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Slow Cooker Mexican Delight!

>> Saturday, August 29, 2015

The other day, as I walked down to our clinic kitchen to get my lunch, I was greeted by mouthwatering aromas of Mexican spices filling the air... I turned the corner to find my dear friend and coworker Chantelle heating up her delightful lunch that she had brought from home.  She graciously packed a lunch for me at work the next day, and it tasted even better than it smelled... this recipe needs to be shared!!


  • 5 chicken breasts
  • 1 onion, diced
  • 1 green pepper, diced
  • 1 red pepper, diced
  • 3 garlic cloves, chopped
  • 1 can of tomatoes (796 mL size)
  • 1 can of corn (341 mL size)
  • 1 can black beans (540 mL size)
  • 1 package of low sodium taco seasoning
  • 1 tsp cumin
  • 1 tsp oregano
  • 2 cups chicken stock
  • And a little bit of love

DIRECTIONS: (slow cookers are so easy! :)

1.  Throw all ingredients in the slow cooker.  Cook for 4 hours on high or 6 hours on low. 

2.  Shred the chicken in the mixture and leave it on low for another hour or two – just to get the flavor all the way through the chicken.'re done!

This dish can be enjoyed as is or in a taco, but my favorite option is to put it over a mixed green salad!  This adds lots of FreeVeg to the meal.  If you put it over a salad or in a taco, drain fluid first.

Makes 10 servings.  Per serving: 
  • calories: 183
  • carbs: 20g
  • fat: 2g
  • protein: 19g

Thanks so much to my dear friend Chantelle, and her friend Amy, for the delicious recipe!

Follow me on twitter! @drsuepedersen © 2015


Diabetes Medication Empagliflozin Reduces Cardiovascular Events

>> Friday, August 21, 2015

BIG news in the diabetes world this week - empagliflozin, a medication used to treat Type 2 Diabetes, is the first diabetes medication to show a reduction in cardiovascular risk in a rigorous clinical trial.

The EMPA-REG trial enrolled over 7,000 type 2 diabetic patients who were considered to be at high risk of cardiovascular events and had suboptimally controlled diabetes, and randomized them to received either empagliflozin 10mg, empagliflozin 25mg, or placebo.  The primary outcome was time to first occurrence of cardiovascular death, non fatal heart attack, or non fatal stroke.  Treatment with empagliflozin was in addition to usual standards of diabetes care.

The trial found that empagliflozin reduced the risk of cardiovascular events compared to placebo.  I would love to look at further details today - but the data is embargoed until the European Association for the Study of Diabetes (EASD) meeting in Stockholm on September 17th.  Data on just how much CV events are reduced, or which patients may benefit most, is not yet available.

Empagliflozin (trade name Jardiance) is one of a class of newer type 2 diabetes medications called SGLT2 inhibitors.  They block the kidneys' ability to reabsorb sugar from the urine back into the bloodstream, with the result that sugar is excreted in the urine (ie it causes you to pee sugar).  In addition to reducing blood sugar and improving diabetes control, these medications also reduce blood pressure (they have a diuretic like activity) and also cause an average weight loss of around 10 lbs.  Another excellent feature is that they do not cause low blood sugars as a side effect.  While the details of the EMPA-REG trial haven't been released yet, it is likely that all of these mechanisms of action contribute to the reduction in CV risk that was seen.

Empagliflozin has just been approved in Canada and will be available on shelves soon.  Canagliflozin (trade name Invokana) and dapagliflozin (trade name Forxiga) are available already.  The clinical trials of canagliflozin (called the CANVAS trial) and dapagliflozin (DECLARE trial) are currently underway, with results expected in a few years' time.  Clinical trials of other classes of type 2 diabetes medications are also underway, with results also rolling out over the next few years.

Until now, we have not had robust evidence that any particular diabetes medication clearly decreases the risk of CV events.  Metformin has some less robust data behind it in this regard; this data is one of the main reasons why it is considered the first line treatment for type 2 diabetes worldwide.   As the data and details of this study (and the other studies of medications in this class) become available to us, it will be interesting how these results may change the shape of how we approach type 2 diabetes treatment.

