April 10, 2013
Adipose Tissue Resting Energy Expenditure Higher in Women than Men

Apologies for the period of dormancy.  I’m back and I’m bringing you new articles every Wednesday.  With that said, here we go.

Introduction:  Men and women store fat on different areas of the body.  Women store fat in larger amounts of subcutaneous adipose tissue (the fat under the skin) and men store more visceral fat (the fat around the organs).  In general, women have more body fat than men.  How much adipose tissue contributes to whole body metabolism is not well known; therefore, this was the aim of the study.

Methods:  This was a large cohort coming from hundreds of men and women.  The researchers looked at adipose tissue gene expression as well as expression of genes involved in mitochondrial function.


  • For the two sexes, fat mass and fat free mass positively correlated with resting metabolic rate (when one went up, the other went up).  
  • Women have a higher metabolic rate per kilogram adipose tissue than men.
  • Women have a higher expression of genes related to mitochondrial function than men.
  • Women have a higher number of brown adipocytes in subcutaneous adipose tissue than men.

Discussion:  Just to give you an idea of the relative contributions of tissue to basal metabolic rate (BMR), the brain and internal organs account for 70-80% but only make up 5% of the body weight.  Skeletal muscle, which everyone in your gym says influences BMR the most, is 20 times lower than the internal organs.  Skeletal muscle accounts for about 15% of a person’s BMR.  Adipose tissue falls in at around 6% of BMR so we can say it is not that active of a tissue.  

From the lab to the gym: So what’s the main takeaway of this study?  The practical message is from bullet point 4 of the results and particularly a molecule found in those brown adipocytes known as UCP1.  UCP1 is a protein that allows the mitochondria to create heat in the brown adipocytes.  Women have a higher amount of UCP1 in their subcutaneous adipose tissue (the fat you want to lose under your skin).  Therefore, this study suggests that women have a higher capacity to burn calories by converting energy to heat.  Of course the internal organs and muscle are going to contribute the most to your BMR, but the higher metabolic rate of adipose tissue in women gives them an advantage to burn more calories in a resting state than men.

Nookaew et al J Clin Endocrinol Metab. 2013 Feb;98(2):E370-8.

November 28, 2012
Nighttime snacking reduces whole body fat oxidation and increases LDL cholesterol in healthy young women.

This one is for the night-eaters. The ones who find themselves diving into some snacks before bed.  You know who you are.  Did you know they actually consider this a syndrome though?

Introduction:  Night eating syndrome is classified as a delay in the circadian timing for food intake which can alter metabolism and eventually lead to obesity.  This syndrome is diagnosed as ingesting a quarter of your total energy for the day after an evening meal up to three times per week.  The aim of this study was to see how two weeks of snacking either during the day or at night, without changing meal frequency, would alter energy metabolism in lean young women.

Methods:  13 lean healthy women were recruited with 7 of them being randomly assigned to the snacking during the day group (10:00am) and the other 6 to the snacking at night group (11:00pm).  After the two weeks, their energy expenditure and substrate utilization were measured in a whole-room respiratory chamber for one day.  The snack consisted of merely 200kcal.  Breakfast, lunch, and dinner were given at 9:00am, 2:00pm, and 7:00pm for each group during the two weeks.


During the afternoon, the group that snacked at night had a significantly higher RQ (using more carbohydrates instead of lipids for energy) and significantly lower fat oxidation.  There was a small decrease in 24-hour fat oxidation with the group that snacked at night but this was not statistically significant.  LDL cholesterol levels significantly increased as well in the group that snacked at night.

My input:  A major strength of this study was the strict control of meal frequency during the two weeks.  However, the groups were small and likely underpowered when it came to statistical significance, particularly with the slight decrease in 24-hour fat oxidation which could have been significant had they recruited more volunteers.  Regardless, this study shows the importance of nutrient timing and how eating at specific hours of the day can alter our metabolism due to the hormones naturally controlled by circadian rhythms at those hours.  It is a necessity for the nutritional science field to step away from calories in versus calories out and start looking more towards nutrient timing at different hours of the day under different conditions (rest versus pre/post-exercise).

Hibi et al Am J Physiol Regul Integr Comp Physiol. 2012 Nov 21

September 17, 2012
Nutritional regulation of muscle protein synthesis with resistance exercise: strategies to enhance anabolism.

Maximize your muscle protein synthesis after weight training, bros.  I’ll highlight for you a recent review, which the scientist nerds can read entirely for free here, from Dr. Stuart M. Phillips.  I encourage you to take the time to read this one.

