My name is Nick and I am currently doing my PhD in physiology with an emphasis in muscle physiology. Welcome to my exercise science blog. Unlike a lot of fitness blogs out there, this one is unique because it is backed by true science. You will find only articles that have been peer reviewed and published in top tier science journals on this blog. For the fast easy read, just read the bold type. If you have any questions do not hesitate to ask me. I am at your disposition for any advice in exercise or just basic physiology. This is not a progress blog to benefit myself but rather to share some of my knowledge and expertise with you that I have gained over my years dedicating my career to exercise science. If I do not know the answer, I will do my best to search through the journals to find it for you. Although I am in biomedical research, I am not a licensed medical professional so please consult a physician before entering any exercise or nutrition program.
Are you a girl who regularly skips breakfast? Read on because this well-controlled study is for you.
Introduction: Breakfast skipping is strongly associated with a greater chance of weight gain. Furthermore, this trend is also linked to poorer food choices. Higher protein meals are becoming more popular as a way to improve satiety and appetite control. The purpose of this study was to examine if it is better to skip breakfast or eat one higher in protein in regards to appetite control throughout the remainder of the day.
Methods: Twenty overweight or obese girls between the age of 15-20 who normally skip breakfast were recruited for this study. They were tracked for 7 consecutive days and randomized to one of 3 groups: breakfast skipping (BS), a normal cereal meal for breakfast (NP), or a high-protein breakfast (HP) consisting of beef and eggs for breakfast. Breakfast and lunch were controlled but the rest of the day they were free to eat as much as they wanted.
NP & HP led to a 60% reduction in daily hunger.
HP lead to a greater increase in total fullness.
NP & HP led to a 30% reduction in daily desire to eat.
HP breakfast but not the others suppressed an important hunger stimulating hormone (ghrelin) by 20%.
HP breakfast but not the others increased an important satiety-stimulating hormone (PYY) by 250%.
BS & NP led to greater evening snacking than HP.
Discussion/Conclusion: A small breakfast of merely 350kcal led to reductions in perceived hunger, the desire to eat, and prospective food consumption. In addition, it also increased fullness. What is even more interesting is that the high-protein breakfast group had additional benefits of a reduction in the hunger-stimulating hormone ghrelin, increases in PYY (a hormone that makes you feel fuller), and decreases in evening snacking, particularly of high-fat foods. The authors note that a limitation of this study was that the breakfast skipping group and the high-protein group had similar total amounts of calories consumed during the day. Although this study looked at 1-week of food consumption, it is not certain if eating a high-protein meal for longer periods of time (a year or more) would prevent weight gain.
My input: The most obvious inferences that the authors draw come from the simple fact that the breakfast skipping group is fasted. Of course, their perceived hunger/fulness, desire to eat, and prospective food consumption will be higher in the morning because they just woke up. I think the most powerful part of the study came from the blood draws and the actual measurable physiological significance that a high-protein breakfast did decrease a hormone responsible for making you want to eat and increase a hormone that tells your brain that you are full.That is what truly stands out as powerful rather than all the other results based solely on questionnaires. For that reason, I’d suggest trying out the high-protein diet over your standard cereal-based breakfast and seeing how it works with your own feelings of satiety throughout the day.
A fresh article was published in the New England Journal of Medicine yesterday that looks at the most common myths, presumptions, and facts about obesity. What really makes this paper intriguing is that the authors used internet searches to find these. Since some of you might not have assess to the full text, or not have the time to read the entire article, I’ll highlight some of them for you below.
The myths (the authors define myths as “beliefs held true despite substantial evidence refuting them”)
Small sustained changes in energy intake or expenditure will produce more substantial long-term weight changes.
Setting realistic goals for weight loss is important; otherwise, people will become frustrated and likely lose less weight.
Slower gradual weight loss is better than large rapid weight loss in regards to long-term outcomes.
PE classes in school play an important role in reducing or preventing childhood obesity.
A bout of sexual activity burns 100-300 kcal for each participant. (The authors state the actual numbers are more like 14-21 kcal considering the average sexual experience lasts 6 minutes, ouch).
The presumptions (the authors define presumptions as “unproved yet commonly espoused propositions”)
Eating breakfast each day as opposed to skipping it is protective against obesity.
Eating more fruits and vegetables will result in weight loss or less weight gain, regardless of any other behavioral or environmental modifications.
Weight cycling (yo-yo dieting), is associated with increased mortality.
Snacking contributes to weight gain and obesity.
An individual’s environment (parks, recreational playgrounds, etc.) influence the incidence and prevalence of obesity.
THE FACTS (“sufficient evidence to be considered empirically proved”)
How would you like to be in a study where they fatten you up for 2 months? Well, this group recruited volunteers just for that and have provided a significant advancement in what is known about adipose tissue structural changes during the first several weeks of weight gain.
Introduction: The purpose was to examine molecular changes in adipose tissue structure after 2 months of an overfeeding protocol.
Methods: Forty-four healthy males were recruited and told to increase their daily caloric consumption to excess of 760 kcal/day. To accomplish this, they added 100 grams of cheese, 20 grams of butter, and 40 grams of almonds to their usual diet. Fat biopsies were taken at 2 weeks and again at the end of the 2 months.
