflammation than mice fed the same high-fat diet without the supplement, said Joshua Lambert, associate professor of food science. The mice ate the human equivalent of 10 tablespoons of cocoa powder -- about four or five cups of hot cocoa -- during a 10-week period.

"What surprised me was the magnitude of the effect," Lambert said. "There wasn't as big of an effect on the body weight as we expected, but I was surprised at the dramatic reduction of inflammation and fatty liver disease."

The researchers reported that several indicators of inflammation and diabetes in the mice that were fed the cocoa supplement were much lower than the mice that were fed the high-fat diet without the cocoa powder and almost identical to the ones found that were fed a low-fat diet in the control group. For example, they had about 27 percent lower plasma insulin levels than the mice that were not fed cocoa. High levels of insulin can signal that a patient has diabetes.

The cocoa powder supplement also reduced the levels of liver triglycerides in mice by a little more than 32 percent, according to Lambert, who worked with Yeyi Gu, graduate student in food science, and Shan Yu, a graduate student in physiology. Elevated triglyceride levels are a sign of fatty liver disease and are related to inflammation and diabetes.

The mice also saw a slight but significant drop in the rate of body weight gain, according to the researchers, who reported their findings in the online version of the European Journal of Nutrition.

While researchers have linked obesity-related chronic inflammation to several diseases, including type 2 diabetes and fatty liver disease, the reason for the inflammation response is not completely known. Lambert said two theories on inflammation and obesity that have emerged may help explain cocoa's role in mitigating inflammation. In one theory, Lambert said excess fat may activate a distress signal that causes immune cells to become activated and cause inflammation. The cocoa may reduce the precursors that act as a distress signal to initiate this inflammatory response.

Lambert said that another theory is that excess fat in the diet interferes with the body's ability to keep a bacterial component called endotoxin from entering the bloodstream through gaps between cells in the digestive system -- gut barrier function -- and alerting an immune response. The cocoa in this case may help improve gut barrier function.

Cocoa, although commonly consumed in chocolate, actually has low-calorie content, low-fat content and high-fiber content.

"Most obesity researchers tend to steer clear of chocolate because it is high in fat, high in sugar and is usually considered an indulgence," Lambert said. "However, cocoa powder is low in fat and low in sugar. We looked at cocoa because it contains a lot of polyphenolic compounds, so it is analogous to things like green tea and wine, which researchers have been studying for some of their health benefits."

Lambert said he expects future research will be conducted to better identify why the cocoa powder is effective in treating inflammation, as well as determine if the treatment is suitable for humans.

The National Institutes of Health supported this work

Copyright from Science Daily....
.

A great way to cure Diabetes through your diet!!!!!!

Here is an extremely amazing, healthy, safe and foremost natural way to cure the deadly syndrome DIABETES TYPE 2 .By a detailed study of previous article that is the "role of Adiponectin and Leptin in diminishing Insulin Resistance" I have revised a method of equipping few food substances which have the capability of sensitizing both Adiponectin and Leptin to a good extent when included in diet.

And the wonderful diet when followed regularly which will take you one step ahead to lead a healthy life without diabetes is here.

Before that please check your ORAL GLUCOSE TOLERANCE TEST:

follow these steps:

A standard dose of glucose which is 75grams  is ingested by mouth  and the blood sugar levels(mg/dL)                       should be checked  after 2 hrs. This test is to be performed morning and the glucose is to be drunk within 5 minutes.

Normal values for a 75g -oral glucose tolerance test for TYPE 2 DIABETES are:

fasting: 60-100 mg/dL

1hour :less than 200mg/dL

2hour:less than 140 mg/dL

If the value you received are  between 140-200 mg/dL

then you have impaired adipocyte differentiation

If the value you received are above 200 mg/dL the you have a 

higher sign of diabetes

After that follow this as your morning diet(breakfast):

 1)Robusta cofee,without much roasting, without milk(better if preffered)-207ml-gives you required (70mg    to 350 mg) of chlorogenic acid.