Introuction:  When scientists talk about muscle protein synthesis they are referring to accruing muscle proteins in an overall net positive balance.  That is to say, taking the most basic form of proteins, amino acids, and eventually creating structural muscle (aka hypertrophy).  Normally, this is done by adding to already existing contractile machinery of the muscle cells.  Researchers suggest that muscle protein synthesis (MPS for now on) is controlled by certain factors including dose, food source, and timing.  Let’s see what Dr. Phillips has to say about each of these areas.

"The anabolic window" -Timing

It’s like the holy grail of muscle growth for bros.  ”You can’t miss the window or you ruined the entire workout.”  Well, that’s a bit exaggerated.  Phillips states that, "It is now unequivocal that immediate post-exercise amino acid provision is an effective nutrition based strategy to enhance MPS above rates observed with exercise alone.”  Early post-exercise ingestion of amino acids or protein comes from studies that showed that exercise induced increases in rates of MPS are greatest right after exercise; approximately 100-150% above basal rates.  However, it may not be that big of a deal if you miss this window.  If you look at the figure below, the increase in MPS is in fact greater after exercise but can remain elevated for up to 48 hours.  Phillips suggests that consuming protein during these later times as well can be just as beneficial as ingesting protein directly after exercise.

MPS after resistance exercise

More importantly, Philips discusses the importance of actual exercise intensity and how it relates to muscle failure.  This is in lines with a study I touched upon in the past.  Looking at yet again another figure below, you can see that groups that take resistance exercise to failure, regardless if they’re using heavy load and low volume, or a light load and high volume had an enhanced amino acid sensitivity to muscle protein synthesis.  Let me say that again, IRREGARDLESS OF HOW MUCH WEIGHT YOU USE, as long as you are taking the muscle to failure, you will increase your rates of muscle protein synthesis more than loads not till failure. 

High vs low load

Protein source

Let it be noted that whey, egg albumin, soy, casein, and beef have all been shown scientifically to be able to stimulate MPS.  However, the Philips group has shown in the past that whey and milk can increase MPS greater than soy products following resistance exercise (this could be due to differences in amino acid profiles and/or digestion kinetics).  Why is whey fast-digesting and casein slow-digesting?  Every one knows that or will tell you that but do they even have an explanation why?  Phillips drops a knowledge bomb with one sentence, Whey protein is acid soluble and is associated with a very rapid, large, but transient increase in postprandial amino acid availability,  while casein coagulates and precipitates when exposed to stomach acid and the resultant dairy curd is slowly released from the stomach resulting in a much more moderate but sustained rise in plasma amino acids.”  I love knowledge bombs.


It is still accepted that in young healthy individuals, approximately 20-25g (which corresponds to approximately 8-10g of essential amino acids) of a rapid digesting protein source (whey or milk) can help maximize stimulation of MPS after resistance exercise. 

There you have it.  Now, I’m off to eat some beef.

March 14, 2012
Fitness or Fatness?

A few questions ago someone asked me how to find creditable journal articles.  Write this name down, Steven N. Blair.  One of the number one, if not the #1 person, for exercise interventions and large popluation studies in fitness.  His group just published a new article that I will highlight for you below.

Introduction:  How fit someone is as well as how fat someone is are both strong predictors of cardiovascular disease (CVD) risk factors and mortality.  Some studies suggest that being fit can attenuate the harmful effects of being fat.  That is to say, you can be overweight but as long as you are fit, it helps eliminate risk factors of CVD.  However, this group points out that there is a continuous change between being fit or fat, which could skew the results.  Therefore, the purpose of this study was to examine the independent and combined associations of changes in fitness and fatness within the development of risk factors of CVD; hypertension, metabolic syndrome, and hypercholesterolemia.

Results:  After a 6 year follow-up, participants (all 3,148 of them) who maintained or improved fitness had 26% and 28% lower risk of hypertension, 42% and 52% lower risk of metabolic syndrome, and 26% and 30% lower risk of hypercholesterolemia compared with those who last fitness.  On the other hand, those who increased in percent body fat, had 27%, 71%, and 48% higher risk of hypertension, metabolic syndrome, and hypercholesterolemia.  Interestingly, every 1-MET improvement in fitness between the beginning of the study and the follow-up was associated with a 7%, 22%, and 12% lower risk of subsequent incidence of hypertension, metabolic syndrome, and hypercholesterolemia.  On the fat side, every unit increase in BMI or percent body fat was associated with increases in higher risks of these CVD risk factors.  Similar results were found when looking at just waist circumference. Finally, both losing fitness regardless of fatness and gaining fatness regardless of fitness change were associated with a higher risk of developing metabolic syndrome.

