#Diabetes - Dawn Phenomenon

Another interesting article I want to post - helps to share and helps me to find it again for future reference.




Dawn phenomenon

by Jim Hartmann

One of the most frustrating things that diabetics deal with is an unexpected rise in blood glucose overnight. You go to bed with a BG of 100 mg/dL (5.6 mmol/L), and wake up with a BG of 130 (7.2)! You didn’t eat, so what happened?

This results from two distinctly different processes: Dawn Phenomenon and Somogyi Effect. Here are some basics.

DAWN PHENOMENON

Everyone, diabetic or not, exhibits some Dawn Phenomenon. It is a natural part of our bodies’ circadian rhythms. Some have said it is the way our ancestors had the strength to rise and slay a woolly behemoth for breakfast.

Since most of us fast while sleeping, with teenagers a possible exception, our bodies use stored energy during sleep. The body uses all three macro-nutrients (carbohydrates, proteins, and fats) to store energy.

The most easily used is the storage medium of carbohydrates, called glycogen. Glycogen is made from glucose, and is stored in the liver and muscles. Since it is basically nothing more than a complex matrix of glucose, it is easy for the body to store and use, something the body does all day long. The technical term for the act of creating and storing glycogen is glycogenesis. When the body calls for the conversion of glycogen back to glucose it is called glycogenolysis.

Another macro-nutrient that is available to be converted to glucose is protein. Most of us think of our protein as being stored in muscle, but the body has protective mechanisms to make muscle wasting its last choice. One of the most useful and readily available sources of protein storage is in blood components, i.e., albumin (plasma). The body uses a process performed in the liver to convert amino acids, the building blocks of proteins, into glucose. The name for this process is gluconeogenesis, literally “the creation of new glucose”.

So, what does all this have to do with a high fasting BG? Overnight, usually between 4am and 11am, your body releases some hormones. These are Growth Hormone (GH) from the anterior pituitary gland, cortisol from the adrenal cortex, glucagon from your pancreatic alpha-cells, and epinephrine (adrenalin). These hormones cause an increase in insulin resistance, raising your BG. In addition, these hormones trigger glycogenolysis and gluconeogenesis, adding stored or new glucose to your bloodstream.

Dawn Phenomenon, and its associated increase in insulin resistance, is the reason most diabetics are far more sensitive to carbs in the morning.

Dealing with Dawn Phenomenon

There are many ways of defeating Dawn Phenomenon. You will have to experiment with the following suggestions to see what works for you.

1. Try eating no food after dinner. This works for people whose Dawn Phenomenon isn’t very strong. Basically, it lowers their baseline BG, so that when DP does hit them, the increase keeps them below a certain level, usually 120 (6.7).
2. Try eating a small snack of fat and protein before bed. Most find that a tablespoon of peanut butter, or some cheese and deli meat are effective. The theory here is that the slow-digesting fat and protein holds their BG high enough overnight to avoid Somogyi Effect (see below).
3. Eventually, you will learn how the two disparate approaches above work for you. Hopefully, you will set personal targets to guide you, eg., if my BG is below XXX (insert your target here), I need a snack. If my BG is over XXX, I don’t need a snack.
4. The prescription medication Metformin HCl (Glucophage) is often very effective in limiting Dawn Phenomenon for Type-2s and insulin resistant Type-1s. Of course, Type-1s can adjust their basal (slow) insulin regimen to account for Dawn Phenomenon.
5. Lastly, EAT BREAKFAST. The resulting increase in blood glucose from food will often turn off the continued rise. If you don’t, some diabetics will continue to rise until 10-11 am.

SOMOGYI EFFECT

Somogyi Effect, named for Dr. Robert Somogyi, its discoverer, is a high morning BG due to a low overnight. It is most commonly seen with insulin using diabetics, but is also seen with overnight reactive hypoglycemics.

The mechanism is a low overnight, which causes the body to react by releasing many of the same hormones seen in DP. The strongest blood glucose increasing hormone, glucagon, plays an important role. It tells your liver to start glycogenolysis and gluconeogenesis to provide enough glucose for your body to survive. This is sometimes referred to as a Liver Dump. Often, this mechanism over-produces, and you wake to a significantly higher BG.