 2)Navy beans-1/2 cup (cooked)-gives you around 9.8g of amylose resistant starch

 3) Barley (ground)-100g  in 300ml of drinking water-gives you 4.3 to 5.5g of beta-glucans.

 4)Flax seeds(ground) -1 tablespoon (can be incorporated in diet anyway possible)-gives you 1.6g omega-3 fatty acid and 

5)Grapes-75g -gives you required amount of osmotin (which is said to mimic the role of adiponectin).

6)Eating wheat breads also would give you a considerable amounts of beta-glucans.

After having the above diet follow  these steps:

check  your blood sugar levels for 10min,15min,30min,60min and 120 min after this and note them down. I'm sure you do find some difference in the former and the latter values!!!

There you go, you have made a step ahead in leading  a healthy life. Follow this regularly for better results.

I request you to write about this diet you have followed and all the values before and after having the diet.

contact me in:  vaishnavinulureddi@gmail.com

post comments on how you feel about this.

Sources cited;

Very few considerably safe Drugs for Diabetes due to side-effects

When someone with type 2 diabetes needs a third medication to control blood sugar levels, the choice may come down to which drug has the least undesirable side effects, because the available medications all lower blood sugar in a similar manner.

That's the conclusion of a new review of data that shows there were no great differences in the ability of various classes of medication to lower blood sugar among type 2 diabetics, when used as "third-line" treatment (after a first and second drug don't suffice).

However, the study also found that some medications could cause weight gain, and some caused episodes of low blood sugar levels (hypoglycemia).
In any event, "type 2 diabetes is a progressive disease and most patients will need the combination of two or three anti-hyperglycemic agents to reach good glucose control in the long-term," noted the study's lead author, Dr. Jorge Gross, a professor of medicine at the Hospital de Clinicas de Porto Alegre, Brazil.

"The choice of the third agent should be individualized according to the characteristics of the patients and the undesirable effects of the medications, so you can't elect one agent to be used in all patients with type 2 diabetes," he explained.

The study results were published in this week's issue of the Annals of Internal Medicine.
Metformin, an older medication that's available as a generic, is generally recommended as a first-line treatment for type 2 diabetes, along with physical activity and diet changes. If metformin and lifestyle changes fail to control blood sugar well, a second drug is generally added.

For this study, the researchers chose the commonly used combination of metformin and a sulfonylurea. Drugs in the sulfonylurea class are usually available as generics and include: glyburide, glipizide, chlorpropamide, tolbutamide and tolazamide.
"This study looked at what's probably the most common combination of diabetes medications, but even the second-line therapy should be individualized based on the patient's needs," said Dr. Robert Henry, president of medicine and science for the American Diabetes Association.

Third-line medications in the current study included alpha-glucosidase inhibitors (acarbose), thiazolidinediones (which include Avandia and Actos), glucagon-like peptide-1 (GLP-1) agonists, and dipeptidyl peptidase-4 (DPP-4) inhibitors.
The review included 18 clinical trials with a total of more than 4,500 people. The studies lasted an average of more than 31 weeks.

When the researchers compared reductions in hemoglobin A1C (HbA1C) levels, they found no statistically significant differences between the third-line medications. HbA1C is a blood test that measures long-term (about two to three months) blood sugar levels.
Weight gain was more common in people taking insulin or a thiazolidinedione. The average weight gain for those on insulin was about six pounds, according to the study. For those on thiazolidinediones, the average weight gain was more than nine pounds.

An average weight loss of 3.6 pounds was seen in people taking GLP-1 agonists, reported the study. Insulin was most likely to reduce blood sugar levels too much, raising the odds for hypoglycemia, according to the study.
Dr. Joel Zonszein, director of the clinical diabetes center at Montefiore Medical Center in New York City, stressed, however, that "these are mostly drug company studies, and they're not long-term studies."

This review "shows that giving a third agent can help, and it also shows us that these medications have both good and bad effects," he said. "But we really need long-term studies on combinations that aren't sponsored by the pharmaceutical companies."
The bottom line, according to Zonszein: "Each patient should be treated individually. Are they obese? If yes, there are certain medications like insulin and thiazolidinediones that may cause weight gain we don't want."

