Sunday 6 January 2013

On Being a Diabetic

On being a diabetic...

Most people don't really want to know anything more about diabetes than they have to.  They certainly don't want to have to find out about it first hand.  I know because I am one of those people. Diabetes is for other people, not me.  I try to ignore the rising numbers of new cases across the continent...the percentages that seem to grow year after year.  Focusing on the negative could lead to hysteria, and who needs that, right? 

After all, what's wrong with these people that they don't know how to eat right?  If they just exercised and quit eating poorly, maybe they'd smarten up.  That's the message I had heard most of my young life... in the fifties, sixties, seventies, or as Buzz Lightyear says now, "to infinity and beyond".  It was a common way of thinking, blunt and to the point with little empathy for the daily struggle that diabetics must endure to stay on track.  Even armed with that simple formula, many diabetics die too young, but mostly not directly from diabetes, usually from other more insidious causes like heart disease or stroke.

Prior to the invention of insulin, diabetics literally dehydrated to death.  The higher the blood sugar, the sleepier the person became.  If it's high enough, they (you) could lapse into a coma.  I understand the dehydrating part because I use Tears eye drops for dry eyes.  My skin needs to get lathered with lotion, especially my feet. I remember camping in my Boler camper while attending summer classes at university sometime in the 1990's.  I am a sucker for Licorice All Sorts and ate most of a bag over the course of one evening.  I didn't put two and two together, but I got really, really tired and went to bed early.  It wasn't a fitfull sleep and I realize now, the licorice was definitely not a good choice and of course, my blood sugar was sky high. 

Carbohydrates warm your body up, so have a carb snack before you go to bed if you have trouble falling asleep. (Not a whole bag of licorice!)  Protein has the opposite effect, so have protein at lunch if you have a problem staying awake in the afternoon.  A good bedtime snack (if you need it), is a slice of whole wheat toast with peanut butter.  In case you don't know, fat holds the blood sugar at whatever level it's at for a little longer time.  Of course, peanut butter is a protein with fat and toast is a carbohydrate.

There's always the fear of the pendulum swinging too far in the other direction.  Insulin and certain diabetic medications have the potential to cause a low blood sugar. Diabetics with low blood sugar start to shake and sweat and their vision blurs. They may look drunk and have a fruity odor to their breath.  This happened in the parking lot of a mall one morning.  This guy had been trying to walk to McDonald's for breakfast and didn't quite make it.  Most people walked right by him thinking he was under the influence.  Luckily, one lady recognized the signs and decided to do something about it.  She had to fight with the clerks and the people ahead of her in the line to make people understand the urgent need this man had for food!  A student came running to my office since I was the health nurse at that school.  She said a woman was acting very strangely.  She was sitting at the lunch table, not eating, not moving, just staring straight ahead. She would speak in almost guttural tones if asked a question.  No one knew she was a diabetic.  As a latch ditch effort, I held up a glass of juice and made her drink...It was unbelievable to watch as she started coming back to life.  These are the weird things that can happen with low blood sugars.

A daily drink of dry, red wine can also serve to lower your blood sugar.  I said ONE drink.  Remember that if you're on insulin, this could backfire if you prefer to have a few.  First off, if you have a low blood sugar over night when you're sleeping, your liver will come to the rescue by releasing glucose into your blood stream.  When you drink too much alcohol though, your liver doesn't work in the same way, so please be careful. 

I understand that at some time this century, it was observed that those who ate less and did hard, physical labor (such as prisoners of war) survived with diabetes.  A simple case of diet control and exercise lead to more normal blood sugars and few symptoms.  I figure there were fewer cases of diabetes then in general, because people didn't have the many luxuries we enjoy today.  First off, they didn't have televisions or cars.  They had to stoke the stove with wood or coal, not touch the thermostat.  They worked hard, just to survive, not sit in front of the computer.  They had to saddle and feed a horse, then ride it which are all weight loss activities.  They walked most places they went and had, for the most part, far leaner body masses than we see today.  A few years later, they still had to get up off the couch and change the dial on the TV, or walk to the phone and dial the number.  They had to wash their own dishes in the sink, put their clothes through the wringer washer and hang them on the line.  They often went to community dances.  You understand what I'm saying as you hit the button for your garage door to open by itself.  :-)  We have already witnessed the age of the gigantic supersizing of pop and french fries for example.  These are fizzling out for a good reason.  While working as a nurse in the hospital I witnessed a young woman come in because she had gone blind in one eye.  Her blood sugar on the Canadian scale was 60 and I didn't even know they could measure it at that stage.  (The normal is between 4 and 6 mmol/dL).  She had been drinking a gigantic Slurpee every day for God knows how long.

Like most people, we too started out with diabetics in our extended family. All Type 2's.   (Type 1's are generally young and are born without or suddenly are found to have zero body insulin.  Sometimes a person is faced with injecting insulin following a viral infection that appears to wipe out their pancreatic beta cells.  ).

These Type 2's  in my family were and are all relatively normal (whatever that is).  Some were and are overweight and some slender.  All exhibit insulin resistance.  Rare were those with additional health problems initially, and all seemed to have inherited the disease. 

First my grandfather on my dad's side.  He died fairly young at 72.  Although he was admired for looking after my grandma after she had multiple strokes, he was said to have a miserable streak, due in part to the diabetes.  It's true, if your blood sugar is either too high or too low, it can affect your mood.  He was on insulin and in those days they called him a "brittle diabetic"...a term you hardly hear any more.  Next was his eldest granddaughter, (my first cousin).  She lived far away and one time when she visited, I learned she was taking four needles of insulin a day.  I shuddered. She said that everything you eat has sugar in it, even protein.  She was seeing all sorts of different doctors and alternative therapists and finding out the latest, breaking news on treating the illness.  Unfortunately, she passed away during surgery a few years ago.  She was in her late fifties or early sixties, I believe. 