Setting your bedtime BG target a bit higher, will usually prevent you from having a hypoglycemic event overnight.

Source: Diabetes Support Information Exchange UK

New to #Diabetes? Ask Your Doctor These Questions!

Posting to save and share:

Being diagnosed with diabetes can be a scary time for most patients. There is typically much uncertainty and an overload of information. If you have gotten the call to come in and talk with your doctor about your recent blood glucose testing, have this list of questions ready so that you can better understand your new diagnosis.

1. What is my fasting blood sugar? The fasting blood sugar is used to determine if a patient has hyperglycemia, or high blood sugar, or if the patient has diabetes. Any fasting value above 100 mg/dl is considered abnormal. A fasting blood sugar higher than 126 is diagnostic for diabetes. Anything in between these numbers is borderline high and at risk for developing type 2 diabetes.

2. What is my HbA1c? A hemoglobin A1c is a test that measures your blood sugar over 2-3 months. It gives an idea of what your average sugars have been. To manage diabetes with diet and exercise, the HbA1c should be below 7.0%. Anything higher than this may require the use of medications.

3. Do I need to see any specialists? Ask your doctor for a referral for an eye exam and ask if you need to see a foot doctor.

4. Can I test my sugars at home? Ask your doctor for a blood glucose machine, testing strips and lancets. Keep a daily log of readings and your food intake.

5. Can I see a certified diabetic educator? This may be the most valuable referral! These professionals will explain your condition and work with you to develop a personalized management plan.

6. Is it safe for me to exercise? You may need testing on your heart before you begin but weight loss and exercise are important parts of managing diabetes. Be sure that your doctor thinks that you are healthy enough to exercise before your begin.

7. Do I need any medications? As above, the need for medications depend on your blood sugar readings.

8. How often do I need to see my doctor or have blood work? You will likely need blood work checked every 3-6 months.

9. Is my blood pressure acceptable? Blood pressure readings should be less than 130/80 in diabetic patients.

10. Is my cholesterol acceptable? Your cholesterol should be in good control. Ask your doctors if your numbers are in line with the current recommendations for diabetic patients.

Bring this list with you to your appointment if you are overwhelmed and not sure which questions to ask. Understanding your diagnosis is the first step in learning how to live with diabetes and improve your blood sugars.

SOURCE:  eZine Health and Fitnes
s

Leptin May Prevent Type 2 #Diabetes

(Found an article I want to "Save and Share")

Pre-Existing Drugs May Restore Sensitivity to Leptin, an Appetite Suppressing Hormone

Jan 22, 2009

Hearts in the medical community beat with considerable excitement at the discovery of leptin in 1994. A hormone produced by fat, leptin has a very useful talent: it tells the brain when to stop eating. So hopes were high that leptin would become the basis of an anti-obesity treatment. What could be simpler than to dose an obese person with a hormone that says, "You're not hungry any more, and you want to stop eating."

Unfortunately, a snag soon emerged. Obese people do not respond to leptin. Scientists faced two mysteries: First, how do people become resistant to leptin in the first place? And second, are there any drugs that increase sensitivity to leptin?

Those questions have remained unanswered for a long time. But a Children's Hospital Boston study, published in the January 7 issue ofCell Metabolism, may have found the answers to both.

First, it appears that a stress-induced condition causes the hypothalamus, the region of the brain that responds to leptin, to resist the hormone.

Second, two drugs (4-PBA and TUDCA), which are already approved by the FDA for use in other medical applications, appear to greatly increase leptin sensitivity. The receptivity of lab mice resistant to the hormone increased as much as 10-fold when the two drugs were used as "chemical chaperones" to prime the mice for leptin injections.

The Boston study found that a condition called "endoplasmic reticulum" stress in the body's peripheral organs leads to leptin resistance. The endoplasmic reticulum (ER) is a cellular component that produces proteins. Other cellular components, called "molecular chaperones," then fold the protein into its ultimate three-dimensional shape and transport it. When the chaperones can't keep up, a stress response is triggered, called "unfolded protein response" (UPR).

The researchers suspected that ER stress and UPR blocked leptin's action in the brain and were at fault for the hypothalamus's leptin resistance. Previous studies had already shown that mice bred to have ER stress were leptin-resistant and tended to obesity. Once the researchers ascertained that such was the case, they turned to an experimental drug therapy that involved using 4-PBA and TUDCA as chemical chaperones.

