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Smoking and Diabetes: A Deadly Combination

>> Sunday, January 30, 2011



It comes as no surprise to anyone reading this blog that smoking is bad for your health. Interestingly, the risk goes far beyond cancer risk and heart disease - smoking has an important impact on diabetes as well.

As reviewed by Patasi and Hall, several studies have demonstrated that smoking increases the risk of developing type 2 diabetes 2- to 3- fold. The likely reason behind this fact is that smoking decreases the body's ability to use insulin. In fact, smoking 1 cigarette reduces the body's ability to use insulin by 15% for an entire day! We also see that amongst patients with type 2 diabetes, smokers have higher blood sugars than nonsmokers.

Vascular disease is a complication of both smoking and diabetes, so it should come as no surprise that having both risk factors compounds the risk. Smoking diabetics are more than 10 times more likely to develop peripheral vascular disease than nonsmoking diabetics, and also have a higher risk of small vessel diabetic complications such as nerve, eye, and kidney damage. Smoking can also lead to impotence amongst diabetic men. And that's not all - the list goes on.

Given that we know that smoking increases the risk of several cancers as well as the risk of vascular disease, and that 80% of diabetics will die as a result of heart disease or stroke, smoking and diabetes are truly a deadly combination.

Dr Sue Pedersen www.drsue.ca © 2011 drsuetalks@gmail.com

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Are Genetics Important in Diabetes?

>> Saturday, January 22, 2011





In a world where the epidemic of diabetes threatens to spiral out of control, our understanding of the influences that put people at risk of developing the disease is crucial.  As a second part to my recent blog about the important genetic influence on the development of obesity, it is also very important to consider the genetic contribution towards diabetes.

In North America, approximately 80% of diabetes is caused by Type 2 Diabetes, which is a condition of elevated blood sugars caused by resistance of the body's organs and tissues to the effects of insulin, to the point where the pancreas is not able to produce sufficient insulin to overcome this state of insulin resistance.  Insulin resistance and Type 2 Diabetes worsen with weight gain and improve with weight loss; however, there are a subset of people with Type 2 Diabetes who are normal weight.   About 10% of diabetes is Type 1 diabetes, where the immune system attacks the pancreas and causes it to fail to produce insulin.  The final 10% of diabetes is causes by various rare genetic disorders.

The evidence for a strong genetic tendency towards developing Type 2 Diabetes is strong.  For example:
  • some ethnic groups residing in North America (such as Hispanic, South Asian, and Aboriginal) are at 2-6 fold higher risk of developing Type 2 Diabetes compared to North American Caucasians
  • a twin of a person with Type 2 Diabetes is at 90% risk of developing the disease (as compared to Type 1 diabetes, where the risk is lower at 50%)
  • nearly 40% of patients with Type 2 Diabetes have at least one affected parent (whereas in Type 1 Diabetes, the risk of the child of a Type 1 Diabetic parent getting the disease is only 6%)
  • the lifetime risk of a person getting Type 2 Diabetes is 5-10 times higher if they have a first degree relative with the disease, compared to not having a relative with the disease

As reviewed by Dr McCarthy, the search for genes connected to Type 2 Diabetes has really taken off with the ability to search the entire human genetic makeup (called the 'genome') in recent years.  In fact, there are at least 40 genetic spots (called 'loci') in the human genome that have been found to be associated with a susceptibility to developing Type 2 Diabetes.  These genetic variants are associated with a variety of disturbances that affect the risk of developing Type 2, including alterations in the development of the pancreas, insulin synthesis, and insulin secretion.  The genes that contribute to development of obesity (as blogged previously) likely contribute to the risk of type 2 diabetes as well, as the insulin resistance that characterizes type 2 diabetes worsens with weight gain.

In terms of the influence of these genetic variants on the risk of Type 2 Diabetes, it appears that in some cases, having two abnormal copies of these genes may as much as double the risk of getting diabetes, compared to having two normal copies of these genes. 