Over the years, and one by one at least five and possibly six of my dad's eight brothers and sisters were diagnosed with diabetes.  Most were started on diet and exercise then had various pills added and finally were put onto injections of insulin.    One had an amputation of a lower extremity, but those closest to him said it was from wearing rubber boots all the time.  These people were all grandparents by the time they were diagnosed, whereas my eldest cousin had it as a young person.

Nowadays, my dad's side of the family could be the poster child for the diabetes family tree, it is so prevalent among us.  Males and females alike have the thing.  It's 50% prevalent in my family, which includes my older brother and I and that's all we know so far for us.  In the other seven families, it's a similiar story.  Diabetes is dotted throughout and being coped with by all.  One family has three out of five diagnosed.  That side of the family alone could start our own support group as a matter of fact.  Occasionally, some of us do get together and compare notes about what treatment we are currently on and what information we've received that might be new or different.  My generation is lucky that the blood glucose meter came into being and can give a more accurate measure.  Our parents and grandparents often could only test with urine test strips.

Next, my grandpa on my mom's side was diagnosed and not that many years later, my mom too.  I'm surrounded with it and I think it's pretty common knowledge that there's a genetic link.  I have two kids and four grandchildren myself, the rest of the families on both sides have countless offspring now.  You can almost guess at the new, future numbers of this little club that will present themselves within the next decade at this rate.

Nowadays, there are diabetes nurses and nurse practitioners to assist physicians with their diabetic patient caseload.  It becomes an onerous task to deal with people struggling and/or in denial.   There are patients who don't follow their treatment regimes, don't exercise, don't eat right, don't watch their cholesterol, don't, don't don't.  There are diabetics who follow a very strict regimen, but since diabetes sufferers are only human and under constant pressure to do the right thing, like anybody else, we fall off the wagon sometimes.  A considerable amount of our lives are spent  trying to get back on the track so we can get to a better place and to do the right thing.  Everyone gets burned out after awhile from the patients to their formal and informal support persons.  Our health care providers do everything they can and I am so thankful for their guidance, support and encouragement.  We are empowered through the Saskatchewan Health Quality Council's evidence-based standards to have "standing orders" for bloodwork at the lab.  We get our micro albumin checked annually (mine is in March).  Twice a year (March and September) I have a fasting C&T HDL and LDL (cholesterol).  Quarterly, I have my HgA1C checked.  This is a test that gives an indication of the average blood glucose level over the past three or four months. (March, June, September and December).

Nutritionists and dieticians are also available to educate and support diabetics.  When you as a diabetic finally make the leap to the idea that you actually have the disease and not just a little bit is when you might be able to absorb some training.  I attended various sessions over the years, and listened and changed the way I did things every time, but it wasn't until I was faced with going on insulin via needle that I came to attention.  I guess I had been in denial up until that very day, i.e. eight years later.  I was diagnosed in 1998 and fiddled with more different oral medications along with their multiple side effects than you can shake a stick at.  I did that until I finally bit the bullet and allowed myself to be started on an intermediate-acting insulin, NPH, once at bedtime.  You never saw anybody get dragged kicking and screaming to that point more than me.  This was about 2006. 

Unfortunately, that med gave me too many lows and about that time there were some really good basal insulins out.  I was started on Levemir, again with too many lows overnight.  Levermir seems to build up in your tissues and suddenly when the stars align in just a certain way, there you are with a low.  I've been lucky in that when I have a low while sleeping, I develop a serious case of heartburn-like symptoms and it wakes me up.  I can only hope and pray that continues to be the case.  I was finally started on Lantus basal insulin and quit the oral meds completely (except for Metformin which I will always be on) in February, 2011.  In addition to Lantus at bedtime, I take Humalog with every meal.  Even with four needles a day, I have had very few lows since.

Diabetes classes are more informative than you can imagine.  I learned a whole new way of thinking about the disease with classes I took from the Saskatoon Community Clinic.
 
First off, diabetes is a progressive disease.  I learned that the beta cells in your pancreas keep dying off little by little.  I wish I could lay my hands on the notes I took at my education session, but it was an astounding percentage of beta cells that have already died upon initial diagnosis, even if you're only at the pre-diabetic stage.  This was such welcome news to me (which is ironic) because I was struggling with all the guilt of trying to change my diet and then the regimen of pills and getting enough exercise.  At one point, in those days, exercise wasn't even helping.  I remember telling my doctor that I felt like diabetes was the "disease of guilt".  I was always feeling bad one way or another because I didn't eat exactly the right thing or get enough exercise.  Eventually, when I had my intake of food assessed from a journal I kept, I was told I wasn't eating enough and that made things worse.  Another time, I was told that my snacking was the problem.  I don't have to tell you that there is so much information out there it becomes very confusing.  There's the whole margarine/butter debate.  Don't eat butter, eat margarine.  Don't eat margarine, eat butter. They say margarine sitting on a picnic table won't even be touched by flies.  Yet, when I switched to butter, my cholesterol jumped up.

Diabetes isn't the only thing in your life.  If you are a woman of menstruating age, you may suffer from anemia.  Red meat is marbled with fat, so hard on the cholesterol.  Yet you need iron and you can only eat so many raisins because they are so high in sugar.  You can't always have access to dark, green leafy vegetables in this country.  You must learn to take control and especially reduce your portion sizes.  Stop eating high fat and high salt items like potato chips and chocolate bars.  Yet sometimes, you just want a lift from boring.  Eat more chicken and fish, yet the rivers, streams, and oceans are polluted with mercury and the poultry never sees the light of day and gets fed antibiotics.  I could recite many more of these questions, but you get my drift.