Currently, 4-PBA (buphenyl) is used to treat cystic fibrosis and urea cycle disorders, while TUDCA (tauroursodeoxycholic acid) is used to treat liver diseases. Both are also being studied for possible treatment of Alzheimer's and Huntington's diseases. Because both drugs are already FDA-approved, the researchers believe that it will be easy to move them quickly to human trials.

A side benefit of the drugs' role as chemical chaperones is that they have also been shown to reduce ER stress in mice with type 2, restoringinsulin sensitivity and normalizing blood sugar levels.

Besides being a safe treatment for increasing leptin sensitivity in obese people, the drugs could also enter the rapidly expanding pharmacopeia of diabetes treatment medicines.

SOURCE: DiabetesHealth.com

#Diabetes - Blue Circle - The Universal Symbol for Diabetes

Here is another post that is to share a webpage that I also want to save for future reference and easy access - kinda like to "bookmark it", as it were (source link is at the very bottom). 

BLUE CIRCLE

The blue circle is the universal symbol for diabetes. Until 2006, there was no global symbol for diabetes. The purpose of the symbol is to give diabetes a common identity. It aims to:

• Support all existing efforts to raise awareness about diabetes
• Inspire new activities, bring diabetes to the attention of the general public
• Brand diabetes
• Provide a means to show support for the fight against diabetes

What is the history of the blue circle?

A global symbol for diabetes

The icon was orginially developed for the campaign that resulted in the passage of United Nations Resolution 61/225 "World Diabetes Day."

The campaign for a United Nations Resolution on diabetes was a response to the diabetes pandemic that is set to overwhelm healthcare resources everywhere. The campaign mobilised diabetes stakeholders behind the common cause of securing a United Nations Resolution on diabetes. The United Nations passed Resolution 61/225 ‘World Diabetes Day’ on December 20 2006.

Why a circle?

The circle occurs frequently in nature and has thus been widely employed since the dawn of humankind. The significance is overwhelmingly positive. Across cultures, the circle can symbolize life and health. Most significantly for the campaign, the circle symbolizes unity. Our combined strength is the key element that made this campaign so special. The global diabetes community came together to support a United Nations Resolution on diabetes and needs to remain united to make a difference. As we all know: to do nothing is no longer an option.

Why blue?

The blue border of the circle reflects the colour of the sky and the flag of the United Nations. The United Nations is in itself a symbol of unity amongst nations and is the only organization that can signal to governments everywhere that it is time to fight diabetes and reverse the global trends that will impede economic development and cause so much suffering and premature death.

Who owns the symbol?

The International Diabetes Federation (IDF) holds all rights to the blue circle for diabetes.

Promote the symbol

We encourage everyone to use the blue circle as a reference to diabetes and the millions of people affected by the disease. We welcome the use of the logo in publications: magazines, video, online information, etc.

The symbol may not be used without prior permission by IDF. It may not be used:

• To promote or refer to anything other than diabetes
• As a quality label
• For merchandising or any other form of commercial aim

While IDF holds all rights to the diabetes symbol, we can provide permission for merchandising carrying the diabetes symbol on a case-by-case basis. You can submit your proposal to communications@idf.org. Grounds for permission are (amongst others):

• Type of organisation
• Form of distribution of the material

Examples of how the blue circle can be been used:

• On posters
• On t-shirts
• Flags
• Pins

Please direct any questions related to the usage of the blue circle to communications@idf.org.

SOURCE: http://www.idf.org/node/2064

 

#Diabetes Art Day 2011

Diabetes Art Day 2100

September 1st is Diabetes Art Day, a web-based initiative for the Diabetes Online Community to “tell a story” about life with diabetes though creative visual expression. It’s a way for us to tell our stories so we can connect and share with each other and with our loved ones. It’s a way to generate diabetes awareness outside of the DOC by sharing artwork on Facebook, Twitter, blogs and community websites. Diabetes Art Day is for people young and old with any type of diabetes and their families, so children, spouses, parents, siblings, or anyone who is affected by diabetes can participate. For this one day, you’re encouraged to break out of your linguistic comfort zone, bust out some art materials, and make a piece of artwork – painting, drawing, collage, sculpture, an installation piece, a mixed media something or other, or whatever you can imagine. Whether you have lots of experience making art or none at all, Diabetes Art Day is for you to show the world what it’s like to live with diabetes in that “a picture is worth 1000 words” kind of way.