When it comes to third-line agents, Henry said, another factor may be price. Some medications aren't always available in generic form, which may make them significantly more expensive.
If you have specific concerns, such as weight gain or cost, Henry said it's important to bring these concerns to your doctor's attention when you're talking about adding another diabetes medication.

"If a third medication is needed because glucose control isn't adequate, get one that's tailored to your unique needs," he advised.
"We think that the results of this study offer a wide range of choices of anti-hyperglycemic agents that might be used as the third option in patients with type 2 diabetes not controlled using metformin and sulphonylurea based on efficacy. The final decision would depend on the effects in weight and risk of hypoglycemic episodes," said Gross.

Info from- US NEWS health

The Role of Adiponectin and Leptin in diminishing Insulin Resistance

Introduction

‘A family history, a chemical mystery or a diet and an exercise chemistry’- anything may today

 bring a person down from being healthy. And Diabetes Mellitus is the most common one, more commonly T2DM which is letting millions of people down either due to their sedentary lifestyle or inheritance. Globally, as of 2010, an estimated 285 million people have type 2 diabetes, making up about 90% of the total diabetic cases. There are several deleterious  complications that 

made me throw the spotlight over this aspect like diabetic ketoacidosis, retinopathy, neuropathy, atheroschlerosis, etc.

On reference to many clinical evidences and research papers, obesity happens to be one of the

 most important contributor to the increase in the insulin resistance as well as type 2 diabetes.

 This means insulin resistance is associated with accumulation of body fat like skeletal muscle

 lipid over supply, etc.

ADIPONECTIN

Adiponectin is a protein hormone that modulates a number of metabolic processes, including 

glucose regulation and fatty acid catabolism. Adiponectin is exclusively secreted from adipose

 tissue into the bloodstream and is very abundant in plasma relative to many hormones. Levels

 of the hormone are inversely correlated with body fat percentage in adults .Transgenic mice with increased adiponectin show impaired adipocyte differentiation and increased energy

 expenditure associated with protein uncoupling.  Adiponectin is secreted into the bloodstream

 where it accounts for approximately 0.01% of all plasma protein at around 5-10 μg/mL. Levels of 

adiponectin are reduced in diabetics compared to non-diabetics. Weight reduction significantly increases circulating levels.

Adiponectin automatically self-associates into larger structures. Initially, three adiponectin

 molecules bind together to form a homotrimer. The trimers continue to self-associate and form hexamers or dodecamers.

 Role of Adiponectin in AMPK activation  
 Adiponectin is a protein hormone that has positive metabolic effects like enhancing fatty-acid oxidation and glucose utilization in muscle and adipose tissue as well as in inhibiting gluconeogenesis  in liver where these are associated with the activation of AMPK(1,4) in muscle and liver and the activation of the nuclear factor-kb in muscle cells. Hexameric and HMW forms activate NF-kb in undifferentiated and differentiated c2c12 cells and improve insulin sensitivity in liver whereas trimeric forms activate AMPK in muscle and adipose tissues. (Muscle cells trimeric adiponectin causes a rapid 2-fold increase in 5’-AMP level)AMPK when activated by adiponectin phosphorylates  and inactivates acyl-coA Carboxylase (ACC) which is the enzyme that catalyzes the formation of Malonyl-CoA. Malonyl-CoA is a substrate for the fatty-acid bio-synthesis and inhibits fatty-acid oxidation. AMPK activation by adiponectin results in inhibition of fatty-acids and triglyceride synthesis and stimulation of FA beta-oxidation.

AMPK phosphorylates IRS-1 at ser789 which correlates with a 65% increase in insulin stimulated pl3k activity in c2c12 myotubes, since AMPK activates aPKC which plays a positive role in glucose transport. Adiponectin also increases PPAR-Y ligand activity.