Second, as I said, diabetes often isn't the only thing happening.  There may be a triad of conditions that present themselves simultaneously like with me.  I lovingly refer to it as having "metabolic syndrome" because that's what it's called.  I'm not sure why some diabetics have it and others don't.  I' guess I'm just one of the lucky ones.  The three conditions include high blood sugar, high blood pressure, and high cholesterol.  With one, you will most assuredly have the other two.

Third, you better not only brush up on your nutrition knowledge, but you need to become an expert at it.  Sorry, but you have to.  This part is far harder than taking a pill or shooting in insulin.  This part takes up hours of your week, if you let it.  If you don't, you'll have blood sugars that run rampant.  Planning meals is the ideal and I really wish I was better at it.  Grocery shopping must include reading the Nutrition Facts Labels that are present on most things you buy today.  No longer do you have to weigh and measure everything for portion control.  You can use your hands.  For instance, for fruits, grains and starches you want one fistful per serving.  Open up and fill both hands for vegetables.  For meat and alternatives (egg, chicken, fish, cottage cheeze, cheese, hummus, legumes, peanut butter, shellfish etc.) choose an amount up to the size of the palm of your hand.  Use the tip of your thumb to measure the amount of fat you need to limit yourself to per serving.

* from Beyond the Basics: Meal Planning for Healthy Eating, Diabetes Prevention and Management © Canadian Diabetes Association, 2005.

Today, many diabetics are taught how to do basic carbohydrate counting to manage their diabetes.  That means you have to learn and understand the basic food groups.  You have to understand that foods that contain carbohydrates will raise your blood glucose.  These are Grains & Starches, Fruits, Milk & Alternatives (soy and yogurt), and Other Choices (like sweet foods and snacks - muffins, granola bars, pretzels, and popcorn).  In my father's day, diabetes was managed through an "exchange" system.  Even when I was first diagnosed in 1998, the foods were looked at differently.  For instance, carrots and peas had grams attached to them, whereas now, they don't.  Nowadays, foods are much less restricted.  In fact, diabetics can safely eat almost anything as long as they don't overdo the carbohydrate count.  You can have honey and jam, but try to stay away from sickengly sweet things like syrup too often.  There are brands of jam and syrup with no sugar added.  Remember, honey has natural antibiotic properties and was and is used for healing of severe wounds.

So prior to insulin injections, my suggested number of carbs per meal was between 45 - 60 grams.  Since one slice of bread is 15 grams, one half a medium potato is 15, and a half glass of milk is another 15, that seems pretty easy.  You add the other food groups as recommended by the Canada Food Guide in order to balance out a meal. The confusing part is with non-standard foods like perogies.  What I discovered was six perogies could use up all 45 grams at one sitting, forget about having a glass of milk, a piece of bread, or dessert!  Chinese Food is another food that will rapidly elevate blood sugar as does white rice and white bread. (Surprizingly the little mini chocolate bars don't seem to do much damage for me....they are a fat, even though sweet).   I just have to keep in mind that these little treat add up in the big daily picture.  They do all contribute to your total sugar intake, so keep that in mind.  

That's where the Glycemic Index food list comes in.  Foods with a low number give you a slow, long burn and won't spike your blood sugar like those with a high number.  Get to know this list...  Remember a bagel is considered four breads.  You get half a donut if given the option.


    

First off, insulin is the best thing going....it's not a death sentence, or an indication of how bad off you are.  It's your hope for pete's sake!  It's the thing that can keep your blood sugars as close to normal as possible!  It only takes a little of your time, and you can learn to plan for and live with it. You get so you aren't embarrassed to be seen giving yourself a needle in public, even in a restaurant.  You do have to check your blood sugar more frequently, but after awhile and getting into a groove, things calm down.  I check my blood sugar before a meal.  I have a correction scale to follow, so many units for each number above normal and so many units for each 15 grams of carbohydrates I will be eating.  I generally take 6.0 International Units at breakfast and lunch and 7.0 I.U. at supper.  Believe me, I use a 4 mm long needle and it's so tiny as to barely be seen.  Remember, if you have a lot of body fat, for some reason, it seems you may need a little longer needle.   Often, you don't even feel it, but yes, sometimes you do because you have nerves and blood vessels running through your body.  The site for injection is generally my tummy or my arm or thigh.  I have a cousin who can only use one site because if she uses the others,  it's like she didn't take anything.  No one really knows why.

The saying is, "If you can't make it (insulin) yourself anymore you have to "squirt it in".  What an option to have available when you think that before insulin there was no such luxury.  We are the lucky ones to have something to help us.    There is a realtionship between exercise and using up sugar in the bloodstream.   If you get your muscles warmed up and working, they pull the sugar away from the blood for their own use.  Did you know that if you eat too much, you can go run around the block to bring your blood sugar down. Either that or get on the treadmill or the exercise bike.  Better yet, if you can, join an exercise group and be lead through it on a regular basis.  Daily exercise or even three days a week will do wonders for not only your blood glucose levels, but your blood pressure, and cholesterol.  Get back on the wagon, it's January, you can do it...Do it for yourself and all those that love you. (Can you tell I'm giving myself a pep talk?)

The following are excerpts from the Canadian Diabetes Association website.  Since the loss of pancreatic beta cells is so important, I wanted to first show you that there is Canadian research going on to try to find a cure.  I didn't check internationally, but I do know from taking my Master's degree from the University of Phoenix that research is occurring in various other centres around the world, especially the U.S.A.  It's only a matter of time my friends until a cure is found.