Let your creative spirit soar!

[Above text taken directly from the Diabetes Art Day Website]

For Diabetes Art Day I submitted a picture I had taken of my supply kit that I keep in my den. I changed it to all black and white with a color-pop of pink - my pink meter. I also have a blue meter, which is not in the picture, but if it had been I would have tried doing a double color-pop. Here is my submitted image:

#Diabetes - Food Conversion to Blood Glucose

Saw a similar chart on a facebook page and went  looking for this since I find it interesting  (and good to know).

Food conversion to blood glucose

Chart showing different food groups, the percentage converted to blood glucose

 and the time taken.

Carbohydrate sources: starches, (bread, pasta, potatoes, rice, crackers, cereal), fruits and juices, milk, sugar

Protein sources: meats (beef, pork, chicken, turkey, fish), cheese, eggs

Fat sources: butter, margarine, oil, salad dressing, mayonnaise, nuts, sour cream, cream cheese

Chart source: Diabetes Support Information Exchange UK

#Diabetes - Day 223

Well, still struggling with the glucose control sans Metformin. What kills me is the fasting - start the day so high and add to it with breakfast and just hope it comes back down enough by lunch that I'm not so hesitant to eat. But don't worry, i do eat, even though I may be hesitant. Funny thing with Diabetes - the food raises the glucose but you have to eat it anyway to keep the glucose on an even keel overall. 


But I also hate to think what this is doing to my A1c so if things don't get better in a couple of weeks I will make an appointment to go in and talk to my doctor about trying something different. And then just hope whatever we try doesn't have such adverse side effects.


Until then my logbook is just acting so friendly - greeting me with "high" "high" high" all the time!

#Diabetes - Day 220

Well, it's kinda depressing to see the BG numbers starting to reflect my having come off of Metformin. My good sense knew there was a very high probability this would happen, but my questionable sense held onto the hope that we actually caught my Diabetes and got it in control quickly enough that maybe my body would have forgotten that it was suppose to have Diabetes. I mean, I've seen people post things in discussion boards to the effect of "use to have Diabetes" or "once had" and such as that. And, every time I would see this I thought to myself that this/these person/people are delusional. All of the medical information I have read says that there is NO cure for Diabetes. That's the part my good sense was always referring back to. But I guess my questionable sense kept pushing it's naive wonderings (yeah, that may be one of my made up word) in there by saying that maybe, just maybe that really only applies to Type 1 Diabetes since that seems to actually relate more to a non-functioning pancreas whereas Type 2 Diabetes seems to relate more to an insulin resistance (and I will disclaimer here: I AM NOT A DOCTOR, REGISTERED DIETITIAN OR HEALTH CARE PROVIDER. THAT STATEMENT IS SIMPLY MY THOUGHTS AND CONCLUSIONS, MISALIGHNED OR NOT, REGARDING THE SIGNIFICANT DIFFERENCES BETWEEN T1 & T2 DIABETES). But anyway, my questionable sense kept saying that maybe, just maybe, if caught early enough, and quickly gotten in control, T2 could actually reverse and the body's cell would actually accept and use insulin correctly again. 


Well, I reduced my Metformin last Monday to 500mg per day. I took the last 500mg dose Sunday morning. I am not taking any Metformin at this time . . . and my BG numbers are starting to show it.


Good Sense knew this was a possibility, so why does it make me feel depressed when I see it in my meter? I sure wish Questionable Sense would not be so naughty!!

#Diabetes - Researchers Identify New Target for Treatment of Type 2 Diabetes and Prediabetes

Released: 8/22/2011 12:45 PM EDT
Source: Joslin Diabetes Center
Newswise — BOSTON — Aug. 22, 2011 — 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 type 2 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 Proceedings of the National Academy of Sciences, showed that the enzyme, Sirt3, is decreased in the skeletal muscle of humans and animals with diabetes by at least half, compared to those without diabetes and that this may contribute to development of insulin resistance, one of the earliest manifestations of the disease. Sirt3 is found in the mitochondria, 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 insulin action 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 energy metabolism as they should be.
When the mitochondria become inefficient, they generate what are known as reactive oxygen species (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 skeletal muscle. 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.”
The study was supported by research grants to Kahn and Verdin as well as a grant from the Ellison Foundation and the Mary K. Iacocca Professorship. The study also received support from the Joslin DERC cores laboratories.