Disclaimer: I receive honoraria as a continuing medical education speaker and consultant from the makers of empagliflozin (Boehringer-Ingelheim and Eli Lilly).  I am involved in research of SGLT2 inhibitors as a treatment of diabetes.

Follow me on twitter! @drsuepedersen © 2015


Coca Cola - Helping Families Get.... fIt??

>> Sunday, August 16, 2015

It is a well established fact that sugar sweetened beverages (SSB) are an important contributor to the obesity epidemic we are currently facing.  Fifteen percent of total energy intake in USA is from added sugar, and sugar sweetened beverages are the largest contributor.  The association between SSB intake and obesity in children is particularly strong.

Despite these facts, soft drink giant Coca Cola is working hard to shift our focus away from their unhealthy beverages towards our general societal lack of exercise.  Coke has recently teamed up with scientists and has even provided funding to a new non profit organization called the Global Energy Balance Network, to spread the message that physical activity can offset dietary choices.

The truth is that it is very difficult to offset poor dietary choices with exercise; this is because it takes a very long time to burn calories with activity, but a very short time to consume a large number of calories.  Consider this: a typical person walking briskly for a half hour may burn 140 calories, while a 140 calorie can of Coke can be consumed in seconds.    I'm not saying don't exercise - exercise is important for weight maintenance and has many health benefits.  But it is not where the main focus should be in weight loss efforts.   Not to mention the critical importance of the multitude of other factors influencing weight balance - psychological, genetics, environmental, and many others.

For all the above reasons, add me to to the list of health care professionals that are speaking out against Coca-Cola's misleading and frankly irresponsible behavior.

Follow me on twitter! @drsuepedersen © 2015


Burn Baby Burn... Fat vs Carbs vs Protein vs Alcohol

>> Monday, August 10, 2015

In our daily lives, we have four possible sources of energy: fat, carbs, protein, and alcohol.   Have you ever wondered how your body decides what to use as fuel, and how excess calories get stored as fat?  Or whether our bodies could preferentially choose to burn fat and carbs and store the excess protein as ultra-awesome lean muscle?

Here are the answers to these 'burning' questions.

Our bodies very carefully regulate how much protein is in our bodies, and is quick to balance and dispose of extra protein as needed.  When we eat protein, 20-25% of the calories are actually used up just to digest and deal with the protein.  As we eat protein, it induces a strong fullness response that tells us to stop eating.  Protein is carefully managed by the body for distribution to our cells as needed, and can also be broken down into an energy source directly.  During weight loss, our bodies are careful to minimize protein losses, such that about 2/3 of weight that is lost is fat and the other 1/3 lost is the more protein rich lean body mass.

We store between 200-500g of carbs in our bodies as glycogen, which can be broken down quickly for a fuel source as needed. Carbs are a major source of daily energy.  If more carbs are eaten than what is needed for energy, some is stored as glycogen.  When glycogen stores are full, any excess carbs eaten are converted to fat and stored in fat tissue.

Because our bodies consider alcohol to be a toxic substance, our bodies preferentially burn the calories in alcohol before anything else, in an effort to get it out of our system.  All fat burn stops when alcohol enters our system.  Unlike protein, carbs, and fat, alcohol has no ability to cause a sense of fullness, so the alcohol calories we drink end up being additional to our food intake.

While protein, carbs, and alcohol are carefully balanced, the same is not true for fat.  Fat is the ultimate and essentially endless energy storage depot.  Excess carbs are turned to fat; alcohol is metabolized instead of fat; and excess fat intake is stored as fat.  Fat intake does not promote fat use as an energy source - carbs are used first, and if the carb calories eaten are sufficient, the excess fat calories in the diet go directly to fat storage.  Fat also gives less fullness signals to the brain (protein gives the most, followed by carbs, followed by fat).   Fat cannot be converted to protein or carb - it can only be broken down for energy, or stored as fat.

In people with obesity, there is less capacity to use fat as an energy source, which is at least partly genetically determined.  As people with obesity lose weight, fat is used less and less as an energy source, because the body is trying to defend its energy storage (for times of famine back in evolutionary days).  Exercise can help to increase fat burn during and after weight loss, to help prevent weight regain.  A higher calcium intake, especially from dairy sources, helps to burn fat as a fuel, and also promotes some fat loss in the stool (about 50-75 cal per day worth), as well as helping to control appetite.