Pancreatic Beta Cells

Research about pancreatic beta cells currently funded from the diabetes.ca website are:

Dr. James D. Johnson (Operating Grant funded 2011-2014)

University of British Columbia (Vancouver, BC)
Title: Novel pathways in fatty acid-induced beta-cell death: Gene-environment interactions.
One of the causes of type 2 diabetes is an increase in pancreatic beta cell death, leading to insufficient levels of insulin in the body. Dr. Johnson is trying to determine how high levels of fat in the blood kill these beta cells in type 2 diabetes. This research will improve our understanding of the underlying causes of diabetes, for example, which genes are required for beta cell survival in the presence of high levels of fat, and it may eventually lead to new strategies for the prevention and management of diabetes.

Dr. Timothy J. Kieffer (Operating Grant funded 2011-2014)

University of British Columbia (Vancouver, BC)
Title: Islet Gene Therapy for Diabetes
It has just recently become possible to deliver therapeutic genes directly and specifically to pancreatic beta cells using a viral vector. Dr. Kieffer is planning to use this viral vector to deliver to beta cells a protein, called GLP-1, that can improve their survival and function, and a second protein, IDO, that can protect them from immune attack. This research could ultimately lead to new strategies to cure type 1 diabetes.


Dr. Camille Attané (Postdoctoral Fellowship Award funded 2012-2015)

Centre de Research-CHUM (Montréal, QC)
Supervisor: Dr. Marc Prentki
Title: Role of glycerolipid/free Fatty Acid cycling in beta-cell fuel excess detoxification
In type 2 diabetes, high blood glucose and high blood fats can be toxic to the beta cells (insulin-producing cells) of the pancreas. In order to cope with too much fat and glucose, cells detoxify themselves, but how this happens is not clear. Dr. Camille Attané plans to find out the importance of the cycle of fat production and breakdown and the release and use of glycerol (produced when the body uses stored fats for energy) in beta cell protection. Understanding how beta cells detoxify excess fat and glucose may lead to the discovery of new ways to treat type 2 diabetes.

Ms. Pei-Shan Cai (Doctoral Student Research Award funded 2011-2013)

Ontario Cancer Institute (Toronto, ON)
Supervisor: Dr. Minna Woo
Title: Investigating the role of Rb and Rb-family of proteins in cell cycle regulation of pancreatic β-cells
Beta cells were once thought to be non-dividing cells; however, it is now known that these cells indeed maintain the ability to divide. Ms. Cai is hoping to define the role of two proteins – retinoblastoma (Rb) and p107 protein – that control cell growth and death in pancreatic beta cells. This research will lead to a better understanding of beta cell growth which could lead to new therapeutic strategies for the prevention and treatment of diabetes.

Research previously funded from the same website is:

Dr. Andrea R. Josse (Postdoctoral Fellowship Award funded 2011-2012)

University of Toronto (Toronto, ON)
Supervisor: El-Sohemy, Ahmed, Dr.
Title: Genetic variation in carbohydrate digestion, its effects on consumption and the risk of Type 2 diabetes
Type 2 diabetes represents a significant global health problem, and diet plays an important role in its development. Evidence has linked increased consumption of dietary available carbohydrates to type 2 diabetes, yet this relationship still remains controversial. It is known that inter-individual variation exists in certain genes that encode for enzymes that break down carbohydrates. These slight differences may influence habitual carbohydrate consumption and blood glucose levels. Dr. Josse is investigating several important genes that directly affect carbohydrate digestion, absorption and habitual carbohydrate consumption, and whether they relate to fasting blood glucose levels in a multiethnic population of young adults living in Toronto. This research will help us understand the role that available carbohydrates play in the development of type 2 diabetes. Also, given the ethnic diversity of the Canadian population, these results could have an important impact on public health strategies aimed at treating and preventing type 2 diabetes.

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As you may know, diabetes is fraught with nasty things it can do to the body of the diabetic.  Although the list below is not exhaustive, it gives you a pretty good idea.  I want you to know that one of the early signs besides increased thirst and urination is nocturnal diarrhea.  Again, the information below is from the Canadian Diabetes Association website and I wish to thank them for all their efforts.

After each paragraph outlining the complication, I have inserted examples of the currently funded research that is occurring in Canada.  To me research means hope.  Significant discoveries have been made in my own lifetime through the efforts of research.  I am not the only person with diabetes who would benefit  if a cure could be found.  Can we stop diabetes and its effects?

If only we could....So, for all of us who have diabetes, here is a simple question:  How can we lend our hands, hearts, and minds to improving our own worlds and that of our children and grandchildren?  We know that if nothing changes, our offspring and theirs could be facing the same life we are living now, just over and over... Groundhog Day if you will.   The future has to hold something better in 2013!

"Complications of Diabetes

Complications
Over time, if left untreated or improperly managed, high blood glucose levels can cause a variety of costly and potentially life-threatening complications, including blindness, heart disease, stroke, kidney disease, nerve damage, and erectile dysfunction. Approximately 10% of acute care hospital admissions are related to diabetes and its secondary complications. Fortunately, good diabetes care and management can prevent or delay the onset of these complications.

Dr. Nica M. Borradaile (Operating Grant funded 2011-2014)

The University of Western Ontario (London, ON)
Title: Protective effects of NAD+ on endothelial cell survival and angiogenesis during type 2 diabetes
Blood vessel (vascular) diseases are common complications in patients with obesity and type 2 diabetes. Damage to endothelial cells, the cells which line all blood vessels, is caused by high blood glucose and lipids, and once they're injured, their ability to repair further damage is limited. Dr. Borradaile is investigating whether increasing the level of NAD+ – an important molecule involved in endothelial cell survival – will improve the ability of blood vessels to repair the damage that occurs during obesity and type 2 diabetes. This research could help in the development of new drug therapies that would increase NAD+, improve endothelial cell survival, and reduce blood vessel disease in obese people with type 2 diabetes.
 