Read the full article at newswise.com 

#Diabetes - Day 215

I have been having an awful lot of hair loss since being put on Metformin. Now, none of the literature that comes with Metformin says hair loss is a side effect, but if you search "Metformin and Hair Loss" on the internet you will finds tons of discussion boards where many many people have this same complaint.


I pretty much decided that if I have to choose between my health or my vanity, I will go with my health. If I lose all my hair I will just buy a wig and move on. Heck, I could buy two wigs and have fun with the second one by going completely different than what my hair color really is.


Well, that's all well and good, but there is another issue with this massive hair loss . . . I can no longer go in the kitchen and prepare a meal without constantly removing hair as it visibly drops off my head. It is very annoying. And even though hubby and I both know it is clean hair, really, who wants o pull hair out of their food - clean or not?!?!?


I thought I would have to get a hair turban and before going into the kitchen just wrap my head in a turban and change to a clean shirt, but I also thought my BG numbers are all so good - some almost too good, like a BG89 an hour and a half after lunch on one occasion - that I thought I would just call my doctor and see about getting off the Metformin for a while and see if the hair loss backs off.


Doctor's office of course suggested perhaps it is the thyroid and not the Metformin. Lets check that first. No problem - all it requires is a vial of my blood and a little time out of my afternoon to run down there.


Done. 


And, as a bonus, when I was at the doctors office he had the front desk send me up for a quick look at me and another weight check (lost another 3 pounds - not super great, but considering I had seriously neglected my exercise schedule during the summer while grand-kids were in and out (my justification - they came and went on different days so I was thrown off the "Monday - Friday then a weekend" concept and half the time I wasn't sure what day of the week it was.)). Anyway, I digress, back to the doctors office . . . 


He agreed that my number control had been very good and that I could come off the Metformin and we would see how that went. (Day 211)


Fast forward to yesterday afternoon - The nurse called to tell me that the thyroid test was negative. She said they look for a number between 0 and 4 and my test was a 2 - smack dab in the middle.


Now that thyroid is ruled out the only culprit left is the Metformin. Monday I reduced my daily dosage from 1000mg per day to 500mg per day. I have about 10 tablets left in this prescription and as soon as these run out I will be down to no Metformin at all. 


I realize it took a few months to build up the Metformin to the level that caused the hair loss, so likewise it will take a while for the hair loss to return to what would be (at least in my opinion) normal. 


Now the bigger task at hand to to be even more vigilant in my diet & exercise adherence to be sure I keep my glucose numbers in check. I really want to be able to keep this in control without going back on Metformin, or any meds, for as long as possible. *crosses fingers*

#Diabetes - Type 2 Diabetes: Coping With Your Diagnosis

Another good article I want to save & share. This one is from Everyday Health DOT com. Article located on their website at THIS LINK.

Type 2 Diabetes: Coping With Your Diagnosis

Living with diabetes means accepting the diagnosis and making the necessary changes to your life.

By Madeline Vann, MPH

Medically reviewed by Pat F. Bass III, MD, MPH

"Depressed" and "disappointed" are the words used by New Orleans resident Gary Davis to describe his feelings when he received his type 2 diabetes diagnosis two years ago.

“I am a nurse, so I knew what was happening, what was coming,” recalls the 51-year-old, referring to the long-term damage diabetes can wreak on a person’s health and body. Davis admits that initially, he didn’t want to try to make the changes that would improve his health. “At one time, I didn’t even try, but I try now. Every day I try harder,” he says.

Type 2 Diabetes: Avoid Denial

Receiving a diabetes diagnosis can stop you in your tracks. But for many people, hearing the news is the wake-up call they need to start healthy habits.

A Yale study of 20,221 overweight or obese adults under the age of 75 showed that people who receive a diagnosis of diabetes are more motivated to lose weight than their peers, dropping, on average, three pounds more with their diet plan.