For some individuals, the eventual development of Type 2 Diabetes may be unavoidable, due to their genetic makeup.    However, many cases of Type 2 Diabetes are preventable, as many people develop sufficient insulin resistance to generate full blown diabetes only when they reach a state of overweight or obesity.  While obesity in itself has some genetic predisposition as well, both obesity and type 2 diabetes can be improved with dedicate attention towards a healthy lifestyle.

As for obesity genetics, our understanding of the genetic basis for Type 2 Diabetes is essential, as it will help us in better understanding the disease, finding new targets for treatment, and hopefully allowing us to improve individual strategies towards treatment and prevention.





Dr Sue Pedersen www.drsue.ca © 2011 drsuetalks@gmail.com

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Are Genetics Important in Obesity?

>> Sunday, January 16, 2011





With obesity affecting one third of American adults and one quarter of Canadian adults, there is a critical need to improve our understanding of how obesity develops, including the relative importance of genetic and environmental factors.  As we explore the human genome, we are learning more and more about the important role of genetics in the battle of overweight.

As reviewed by Dr McCarthy in a recent issue of the New England Journal of Medicine, studies of the full complement of human genes (called the ‘human genome’) are full speed ahead in the last few years.  The search strategy that has been the most successful in finding genes linked to obesity has been to search the genome for DNA sequence patters that are seen in association with people who have a higher Body Mass Index (a calculation that assesses weight based on body height, and is used to classify obesity; you can calculate yours here, in the right hand column). 

These genome wide studies have identified at least 30 spots (called genetic ‘loci’) on our DNA which influence body weight.  Many of these involve alterations of a gene called the FTO (fat mass and obesity related) gene, which appears to be particularly important in its influence on body mass index.  

In addition, there are at least 15 loci identified that affect where body fat is deposited in the body.  This is important, as we know that body fat deposited around the organs and around the midline is more metabolically active than fat that is deposited under then skin or to the chest and hips.  Interestingly, these 15 genetic spots that affect body fat deposition patters show stronger associations in women than in men.

There are exceptionally rare cases of obesity that are caused directly by a single gene or chromosome abnormality, such as leptin deficiency, or distinct genetic syndromes such as Prader-Willi sydrome.  However, these are not players in the common case of overweight or obesity.

So, how much does having one or several of the common genetic variants influence the likelihood of being, or becoming, obese?  Well, each individual genetic variant does not appear to have a profound effect; the genes with the greatest impact may make a difference of only 2-3 kg of body weight (4-7lb).  However, having a number of the obesity-predisposing genetic variants may have an additive effect.  As we learn more about these genes, it may be possible in the future to predict or assess one’s risk of obesity based on their full genetic complement, taking into consideration all of the obesity-predisposing genetic variants that they may have.

It is also important to note that an individual is not destined or guaranteed to become obese because of these genetic variants, but these genes may certainly help set the stage for development of obesity, and difficulty in losing weight, in the context of our toxic, obesity promoting environment.  It is poorly understood exactly how these genes are expressed, but it is thought that they may have an impact on fat and cholesterol metabolism, appetite regulation, taste preferences, and tendency towards engaging in physical activity. 

The future of obesity genetics research is bright: in addition to giving us a better understanding of mechanisms of development of obesity, this research may present to us new targets for treatment and prevention of obesity, as well as the potential for personalized treatment and prevention, depending on each individual’s particular genetic makeup.

In my opinion, one of the most important opportunities this research gives us is ammunition with which to combat the stigma of obesity, both in the general community and amongst medical professionals.  Each of us has a different baseline genetic risk of developing obesity, which may result in different trigger points of hunger and satiety, differences in willpower and cravings, and differences in our genetic drive to exercise.  Through a better understanding of these genetics and the mechanisms by which they work, it is my hope that we will become better empowered to understand, prevent, and treat obesity in a patient specific, caring, compassionate, and understanding manner.