 **My own note:  What if somebody invented something to make us exercise while we slept?**
 

Heart disease

People with diabetes are at very high risk of heart disease, also known as cardiovascular disease (CVD) and stroke (cerebrovascular disease). In fact, up to 80% of people with diabetes will die as a result of a heart attack or stroke.  Please see six examples of research currently funded for heart disease below.

Dr. Kathleen M. MacLeod (Operating Grant funded 2012-2015)

University of British Columbia (Vancouver, BC)
Title: Mechanisms and implications of elevated RhoA-ROCK pathway activity in diabetic cardiomyopathy
People with diabetes are at risk for developing a heart disease called diabetic cardiomyopathy, where the heart muscle cells don't work properly and the heart does not beat as well as normal. People with diabetic cardiomyopathy have a higher risk of having, and dying from, a heart attack or heart failure than their healthy peers. There is a specific pathway of chemical signals in heart cells called ROCK. When the ROCK pathway is blocked, the heart beats more normally. Dr. Kathleen MacLeod and her team are examining how blocking ROCK causes this improvement, and what role ROCK plays in the development of heart damage. Finally, Dr. MacLeod will examine if blocking ROCK reduces the damage cause by heart attacks. This research will help better understand the causes of diabetic cardiomyopathy and could lead to new ways to treat this complication.

Dr. Brian B. Rodrigues (Operating Grant funded 2011-2014)

University of British Columbia (Vancouver, BC)
Title: Metabolic basis for diabetic heart disease: role of cardiac lipoprotein lipase
Diabetes increases the risk and severity of heart attack and stroke because the heart of a person with diabetes, which normally uses glucose for energy, switches to using only fats. This has negative end results, including the generation of noxious by-products which kill heart cells, reduce heart function and, ultimately, result in an increased morbidity and mortality. Dr. Rodrigues is examining the role of an enzyme, called lipoprotein lipase (LPL), in this process. This research could help us identify and devise new ways to treat, prevent or delay heart disease in people with diabetes.

Dr. Garry X. Shen (Operating Grant funded 2011-2014)

University of Manitoba (Winnipeg, MB)
Title: Regulatory mechanism for glycated LDL-induced oxidative stress and monocyte-endothelial interactions
Inflammation plays a key role in diabetes and heart disease. Dr. Shen is examining the effect of glycated low density lipoprotein (LDL) or "sugar-modified bad cholesterol" on oxidation and inflammation in vascular cells and animals with diabetes. This research will help to understand the cause of increased heart disease in patients with diabetes, and could help to identify new treatments for improving the management of heart and vascular disease in patients with diabetes.

Dr. Sally Y. Shi (Doctoral Student Research Award funded 2012-2015)

University of Toronto (Toronto, ON)
Supervisor: Dr. Minna Woo
Title: Investigating the role of hepatic JAK2 in the development of diabetes and its cardiovascular complications
People with type 2 diabetes have a high risk for heart attacks and strokes, and many of them have fatty liver, which further increases their risk. How fatty liver increases the risk of heart attacks and strokes is not known. A molecule, called JAK2, plays a major role in liver fat metabolism and inflammation. Mice that don't make JAK2 in their liver develop severe fatty liver but surprisingly not diabetes. These genetically engineered mice are therefore a useful experimental tool. Ms. Sally Y. Shi hopes to find out how fatty liver alone without diabetes, or with diabetes will affect the development of heart disease or stroke, which could provide new drug targets to improve the quality of life for people living with diabetes.

**My Note:  I was once diagnosed with Fatty Liver as seen on a CT scan.  Within six months, the Fatty Liver nodule was gone...again diagnosed by CT scan.  Does this condition come and go and why?***  Maybe these researchers would like to avail themselves of the knowledge held by me and my family.  Have a family group conference with researchers asking us questions..  We have likely experienced many of the conditions they are looking into!***

Ms. Ying Wang (Doctoral Student Research Award funded 2012-2014)

University of British Columbia (Vancouver, BC)
Supervisor: Dr. Brian B. Rodrigues
Title: Metabolic basis for diabetic heart disease: role of cardiac lipoprotein lipase
In people with diabetes, to compensate for not properly being able to use glucose as a fuel, heart muscle cells start using fats exclusively for energy. This change in fuel source initially helps the heart, but over the long term causes the heart cells to become damaged and leads to heart disease. Ms. Ying Wang aims to investigate how the enzyme called lipoprotein lipase allows the heart cells to make this switching in fuel possible. This may help future researchers find new ways to prevent or delay diabetes-related heart disease.


Dr. Geoffrey H. Werstuck (Operating Grant funded 2012-2015)

McMaster University (Hamilton, ON)
Title: Is Accelerated Atherosclerosis a Microvascular Complication of Diabetes Mellitus?
People with diabetes have a higher risk of heart attack and stroke because of a disease of the large blood vessels (macrovascular disease) called atherosclerosis. People with diabetes can also suffer from vision problems, kidney disease and other circulatory problems that are a result of a disease of the very small blood vessels (microvascular disease). Traditionally microvascular and macrovascular disorders are considered as separate problems. We will investigate the possibility that diabetes causes atherosclerosis by injuring the small blood vessels that supply the walls of the large blood vessels. The result of this research could change the way microvascular and macrovascular diseases are treated.