“The big thing is to avoid denial. It’s so easy to deny,” says Paul Robertson, MD, president of medicine and science for the American Diabetes Association.

Many times doctors are part of this pattern of denial, says Dr. Robertson, especially when they tell patients that their blood sugar is a "little high, but we’ll just watch it." Robertson emphasizes, "That’s the time to jump on it! Don’t deny it — watch your weight, watch what you eat."

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Related: Ease Your Insulin Needle Fears

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Type 2 Diabetes: Make Changes

Two years after getting the news, Davis confesses, “I’m still confused about what I can and can’t eat.”

And, he adds, there are some foods, like white rice, that he can’t give up. Living in the capital of gumbo, jambalaya, and red beans, all of which are accompanied by white rice, this challenge may be understandable. But although Davis takes insulin to control his blood sugar, he is also taking steps to tackle diabetes by changing his diet and increasing exercise.

Based on his experience, Davis offers the following tips for coping with a type 2 diabetes diagnosis:

• Make an effort to change your diet and exercise habits. Even minor changes can help.
• Get educated about diabetes and what you need to do to stay healthy.
• If you can’t shake your sadness and get motivated, talk to a doctor about the possibility ofdepression.

“It’s hard because you have your certain lifestyle for so many years — I had mine for 49 years — and then someone is telling you [that you] have to completely change it,” says Davis.

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Related: Eight Celebrities With Type 2 Diabetes

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Type 2 Diabetes: Get Educated

Still, there is a wealth of good information out there about how to be healthy with type 2 diabetes, notes Davis. “Take advantage of the research projects. Take advantage of the literature. It’s really all about education,” he says.

Good resources for information on type 2 diabetes include your nurse, a diabetes educator, or a dietitian, all of whom can help you develop a plan for lifestyle change that will help control your blood sugar.

Type 2 Diabetes: Cope With Depression

If you find that you have a hard time getting motivated or you are continuing to feel sad or anxious many weeks after your diabetes diagnosis, consider talking to your doctor or a mental health professional about your concerns.

Not everyone who receives a diagnosis of diabetes experiences depression. But those who do may have a harder time taking steps to manage their disease. A study of 2,902 Native American adults showed that while depression does not make a person more likely to have diabetes, it does make it more difficult for people with diabetes to control their blood sugar levels. Treating depression is a necessary step towards blood sugar control.

“It won’t happen overnight,” says Davis. “But if you keep trying, you can succeed.”

#Diabetes - Type 2 Diabetes and Fatty Liver Disease

This article makes me wish I had researched Fatty Liver Disease when my doctor started treating me for that about 18 months before my Diabetes diagnosis. But I didn't, because he put me on medicine that was improving my triglyceride numbers so I figured it was getting in better and it was all good. Now I realize that treating the triglycerides was a band-aid for the Fatty Liver Disease but was not the cure for the cause. The same cause that fed the Diabetes.


But in all honesty, I never knew anyone diagnosed with Fatty liver Disease so I had no fear of it. I had known people with Diabetes and I knew how it had impacted their lives and in many cases how it had complicated other medical issues - so I had a fear of Diabetes. Diabetes made me start doing online research where Fatty Liver Disease did not.


And some might say my doctor should have told me Fatty liver Disease & T2 Diabetes are commonly seen almost hand in hand, but I can't fault him. He did tell me I needed to lose weight when he prescribed the meds for the Fatty Liver Disease. But his style is not to use scare tactics and I'm sure there are other medical complications that could come from Fatty Liver Disease also, so he would have sounded like he was reciting medical journals at that time. No, the fault is my own since I didn't do my due diligence. I took the script and expected the meds to make it all better and make it just go away. But it just doesn't work that way.


Anyway. Here is the article that prompted this post. It is from Everyday Health DOT com and can be found on their website through THIS LINK.

Type 2 Diabetes and Fatty Liver Disease

If you have type 2 diabetes, you are at risk of developing non-alcoholic fatty liver disease. Find out why and what you can do about it.

By Andrea Bledsoe, PhD

Medically reviewed by Lindsey Marcellin, MD, MPH

Non-alcoholic fatty liver disease is a group of conditions in which fat builds up in the liver, leading to inflammation of the cells where it is stored and causing the liver to get bigger. It can progress to more serious conditions, including fibrosis and cirrhosis of the liver.