There is also a complex interplay that determines whether excess fat is stored around the organs (the more metabolically dangerous 'visceral' fat) or whether it is stored in the safer location under the skin (subcutaneous fat).  There is a strong genetic determination of whether a person stores fat in each location.  Higher cortisol levels, which are increased by stress and sleep deprivation,  promote fat deposition in visceral areas.

So, while the way each of us burns fuel definitely has a strong genetic component, there are a number of things we can do to optimize our individual situation:

  • eat a higher protein diet (unless you have kidney problems)
  • minimize alcohol
  • eat an appropriate amount of carbohydrates (as excess is converted to fat)
  • limit fat intake
  • get enough calcium (from dairy if possible)
  • decrease stress in your life
  • and get enough sleep!

Follow me on twitter! @drsuepedersen © 2015


Smoking Brings On Bad Fat

>> Saturday, August 1, 2015

It is unfortunately not an uncommon practice for people (especially women) to use smoking as a method of weight control.  The (evil, evil!) tobacco industry has had a role in this - since the 1960s,  they have added appetite suppressants to cigarettes to attract smokers concerned about body weight.

However, what most of these people probably do not know, is that smoking actually increases the risk of abdominal obesity (which is the metabolically bad fat) and diabetes.

It is true that smokers, on average, weight about 4-5 kg less than nonsmokers.   Why?
  • Nicotine is a stimulant, increasing energy expenditure by about 200 kcal per day per pack of cigarettes.   
  • Nicotine stimulates the release of serotonin, dopamine, and norepinephrine in the brain, which are neurotransmitters that act in the brain modulate appetite and energy expenditure.   
  • Nicotine acts on neurotransmitters that regulate food intake and metabolism such as leptin, neuropeptide Y, and orexins.  
  • The effect of leptin (a fullness hormone) may be enhanced by smoking.
  • Smoking can be a behavioral alternative to eating. (though lighting up can also accompany alcohol and unhealthy food choices/environments)

There are a number of undesirable hormonal effects of nicotine as well.  Tobacco influences fat distribution through hormones like cortisol that increase abdominal fat deposition.  In women, nicotine has an anti-estrogen effect which also favors abdominal fat collection.

One of the results of these undesirable hormone effects is that smoking actually increases the risk of diabetes by 44% compared to nonsmokers, independent of body weight.  This may be due to a direct effect of nicotine on the pancreatic cells that produce insulin, as well as the abdominal fat collection as well, which causes insulin resistance.

When people stop smoking, the tendency is towards weight gain of an average of 4-5kg in a year, with 13% of people gaining more than 10kg.   This is because metabolic rate drops, appetite increases as the appetite suppressing effect of nicotine is gone, and there is a behavioural tendency to eat more, especially foods high in fat and sugar, which activate the same reward pathways as nicotine in the brain.  An enzyme called lipoprotein lipase activity in fat tissue is increased 2-3 fold after smoking cessation, which increases the efficiency of energy storage.

All of the above being said, about 16% of people actually lose weight after smoking - so quitting smoking is not an automatic sentence for weight gain.

What about diabetes risk after quitting smoking?  The risk is intermediate between nonsmokers and smokers; the insulin resistance effect of nicotine is gone but weight usually goes up.  Although the decrease in heart disease risk is dramatic (50% after a year) with quitting smoking, this decrease in risk is not as great if a person gains weight.

Preventing weight gain with smoking cessation has not proven an easy feat.  Nicotine replacement (especially gums) limit weight gain somewhat, but only during the treatment.  A couple of medications (bupropion, which is Zyban, and varenicline, which is Champix) can also limit weight gain; these could help maintain motivation to quit smoking in the initial phases by having less weight gain, allowing the individual to focus on weight related lifestyle change once a little more distant from putting down the cigarettes.

It is clear that helping people quit smoking is not just about putting down the cigarettes - but also about engaging in permanent lifestyle changes to optimize overall health.

Follow me on twitter! @drsuepedersen © 2015



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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