Kidney disease

Over the years, high blood glucose levels and high blood pressure can damage the kidneys and prevent them from functioning properly or even cause them to fail completely. About one-third of people who have had diabetes for more than 15 years will develop kidney disease, but good diabetes management and regular screening can prevent or delay the loss of kidney function.  Please see six more examples of current research happening for kidney disease.

Dr. Andrew Advani (Operating Grant funded 2010-2013; Clinician Scientist Award funded 2009-2014)

St Michael's Hospital (Toronto, ON)
Title: Unravelling the role of SDF-1/CXCR4 signalling in diabetic nephropathy
Kidney disease is a common complication of diabetes. Dr. Andrew Advani is examining the small blood vessels in the kidney that become damaged in diabetes. He is looking at how a certain small protein, called SDF-1, and its receptor interact and if therapies could change this interaction to prevent damage to the small blood vessels.

Dr. David Z. I. Cherney (Clinician Scientist Award funded 2010-2015)

University Health Network (Toronto, ON)
Title: Hemodynamic and molecular mechanisms of hyperfiltration in type 1 diabetes mellitus
Dr. David Z.I. Cherney aims to better understand how diabetes damages the blood vessels, which then causes kidney damage. Kidney and blood vessel damage is caused by a number of factors, including high blood sugar and a system called RAS. When the RAS system is active, it leads to inflammation in the kidneys and blood vessels. Dr. Cherney is investigating the link between high blood sugar, medications that can block RAS, and kidney injury. The aim of this work is to find new ways to stop kidney and blood vessel damage in diabetes.

**My Note:  I have had at least one attack of Gout.  In my research I discovered that Gout is a type of arthritis that can also affect the kidneys.  I believe there is a connection between diabetes and gout.  I wonder if there is any research on this connection...***

Dr. Ivan George Fantus (Operating Grant funded 2010-2013)

Mount Sinai Hospital (Toronto, ON)
Title: Tyrosine kinase signaling in the pathogenesis of diabetic nephropathy
Dr. Ivan George Fantus is examining specific cells in the kidney which respond to a protein called Src. Src is activated when blood glucose is high, and drugs that inhibit Src seem to be able to slow the development of diabetic kidney disease. Dr. Fantus will examine how activated Src contributes to diabetic kidney disease and whether Src inhibitor drugs can be used as treatment and/or prevention.

Dr. Pedro M. Geraldes (Scholar Award funded 2011-2016)

University of Sherbrooke (Sherbrooke, QC)
Title: Role of PKC delta and SHP-1 on poor collateral vessel formation in diabetes
High glucose levels have been suggested as one of the most important causes of impaired blood vessel formation in people with diabetes. Dr. Geraldes is studying the role of hyperglycemia-induced protein kinase C and SHP-1 activation causing inhibition of new blood vessel formation under ischemic conditions. This research will help us better understand the underlying vascular complications related to high glucose levels in people with diabetes. It may also help in the development of new treatments to promote new blood vessels during ischemia, preventing amputation in people with type 1 and 2 diabetes.


Ms. Hui Jun (June) Guo (Doctoral Student Research Award funded 2010-2013)

University of Toronto (Toronto, ON)
Supervisor: Dr. Adria Giacca
Title: Potential treatments of atherosclerosis and restenosis with insulin and insulin sensitizers
Ms. Hui Jun (June) Guo is studying whether resveratrol (a substance found in red wine) and metformin (a blood glucose lowering drug) alone and when combined with insulin, prevent narrowing of blood vessels, as well as decrease fat deposits in blood vessels. This research will find out if resveratrol and metformin treatment has any potential to prevent blood vessel damage in people with type 2 diabetes.

Dr. Joan C. Krepinsky (Operating Grant funded 2011-2014)

McMaster University (Hamilton, ON)
Title: SREBP in the pathogenesis of diabetic nephropathy
Diabetes is a common cause of kidney failure, leading to scarring of the filtering units of the kidneys. High glucose levels cause kidney cells to make a protein called transforming growth factor beta (TGFbeta), which induces cells to make scar proteins. Dr. Krepinsky is investigating how TGFbeta activates another protein, called SREBP-1, and how this contributes to the increase in scar proteins. Preventing or slowing the accumulation of scar proteins is important to preserving kidney function in people with diabetes, and blocking SREBP-1 may be a new way to achieve this.


Eye disease (diabetic retinopathy)

This effect of diabetes on the eyes is the most common cause of blindness in people age 65 years and younger and the most common cause of new blindness in North America. It is estimated that approximately two million individuals in Canada have some form of diabetic retinopathy.  Two examples of eye disease research as it relates to diabetes complications follow.

Dr. Bruce A. Perkins (Operating Grant funded 2010-2013)

University Health Network (Toronto, ON)
Title: In-vivo corneal confocal microscopy as a non-invasive biomarker of early neuropathy in type 2 diabetes
Nerve damage is a complication of diabetes that is important to recognize at early stages, but complications, such as foot ulcers, infection, and the need for amputation, do occur. The best method for detecting early nerve damage is to perform a skin biopsy and examine the structure of nerve endings under a microscope. However, the cornea of the eye has similarities to the skin, including the presence of a nerve layer that can be non-invasively visualized using a high-powered microscope called a corneal confocal microscope. Dr. Bruce A. Perkins is testing if the small nerve fibres of the eye, seen under the confocal microscope, can be used as a non-invasive alternative to the skin biopsy test. If this alternative works, it could be paired with routine eye exams for people with diabetes.