Discussion/Conclusion:  Maintaining a certain level of fitness or improving on that level seems to alleviate, although not completely terminate, some of the negative effects of fat gain.  In addition, losing body fat can reduce CVD risk factors associated with a loss in fitness.  It is important to note that both, separately, are important risk factors in the development of CVD.

My input:  Keep in mind when reading these results that they are correlations and that does not give us a cause-effect relationship.  Other than that, I’m going to let Dr. Blair give you his final input this time (I urge you to please click this link) on this topic because he says it so much better than I could:

"My recommendation is to focus on good health habits, no matter what number you see on the scale. Give fruits, vegetables and whole grains a major place in your daily diet. Be moderate about fat and alcohol. Don’t smoke. Work on managing stress. Perhaps most important, get out
of your chair and start moving for at least 30 minutes every day.”

Lee et al J Am Coll Cardiol. 2012 Feb 14;59(7):665-72.

February 12, 2012
Sugar Month: The Conclusion.

Finally, we’ve come to the end of sugar month when I will now gather all of the thoughts to bring you the key points of what we know now in the scientific community in regards to sugar.

  1. Sugar when given in large amounts can have deleterious effects.  The key to this sentence are the words in bold.
  2. The effects are essentially on hepatic lipids, plasma lipoproteins, and hepatic insulin sensitivity. 
  3. The effects are related to fructose more than glucose.
  4. The effects of high-fructose corn syrup and sucrose are the same.
  5. The effects of fructose can be attenuated by exercise.

It is important to note that intervention studies, that is to say, studies over long periods of time are necessary and needed to truly elucidate whether or not increases in sugar are harmful over a substantial period of time.  Until these are accomplished, it is difficult to conclude true health consequences of sugar ingestion.

Hope you learned something from all of this and that you can apply the knowledge given here to better your health and lives.  

All the best,


February 10, 2012
The Toxicity of Sugar: You’ll want to read this one.

Last April, there was a very popular article published in the New York Times about how sugar is toxic to the body.  Although it is not entirely scientifically sound, it is still a well written piece, stemming from the original, and hugely popular, video from Dr. Robert Lustig posted on YouTube back in 2009.

Dr. Lustig publicly proclaims that sugar is indeed toxic to the body as that of tobacco products or alcohol.  This acclimation began with a publication in the American Dietetic Association journal back in 2010 when Dr. Lustig wrote an entire detailed review on fructose having similar properties to ethanol.  In summary, Dr. Lustig states that fructose has deleterious effects on the liver similar to that of ethanol in that it:

  1. Drives de novo lipogenesis, resulting in dyslipidemia, steatosis, and insulin resistance.
  2. Increases the amount of reactive oxygen species which in turn increases the risk for liver cell damage.
  3. Activates reward centers in the brain by blocking leptin and promoting sensations of hunger, which contributes to a positive feedback pathway for continuous ingestion of food, even when you’re not hungry.

Although these consequences of consuming excess sugar are possible, Dr. Lustig also provides two “antidotes” to combat the harmful liver effects from fructose:

  1. Exercise:  which increases hepatic TCA cycle maximal velocity leading to a process of biochemical events that will eventually provide less substrate for the creation of triglycerides.  In addition, improving the activity of mitochondrial proteins involved in promoting insulin sensitivity. 
  2. Fiber:  by reducing glycemic load and rate of carbohydrate absorption, fiber reduces the content of energy from the food the liver has to metabolize which in turn again, reduces triglycerides and improves insulin sensitivity.  Also, fiber is well known to increase satiety which would reduce consumption of more sugar.

Dr. Lustig also adds that although fructose is considered a carbohydrate, it is metabolized more like fat substances.

More recently (as of last week), Dr. Lustig is back at it again, publishing a comment article in Nature where he states some dramatic proposals in regards to fighting the war on increased sugar consumption.  Again he drives home the point that sugar is analogous to consuming alcohol claiming that it is unavoidable in society, toxic, has the potential for abuse and creates a negative impact (metabolic syndrome) on society.  There is even a link between sugar consumption and increases in the likelihood of cancer.  He then proposes that there should be a tax on any processed foods that contain any form of added sugars including soda, juice, sports drinks, and chocolate milk.  Does this seem extreme to you?  Would this really reduce consumption?  Statistical models show that for this to have an impact, companies would have to double the prices of all of these drinks to reduce intake.  Furthermore, Dr. Lustig states that there should be a limit on the availability of these products, such as limiting the hours retail stores are open to sell these products, regulating the location and amount of retail markets, and setting a limit as to who can legally purchase these items.  Yes, that’s right, Dr. Lustig feels you should be at least 17 years old to purchase drinks with added sugar.  