Dr Sue Pedersen www.drsue.ca © 2011 drsuetalks@gmail.com

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After Gestational Diabetes: What's Next?

>> Sunday, January 9, 2011



Gestational diabetes, or diabetes diagnosed for the first time during pregnancy, is a common condition, affecting approximately one in 25 pregnant women in Canada. After the baby is born, women who had gestational diabetes may be eager to leave their blood sugar concerns behind, but beware: women who have had gestational diabetes are at high risk of developing type 2 diabetes.

In pregnancy, there are several factors that contribute to the development of gestational diabetes, including increased food intake, weight gain, decreased exercise, and the production of several hormones by the placenta that make the mother more resistant to the effects of insulin. As the development of gestational diabetes identifies women whose pancreas is not able to keep up in the face of the stress of pregnancy, it also identifies women who are at future risk of developing full blown type 2 diabetes (outside of pregnancy). In fact, having had gestational diabetes increased the risk of developing type 2 diabetes later in life by up to 12 fold.  Further, some cases of gestational diabetes were likely type 2 diabetics before the pregnancy started, but they did not come to medical attention until the pregnancy began.

Because the impact of undiagnosed type 2 diabetes postpartum is of serious consequence to the mother's health, and also has implications for future childbearing, it is essential that these women undergo screening for type 2 diabetes postpartum. Blood sugars will be checked following delivery in the hospital, but this alone is not enough, as diabetes can return after discharge home when normal life and eating patterns resume.

All women who have had gestational diabetes must undergo a glucose tolerance test within 6 weeks to 6 months postpartum. This involves drinking a glucose containing drink, with measurement of blood sugar before and 2 hours after the drink is taken. Checking fasting blood sugars is not enough, as this will miss 40% of type 2 diabetes in the postpartum population.

Additionally, women with previous gestational diabetes must be screened for type 2 diabetes:

  • before any future pregnancies
  • every 3 years, or more often, depending on other risk factors

Unfortunately, as few as 25% of women who have had gestational diabetes complete this important postpartum testing. Having undiagnosed type 2 diabetes can cause injury to blood vessels supplying vital organs including the heart, kidneys, and eyes. Having undiagnosed type 2 diabetes at the time of the next pregnancy can have devastating consequences to the fetus, including congenital malformations and miscarriage.

If you have or have had gestational diabetes, speak to your doctor to be sure that you have undergone, and continue to undergo, the appropriate screening.


Dr Sue Pedersen www.drsue.ca © 2010 drsuetalks@gmail.com

Follow me on Twitter for daily tips! @drsuepedersen

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Video Blog: Portion Control Your Breakfast!

>> Sunday, January 2, 2011


Breakfast is an important start to your day, so consider a new breakfast strategy in your 2011 weight management program!

In this video blog, Dr Sue emphasizes the importance of eating breakfast in maintaining a healthy body weight or losing weight. She describes three ways you can easily portion control your breakfast: use of a portion control tool such as The Diet Bowl (which Dr Sue studied in a research trial); storing a measuring cup directly into your cereal container; or using a coffee mug as your breakfast bowl!



Dr Sue Pedersen www.drsue.ca © 2011 drsuetalks@gmail.com

Follow me on Twitter for additional tips and pearls! drsuepedersen

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A HEARTFELT WELCOME!

I am excited that you have arrived at my site, and I hope you are too - consider this the first step towards a Healthier New You!! As a medical doctor, Endocrinologist, and obesity specialist, I am absolutely passionate about helping people with weight management. Though there is certainly no magic cure for obesity, there IS a successful treatment plan out there for you - it is all about understanding the elements that contribute to your personal weight struggle, and then finding the treatment plan that suits your needs and your lifestyle. The way to finding your personal solution is to learn as much as you can about obesity: how our toxic environment has shaped us into an overweight society; the diversity of contributors to obesity; and what the treatment options out there are really all about. Knowledge Is Power!!


Are you ready to change your life? Let's begin our journey together, towards a healthier, happier you!!




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