   
Adiponectin and acyl-coA synthase

 Acyl-CoA synthetases catalyze the 1^st step of fatty acid metabolism;

  FA + CoA + ATP ͢Fatty acyl CoA + 5’ AMP +2 Pi and the activation of FFA’s to their CoA derivatives by these enzymes generate 5’ AMP. The resultant formed during the attachment  of FA’s  to CoA would then activate AMPK.( The result is ATP consumption and  AMP production)

LEPTIN

Leptin  is an adipose derived  protein hormone that plays a key role in regulating energy intake and energy expenditure, including appetite and metabolism. It promotes appetite suppressants  like α-MSH and lowers the hunger. Leptin acts directly on the cells of the liver and skeletal muscle where it stimulates the oxidation of fatty acids in the mitochondria. This reduces the storage of fat in those tissues (but not in adipose tissue). The absence of leptin leads to uncontrolled food intake and results in obesity. The obese people have high levels of leptin and consequently result in leptin desensitization. In a report, baseline plasma leptin did not significantly differ between subjects with newly diagnosed or long-standing type 2 diabetes compared with non diabetic controls matched for BMI; however, plasma leptin responsiveness to dexamethasone was impaired in the diabetic groups. Leptin may improve glucose uptake by muscle and decrease hepatic glucose production . Finally, there is evidence that leptin may protect against the adverse effects of fat accumulation within non adipose cells. Less circulating leptin may lead to improved sensitivity to leptin, possibly offsetting the consequences of the reduction.

Role of leptin in AMPK activation
  Leptin  stimulates phosphorylation and activation of the alpha2 catalytic subunit of AMPK           (alpha2 AMPK) in skeletal muscle, thus establishing signalling pathway for leptin. Early activation of AMPK occurs by leptin acting directly on muscle, whereas later activation depends on leptin functioning through the hypothalamic-sympathetic nervous system axis. In parallel with its activation of AMPK, leptin suppresses the activity of ACC, thereby stimulating the oxidation of fatty acids in muscle. AMPK activation inhibits the phosphorylation of ACC stimulated by leptin. We can identify AMPK as a principal mediator of the effects of leptin on fatty-acid metabolism in muscle

COMBINATION OF ADIPONECTIN AND LEPTIN

Through analysis of multi-variated research studies it can be suggested that the combination of

 leptin and adiponectin at the molecular level would completely reverse the insulin resistance syndrome. Other studies have shown that insulin resistance in lip atrophic mice can be effectively reversed by the combination of physiologic doses of adiponectin and leptin, but only partially by

 either alone.

HYPOTHESIS

It has been hypothesised that combination of both adiponectin and leptin would lead to a rapid increase in the AMPK activity rather alone and combining these would double the positive effects in reducing Insulin Resistance. They may suppress the ACC activity at a better potential.

The combination of  the  aspects that lead to insulin sensitivity and addition of these to the

 existing drugs for IR may improve the medication and help many people get away from this

 deadly metabolic syndrome or  may also give rise to a completely new drug to treat T2DM and

 IR. It would also more effectively help in reducing the wide-spread obesity and prevent its further complications.

REFERENCES

       Skeletal muscle lipid deposition and insulin resistance: effect of dietary fatty acids and exercise

       Michael P Corcoran,Stefania Lamon-Fava, and Roger A Fielding

       Intramyocellular lipid kinetics and insulin resistance     ZengKui Guo

       Novel role of FATP1 in mitochondrial fatty acid oxidation in skeletal muscle cells   David Sebastián*§,  Maria Guitart§**, 

         Contraction of insulin-resistant muscle normalizes insulin action in association with increased mitochondrial activity and fatty acid catabolismJohn P. Thyfault1, Melanie G. Cree2, Donghai Zheng3

       Adiponectin and Leptin in Relation to Insulin Sensitivity

GEETHA R. SOODINI, M.D., and OSAMA HAMDY, M.D., Ph.D.

    www.resistantstarch.com/NR/rdonlyres/

    A Potent and Selective AMPK Activator That Inhibits de Novo Lipogenesis

    Efficacy of Metreleptin in Obese Patients With Type 2 Diabetes: Cellular and Molecular Pathways Underlying Leptin Tolerance

-Vaishnavi.NR