Dr. Przemyslaw (Mike) Sapieha (Operating Grant funded 2011-2014)

University of Montreal (Montréal, QC)
Title: The involvement of neuronal guidance cues in microvascular degeneration and misguided vessel growth in diabetic retinopathy
Diabetic retinopathy (DR) is the most common complication of diabetes and the leading cause of blindness in working-age individuals. It is characterized by an initial phase of vascular degeneration (blood vessel breakdown) followed by deregulated neovascularization (formation of disorganized microvascular networks). This secondary neovascularization fails to grow into the hypoxic tissue, and instead, these vessels are misdirected toward the vitreous (the clear gel that fills the space between the lens and the retina of the eyeball) and contribute to retinal detachment. Dr. Sapieha is trying to determine if Semaphorin3A (a neuronal guidance cue) – produced by stressed neurons – is involved in mediating the pathological features of DR by participating in retinal vaso-obliteration and by repelling growing neo-vessels from the retina towards the vitreous while hindering desirable retinal revascularization. This research could help in the development of new strategies to prevent and treat retinopathy in patients with diabetes.


Nerve damage

Diabetes affects the circulation and immune systems which, in turn, impairs the body’s ability to heal itself. Over time, diabetes can damage sensory nerves (this is known as “neuropathy”), especially in the hands and feet. As a result, people with diabetes are less likely to feel a foot injury, such as a blister or a cut. Unnoticed and untreated, even small foot injuries like these can quickly become infected, potentially leading to serious complications like amputation. Seven of 10 non-traumatic limb amputations are the result of diabetes complications.  Two examples of current research as it relates to nerve damage due to the complications of diabetes follow.

Dr. Pedro M. Geraldes (Operating Grant funded 2010-2013)

University of Sherbrooke (Sherbrooke, QC)
Title: Role of SHP-1 in PDGF and VEGF inhibition causing poor collateral vessel formation in diabetes.
Dr. Pedro M. Geraldes is looking into blood vessel damage in people with type 1 and type 2 diabetes. This kind of damage can cause injury to the limbs, especially the feet. When blood vessels become damaged, high blood sugar impairs the body's ability to fix the damage. Dr. Geraldes is looking into how high blood sugar causes this impairment, in hopes of finding ways to fix the damage and reduce foot amputations in people with diabetes.

Dr. Douglas W. Zochodne (Operating Grant funded 2012-2015)

University of Calgary (Calgary, AB)
Title: Diabetes and Skin Sensation
A common complication of diabetes is damage to the nerves in the hands and feet that can lead to numbness, pain, and poor healing of wounds (called diabetic neuropathy).Dr. Douglas Zochodne and his team have found that – in both type 1 and type 2 diabetes – local, low levels of insulin (too low to change blood glucose) can act on skin nerve fibres and make them grow. Dr. Zochodne and his team are investigating how insulin and other growth factors in the body cause nerve fibers to grow. He hopes to use these factors to help re‐grow nerves, and will investigate if this re‐growth helps improve numbness and wound healing. Through this research, Dr. Zochodne hopes to find new ways to stop or reverse diabetic neuropathy.

Problems with erection (impotence)

Although erectile dysfunction (ED) affects most men at some point in their lives, it is more common in men with diabetes. In fact, in up to 12% of men with diabetes, ED is the first sign that leads to the diagnosis of diabetes. Older men with a longer duration of diabetes, poor blood glucose control, and those who smoke, have high blood pressure, high cholesterol, and heart disease, are at highest risk.
Sorry, no current research jumped out at me from this website, although there is previous research.  Please see the website.

Depression

Approximately 25% of people with diabetes suffer from depression.  Two examples of research into depression associated with diabetes follow.

Dr. Norbert Schmitz (Operating Grant funded 2010-2013)

Douglas Mental Hospital University Institute (Montréal, QC)
Title: Depression and disability in diabetes: a longitudinal community study
Dr. Norbert Schmitz is looking at depression, disability, and diabetes. Type 2 diabetes is associated with a high prevalence of disability, and depression strikes 10 to 30 per cent of people with diabetes. Dr. Schmitz is examining the relationship between neighbourhood environment, physical activity, diet, depression, disability, and quality of life in people with diabetes. The results will provide useful information for the management of diabetes, depressive illness, and associated clinical and behavioural risk factors.


Insulin resistance and Obesity

Insulin resistance and obesity are not considered "complications", but research is underway since they are both results of or contributing factors for diabetes and need their due.  Two examples follow.
 

Dr. André Tremblay (Operating Grant funded 2012-2015)

CHU Sainte -Justine (Montréal, QC)
Title: Role of the CD36-PPAR pathway in lipid and energy metabolism in fat
Obesity can cause fats to be stored not only in fat tissues, but also in the liver, pancreas and muscle cells. Fat storage in these locations can lead to insulin resistance and type 2 diabetes. Dr. André Tremblay and his team hope to find ways to make the body use fats in better ways to avoid the progression to insulin resistance and type 2 diabetes. Dr. Tremblay's studies are focused on molecular pathways in the body that regulate energy balance in fat cells. These studies will provide new information on how obesity and insulin resistance develop. Dr. Tremblay hopes that his information will help future researchers find new ways of treating these conditions and preventing type 2 diabetes from developing.

Dr. Alain Veilleux (Postdoctoral Fellowship Award funded 2011-2014)

Center de recherche CHU Sainte-Justine (Québec, QC)
Supervisor: Dr. Emile Levy
Title: Intestinal lipid and lipoprotein metabolism in relation with insulin-resistant and diabetic states in humans
Insulin resistance is the central feature of type 2 diabetes, but is also commonly associated with dyslipidemia. Exaggerated hepatic lipid production and impaired lipid clearance by peripheral tissues are believed to play key roles in the development of dyslipidemia. Recent studies have pointed out the intestine as an important regulator of lipid homeostasis, and previous studies clearly suggest that intestine is an important contributor to the development of dyslipidemia in insulin-resistant state. Dr. Veilleux is investigating whether intestine develops insulin-resistance and inflammatory states, and represents a major contributor to diabetic dyslipidemia. This research could help identify treatment strategies to reduce cardiovascular disease risk in patients with diabetes.