Okay, I understand the detrimental effects of sugar on the body and you’ve seen for the past month numerous studies showing them, but accomplishing all of these does not seem feasible in the U.S.  High-fructose corn syrup (HFCS) is not the sole culprit for the increase in obesity and Type 2 diabetes in the United States.  This notion was stated by John White in an article back in 2008 on the content of HFCS where he goes on to break some common misconceptions about this sweetener and sucrose.  As stated in the first week of sugar month, HFCS has a similar content to that of sucrose; 50% glucose and 50% fructose.  The only real difference is, and the reason of the stigmatic popularity to brand this sweetener as the reason for the obesity epidemic, is that it is cheaper for companies to use in their products.  White states that HFCS is not predictive of the rise in US obesity due to these conclusions:

  1. HFCS has the same sugar composition of other “benign” fructose-glucose sweeteners such as sucrose, honey, and fruit juice concentrates.
  2. Increased caloric intake since 1970 was not due to added sugars (including HFCS) but rather due to increased consumption of all caloric nutrients, especially fats, flour, and cereals
  3. Fructose-glucose sweeteners are all metabolized through similar pathways regardless if you ingest them from fruit, sodas, or fruit drinks.

Therefore, in White’s view, switching back to sucrose instead of HFCS in products would have, “no change in basic metabolism and no changes in the rates of obesity” (since sucrose and HFCS are essentially the same two monosaccharides).  ”The one change that consumers would notice is higher prices as sucrose is substituted for the less-expensive HFCS.”

Tomorrow is the conclusion of sugar month but for now I would like to know what some of you think about this post.  Do you think sugar is truly as toxic as Dr. Lustig states and should we take such drastic actions in limiting the consumption and availability of these sugar additives?


February 8, 2012
Simple but powerful thought for Sugar Month

A day of beverages:

8:00am - Orange juice 8 oz (110 calories)

10:00am - Medium mocha (400 calories)

Noon - Regular cola 20 oz (280 calories)

2:00pm - Some fruit drink 16 oz (230 calories)

5:00pm - Sweet tea 16 oz (200 calories)

8:00pm - Beer 12 oz (150 calories)

Total of 1,370 calories, approximately 65% of your standard daily value. 

January 23, 2012

Continuing with fructose, our focus now shifts towards the effects on the liver.  Some of you might have heard of non-alcoholic fatty liver disease, which is the accumulation of fat inside the liver that eventually leads to inflammation, scarring, and finally, cirrhosis (when the scar tissue replaces the actual liver cells).  Through the mechanisms of storing fat outside of normal fat depots (what we call ectopic fat depositions), scientists believe this creates a milieu of metabolites that eventually leads to insulin resistance and, subsequently, Type 2 Diabetes.  I’ll keep it short this time.

If you look at Figure 1, you can see that ingesting large amounts of fructose (in this case it was equal to 4L of soda/day, yikes) causes an increase in de novo lipogenesis from the liver.  It is also known to increase fasting triglycerides, which this study suggests a correlation between the two.  I know this large amount is not comparable to everyday ingestion for a normal person but nonetheless it shows you the possibility.

The second figure is another study that shows increases in ectopic lipids (IMCL = intramyocellular lipids and IHCL = intrahepatocellular lipids) as well as triglycerides.

In regards to insulin resistance, the third figure from another study actually done here in the department of physiology shows indeed, even fructose overfeeding decreases hepatic insulin sensitivity.

Finally, the last figure is a proposed pathway by Prof. Luc Tappy on how fructose can lead to insulin resistance through several different mechanisms.

Figures adapted with aid of Prof. Luc Tappy MD, PhD

January 18, 2012

 For those who did not see, I received this question last week in regards to artificial sweeteners:

For the first part, there is a fairly recent study looking at the effects of stevia, aspartame (the most popular artificial sweetener found in diet soda), and sucrose on food intake, satiety, and post-prandial glucose and insulin levels.  As you can see in the first figure, aspartame did well indeed cause an increase in insulin after ingestion but I would not consider this a “spike” (clearly it is not as much as sucrose).  The researchers didn’t speculate on this subtle increase but it does show that the artificial sweetener, aspartame, can indeed increase insulin levels but it is worth noting that this is not that high.  As far as energy intake, you can see in the second figure that the three different loads of either stevia, sucrose, or aspartame did not effect hunger levels throughout the day at other meals.  The only difference was total energy intake but this makes sense since aspartame has no calories compared to sucrose.