Fatty liver disease "is so common. It’s present arguably in a majority of type 2 diabetics,” says Daniel Einhorn, MD, clinical professor of medicine at the University of California, San Diego and the medical director of the Scripps Whittier Diabetes Institute. “None of us thought about it more than about 10 years ago, then all of a sudden we discovered it and see it all the time.”

Fatty Liver Disease and Type 2 Diabetes: The Connection

Diabetes does not cause fatty liver disease. Instead, the two diseases tend to occur in the same people because the same conditions cause both problems. “So, it’s not the diabetes per se. People with diabetes also have obesity and insulin resistance, and so the fatty liver is thought to be part of that,” Dr. Einhorn explains.

Einhorn says that most cases of fatty liver disease do not cause any harm. However, since type 2 diabetes and obesity are so common in the United States, fatty liver disease is now a leading cause of end-stage (fatal) liver disease requiring a liver transplant, along with alcohol abuse and hepatitis.

Fatty Liver Disease Diagnosis

Fatty liver disease has no symptoms. People who are being treated for diabetes will have liver enzyme tests as part of their routine blood work during medical exams. Ninety-nine percent of the cases of fatty liver disease are detected by this test, says Einhorn. In some cases it will be picked up during the physical exam or in imaging studies, like a computed tomography scan of the abdomen or a liver ultrasound.

Einhorn says that fatty liver disease is not treated as a separate disease; therefore, doctors do not usually pin down the diagnosis with any additional studies unless liver enzymes are elevated unexpectedly, such as in a person without diabetes or obesity, or if the levels are very high and it appears that something else may be going on.

Fatty Liver Disease Treatment

There are no drugs that treat fatty liver disease. Instead, this condition is treated indirectly with lifestyle changes such as losing weight, getting in better physical shape, and controlling blood sugar and triglycerides — fats in the blood that can contribute to fatty liver. “You try to get the best possible control and hope that the fatty liver responds to that control,” says Einhorn.

Diabetes medications known as “insulin sensitizers” have been shown to have an effect in reducing fat in the liver; these include thiazolidinediones or glitazones such as pioglitazone (Actos) and rosiglitazone (Avandia), which are used to treat insulin resistance. It makes sense to use them if insulin resistance is part of fatty liver, explains Einhorn, but they are not U.S. Food and Drug Administration-approved for treating fatty liver disease.

Fatty Liver Disease Prevention

Type 2 diabetes, obesity, and fatty liver disease seem to go hand-in-hand. But it is not a given that if you have type 2 diabetes you will automatically develop fatty liver disease. Since obesity, insulin resistance, and high levels of triglycerides in the blood increase the risk of fatty liver disease, treating these other conditions can prevent its development.

Maintaining a healthy weight or losing weight if you are overweight or obese; exercising regularly; and controlling your blood sugar and triglyceride levels will go a long way toward safeguarding against fatty liver disease.

source: http://www.everydayhealth.com/type-2-diabetes/fatty-liver-disease-connection.aspx

 

#Diabetes - This Day in History - Insulin isolated in Toronto

Jul 27, 1921:

Insulin isolated in Toronto

At the University of Toronto, Canadian scientists Frederick Banting and Charles Best successfully isolate insulin--a hormone they believe could prevent diabetes--for the first time. Within a year, the first human sufferers of diabetes were receiving insulin treatments, and countless lives were saved from what was previously regarded as a fatal disease.

Diabetes has been recognized as a distinct medical condition for more than 3,000 years, but its exact cause was a mystery until the 20th century. By the early 1920s, many researchers strongly suspected that diabetes was caused by a malfunction in the digestive system related to the pancreas gland, a small organ that sits on top of the liver. At that time, the only way to treat the fatal disease was through a diet low in carbohydrates and sugar and high in fat and protein. Instead of dying shortly after diagnosis, this diet allowed diabetics to live--for about a year.

A breakthrough came at the University of Toronto in the summer of 1921, when Canadians Frederick Banting and Charles Best successfully isolated insulin from canine test subjects, produced diabetic symptoms in the animals, and then began a program of insulin injections that returned the dogs to normalcy. On November 14, the discovery was announced to the world.