I hope that one day in my lifetime, a cure can be found.

 

Saturday 5 January 2013

Snippits of Humour


Happy New Year 2013. 

Yesterday, I spent part of the afternoon laughing my head off watching Bill Murray in the movie "Lost in Translation".  He is so hilarious and deadpan, watching him I can't help myself.  He's in Japan.  There's the scene where he's standing in the middle of an elevator, surrounded by the local businessmen. He towers over all of them by at least a foot and can look down on the tops of their heads.  Nobody speaks and the businessmen are majorly  bespectacled with their over-sized black-rimmed glasses.  All eyes are riveted on the numbers above the door opening.  You can see the businessmen actors trying hard not to laugh, but Bill remains straight-faced as ever, except for those dancing, twinkling eyes of his.  You know he's getting a real kick out of the moment. 

Then there's one of the scenes where he's the actor in a TV commercial.  He's raising his glass in a toast, inviting the audience to try some special brand of alcohol. All of a sudden, the director stops everything and starts ranting and raving.  You can guess something went wrong with Bill's delivery, yet you don't know for sure what.  The director's face has turned beet red, he's raised his voice and is spitting a little more with each word.  Bill obviously wonders what he did wrong and looks to the interpreter for explanation. She doesn't move or offer a hint, but sits quietly, stone-faced, until the director's tirade is over. 

When the director is finally finished, he turns on his heel and stalks off, apparently fuming.  Bill braces for the interpretation and can't believe when she dwindles it down to about a three word explanation. Surprized, he asks, "are you sure that's all he said?"   She turns away.  The power of the interpreter...she is arrogant like a cat, and doesn't stoop to answer.  The first time this happens, it confirms our suspicions about interpetors.  You know darn well they aren't telling you word for word what the person said.  I think whole wars may be started because of them.  At the very least, they can and do gloss messages over.  The irony is where the power lies.  He is supposed to be the "star", yet she has got him by the short hairs.

The second and third times you experience this communication glitch, it just gets funnier and funnier.  The reality is, he's trapped in a situation of politics, politeness, and saving face.  There's not a single thing he can do about it, but go with the flow.  Since the director is having a total melt-down and Bill can't figure out what to do with his acting he  starts ad libbing, the way only Bill Murray can.  This initial frustration and eventual abandoning of all convention is the same theme he works through time and again throughout the movie.  Even though trapped in some kind of hell at both this job and in his marriage, he learns to enjoy himself.  One piece of evidence is in his zest for karaoke singing and even though his voice is a little off-key, he sings his heart out with increasingly difficult songs.  All his new friends applaud his efforts. 

Later I watched a few comedians do their bit on video clips from the internet.  I happened in half way through the clip of a man who was raised as the only boy in a family of girls.  He said when he had to fight guys while growing up they learned to stay away.  Why?  Because they knew he would try to tickle them to death.

Joe Braza said that after seven years with his wife, they parted ways because he had started to sound like her, but worse, she had started to look like him.

Jerry Wolski talks about children not being allowed to be stupid any more.  He says kids seems to have to have a diagnosis...they either have ADD or some such thing....not just that they inherited somebody's 'stupid genes'.

 Do you remember when they used to refer to underwear as "drawers"? Men had long underwear with a "trap door" at the back. I can only surmize that in freezing cold winters, with outdoor toilets, these inventions were ever so valuable for the male population. Women had no such luxury. They don't seem as popular any more.  In the winter there were no clothes dryers, so everything got hung outside on the clothes line.  Of course, in 40 below temperatures everything hung out would freeze into a stiff unit...including the long underwear.  If you have never seen this, you don't know what you're missing.  Remember, hanging stuff out in that temperature killed all sorts of things from lice to viruses and all that!

I was teaching my four-year old grandson to play hide and seek".  I know the count is to 100, but I decided to do a shortened version and just count to 10.  He hid his face under a pillow on the couch in full view of me, but I called the age-old, "here I come, ready or not you must be caught!"....There was the typical laughing and tickling when he was "found" and then it was his turn to count.  I said, "Now you count to 10, but he said,  "No, I'll count to 12."  You had to be there, I heard his mother laugh out loud from the other room.  It's bad when your four-year old grandchild thinks you can only count to 10.

For a short time in about the seventies, people started calling little kids "rug rats".  Honestly.  I thought it had died down, but I saw today that there is a kid's cartoon on TV with the same name.  Oh brother.

Sometime in the past few decades,  everything was some kind of "wonder".  You could be anything from a "gutless wonder" to a "one-hit wonder".

Here's a spin-off from the Dukes of Hazzard TV show.  My son was about two years old and a big fan of the Duke Boys.  As you may know, the sherriff on this show was Rosco P. Coltrain.  I have a cousin, Ross, who is a little older than me.  Ross used to visit us quite often and since we called him Rosco, my son soon began to call him "Rosco Peko-train".  It was very cute and soon members of my extended family were also calling Ross - "Rosco Peko-train" or shortened to "Rosco Peko".  If you put it into perspective, that was at least thirty years ago.  We moved away from that community and a few years ago, I happened to be talking to a neighbour of Ross's.   Somehow, she innocently referred to him  as Rosco Peko.  Startled,  I told her about what had happened so many years ago with my little son.  She said, "yea, she knew all about it and ...it stuck!".  WOW!  Unbelievable.