On to the next part of the question and whether or not artificial sweeteners can increase appetite.  This time we’ll use another artificial sweetener, sucralose, or as you might know it, Splenda.  An article published last year states that sucralose cannot effect hormones responsible for the satiety response (GLP-1, PYY), insulin levels, or appetite.

Furthermore, does the human gut respond the same way to sugar and artificial sweeteners?  Well, in this study, glucose seems to be the driving factor in activating mechanisms for appetite whereas other sugars or artificial sweeteners did not.  The authors state that sweetness per se does not effect secretion of gastric peptides but the sugar must have a structural integrity similar to that of glucose for these effects to exist.

Let’s move on now to the brain, specifically the amygdala (sorry Waterboy), which is a part that can respond to food aromas and the insula, which relates oral sensations with internal states.  This study shows that in fact, artificial sweeteners can affect these two regions of the brain and interrupt brain chemistry for sensing normal sugars such as sucrose.

As far as safety, it is documented scientifically in this review that artificial sweeteners are in fact safe to use. 

Et voilà. In summary, artificial sweeteners will not affect your appetite and therefore you can go back to ordering a large fast food meal (no really, don’t) with that barge of diet softdrink.  As far as the insulin response, I feel a lot of people downplay the ability of the brain in regards to hunger or satiety.  It is similar phenomena as Pavlov’s dogs salivating in anticipation of a meal after they hear the tuning fork.  Even at the smell of food, your gut will release gastric hormones in anticipation of the food that will soon be eaten and digested.  It could be the same response as to why there was a slight increase in insulin to aspartame.  The mind thought something sweet was being consumed when in fact it was not.  I hope this clarified some of the issues and answered the proposed question.


January 16, 2012
Excessive fructose intake induces the features of metabolic syndrome in healthy adult men.

Fructose, friend or foe?  It can be so beneficial to endurance athletes but so detrimental to the sedentary person.  These findings may alarm you.

Introduction:  As stated previously during sugar month, large fructose ingestion is linked with an array of health problems.  In this case, researchers link it to the metabolic syndrome, which consists of insulin resistance, dyslipidemia, abdominal obesity, and elevated blood pressure.  The metabolic syndrome often precedes the development of Type 2 diabetes.  Some of these effects are not found with glucose or diets consisting of starch.  Fructose and glucose metabolism differ and one of the consequences is depletion of ATP and production of inflammatory mediators.  The breakdown eventually leads to the production of uric acid, which may have a role in insulin resistance.  Therefore, the researchers are trying to use a drug, allopurinol, as a way to reduce uric acid and see if this can reverse the symptoms of metabolic syndrome after fructose consumption.

Methods:  Participants were 74 males who ingested 200g daily of fructose sipped throughout the day for a total of 2 weeks.  One group received the drug allopurinol and the other did not.

Results:  The following showed significant differences from baseline in regards to fructose ingestion:

  • Increase in ambulatory blood pressure with subtle greater increases in diastolic blood pressure throughout the day (number of participants who fit the criteria of metabolic syndrome for this went from 9 at baseline to 21)
  • Mean increase in fasting triglycerides
  • Reduction in HDL cholesterol
  • Increase in patients with fasting glucose meeting the criteria for metabolic syndrome ( >5.5 mmol/L)
  • Increase in fasting plasma insulin
  • Worsening of liver function tests

In regards to the group that consumed the drug (allopurinol) to decrease uric acid there were significant changes found to:

  • Protect against increases in systolic and diastolic blood pressure as well as mean arterial pressure
  • Protect against metabolic syndrome (32% participants had it before and only 34% after as compared to the fructose only group at 19% to 44% after two weeks)

Discussion/My input:  The first thing you are probably thinking is, “Nick, who would drink 200g of fructose per day, this study is not practical.”  Well, here is an alarming fact; the upper quintile of Americans consume more than 110 g of fructose daily either as additional sugar or as high-fructose corn syrup.  That is pretty close and these changes happened in only 2 weeks!  As far as the drug, it may be something included in the future to combat the metabolic syndrome; however, these results cannot be related to obese individuals or even women.  The researchers state that fructose metabolism can vary between genders.  Once again, fructose might not be the sole reason for the obesity epidemic, but it does lend credence to that notion.

Perez-Pozo et al Int J Obes (Lond). 2010 Mar;34(3):454-61