Two months later, with the support of J.J.R. MacLeod of the University of Toronto, the two scientists began preparations for an insulin treatment of a human subject. Enlisting the aid of biochemist J.B. Collip, they were able to extract a reasonably pure formula of insulin from the pancreases of cattle from slaughterhouses. On January 23, 1921, they began treating 14-year-old Leonard Thompson with insulin injections. The diabetic teenager improved dramatically, and the University of Toronto immediately gave pharmaceutical companies license to produce insulin, free of royalties. By 1923, insulin had become widely available, and Banting and Macleod were awarded the Nobel Prize in medicine.

source: This Day in History

The Discovery of Insulin: the Work of Frederick Banting and Charles Best

1. Robert D. Simoni, 
2. Robert L. Hill and 
3. Martha Vaughan

 

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The Preparation of Insulin
 (Best, C. H., and Scott, D. A. (1923) J. Biol. Chem. 57, 709–723)

The story of the discovery of insulin has been well chronicled beginning with a young physician, Frederick Banting, in London, Ontario, imagining that it might be possible to isolate the internal secretions of the pancreas by ligating the pancreatic ducts to induce atrophy of the acinar cells and thereby minimize contamination of the tissue extract with digestive enzymes. Banting presented his suggestion to J. J. R. Macleod, a distinguished physiologist at the University of Toronto who provided Banting with a laboratory for the summer and some dogs for the experiments. Macleod also assigned Charles Best, a young student, to work as Banting's assistant for the summer. During the summer of 1921, Banting and Best made remarkable progress, and by fall they had isolated material from pancreas extracts that dramatically prolonged the lives of dogs made diabetic by removal of the pancreas. In the winter of 1922, Banting and Best treated their first human patient, a young boy, who's life was saved by the treatment. This was a stunning accomplishment. Consider that from the start of the research in the summer of 1921 to treating a human patient successfully in the winter of 1922, the pace, especially by current standards for clinical treatments, was remarkable.

With that achievement, Macleod, who had been initially unenthusiastic about the work, assigned his entire laboratory to the insulin project. He also enlisted the Eli Lilly Company to aid in the large scale, commercial preparation of insulin although the University of Toronto received the patent for insulin production. By 1923, insulin was available in quantities adequate for relatively widespread treatment of diabetes. Although the success of the insulin project was remarkable, the rewards for the research workers were, it seems, quite controversial. The 1923 Noble Prize in Physiology or Medicine was awarded to Banting and Macleod. Apparently, Banting was annoyed at the omission of Best and gave him half of his share of the prize. There was also, perhaps, the feeling that Macleod had done little in the initial stages of the work and was an undeserving recipient. Macleod split his share of the Prize with J. B. Collip who had made contributions to the later stages of the work on insulin purification.

After the spectacular events of 1921–1923, the University of Toronto established the Banting and Best Department of Medical Research separate from the University. Banting accomplished little during the rest of his career and died in a plane crash in 1940. Best, however, had a long successful tenure at the University of Toronto working on insulin and subsequently other important topics including the importance of dietary choline and the development of heparin as an anticoagulant.

The paper selected as this Journal of Biological Chemistry Classic is not itself “classic” in the usual sense. It reviews very well, however, a remarkable body of classic work. The information regarding various procedures that had been developed quickly and compared in attempts to improve the yield and purity of insulin also contains clues to some special properties of the protein, although so little was known at that time about the structure of insulin (or any protein) that there seemed little rationale for its purification. Insulin was crystallized in 1926 by John J. Abel (1). Virtually all of the information in this Introduction is from Ref.2.

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Frederick G. Banting. Photo courtesy of the National Library of Medicine.

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Charles H. Best. Photo courtesy of the National Library of Medicine.

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Footnotes

• The American Society for Biochemistry and Molecular Biology, Inc.

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References

1. ↵ 
   Abel, J. J. (1926) Crystalline insulin. Proc. Natl. Acad. Sci. U. S. A. 12,132– 136

    

   FREE Full Text
2. ↵ 
   Bliss, M. (1982) The Discovery of Insulin, The University of Chicago Press, Chicago, IL

source: The Journal of Biological Chemistry