Results: MRI revealed a significant increase in abdominal tissue volume both for subcutaneous and visceral. No changes in mean adipocyte (fat cell) surface size or number. There was a significant increase in the density of capillary vessels. As you would expect, there was an increase in the number of genes related to fatty acid and lipid biosynthesis. There was also an upregulation in genes involved in formation of the extracellular matrix and angiogenesis (the creation of blood vessels).
Discussion/Conclusion: Although there was an increase in genes responsible for storing excess fat, there was not yet a significant increase in size or number of fat cells. Interestingly, there was an upregulation in capillary density and genes involved in creating more blood vessels to supply the adipocytes. This could also be a reason why the extracellular matrix was remodeled to create space during initial weight gain.
My input: There were also some other important molecular pathways that were downregulated in this study but for sake of boring you I decided to leave those out. I think the main important finding in this study is the disovery of genes involved in creating new blood vessels for the fat cells. It makes sense if you think about it, that an increase in adipose tissue would demand a larger supply of blood. Therefore, it is necessary to increase the amount of vessels perfusing the cells. This group did well in not only showing this in gene arrays but also in histological staining from the fat biopsies. Another article from a different group found similar results in that the adipose tissue of obese and insulin resistant subjects had larger vessels but fewer capillaries when compared to lean subjects. I would not be surprised to see pharmaceutical studies in the near future aiming at trying to reduce the amount of blood vessels as a way to amerilorate adiposity. After that, I would not be surprised if that is soon the next gimmick in supplement companies’ “fat burners”/thermogenic products.
Where your body deposits fat matters in regards to insulin resistance and future cardiometabolic risk. Here is a figure from a brand new study published by my doctoral adviser in Obesity. Getting around the ugly statistical box plots, what it means to you is simply that subcutaneous thigh adipose tissue appears to show a protective effect when it comes to insulin resistance (Dr. Amati uses Rd in this case, which is rate of glucose disposal, as a marker of insulin sensitivity). The higher you are on the scale, the more sensitive your periphery is to insulin. The worst marker of insulin sensitivity, and what scientists can deem as the dangerous area to store fat, is the visceral abdominal adipose tissue. These results are all regardless of age and gender.
Here we see again the apple vs. the pear story in how one stores fat depots where in this case, the pear seems to win, or at least, be favored.
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.
Sugar when given in large amounts can have deleterious effects. The key to this sentence are the words in bold.
The effects are essentially on hepatic lipids, plasma lipoproteins, and hepatic insulin sensitivity.
The effects are related to fructose more than glucose.
The effects of high-fructose corn syrup and sucrose are the same.
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.
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:
Drives de novo lipogenesis, resulting in dyslipidemia, steatosis, and insulin resistance.
Increases the amount of reactive oxygen species which in turn increases the risk for liver cell damage.
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:
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.
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:
HFCS has the same sugar composition of other “benign” fructose-glucose sweeteners such as sucrose, honey, and fruit juice concentrates.
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
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?
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.
The remainder of “sugar month”, for lack of a clever name, is going to be dedicated to mostly research about fructose. Therefore, it is appropriate that I also give you an introduction to High Fructose Corn Syrup (HFCS) and some background on fructose metabolism. Once again, we’ll keep it simple.
Fructose is found naturally in fruits and honey. It has somewhat of a low glycemic response in that it does not elicit as high of insulin spikes postprandial as other sugars. In fact, sports products that contain fructose are what are responsible for some of the stomach discomfort that endurance athletes experience upon ingesting these drinks during physical activity. HFCS can be a somewhat misleading term in that it is not entirely just fructose. HFCS is extracted from the starch (Amidon) in corn to make a glucose syrup. From this syrup, half of it is made into fructose (because pure glucose does not have a pleasant taste) and the other half is mixed with glucose. Thus, HFCS has a similar composition as sucrose (50% glucose, 50% fructose). This is summarized in the first figure.
As shown in Figure 2, the metabolism of fructose is similar to glucose in that it involves the GLUT2 transporter. Fructose metabolism is not dependent on insulin secretion. The fate of fructose upon ingestion within the organ systems can be seen in Figure 3. In summary, the effects of fructose on the body from numerous studies show that:
Long term fructose ingestion can induce metabolic disorders
In rodents: a high fructose/sucrose diet leads to obesity, insulin resistance, diabetes, dyslipidemia, and high blood pressure.
In humans: high fructose/sucrose diets lead to hypertriglyceridemia
As stated yesterday, increases in HFCS parallel the increases in obesity in the United States but it is unknown whether or not this is the sole factor. Now that you have the necessary background of the sugars and how this corresponds to metabolism, the rest of sugar month will be science articles convincing you that increased ingestion may or may not be a factor in obesity and diabetes.
So I told you that I’m dedicating this month to all about sugar and its effects on health. What I have for you is a plethora of studies and the aid of one of the leaders in the world on sugar metabolism studies in humans, Professor Luc Tappy. Before we begin, I’ll start with a simple introduction because I know those not in the sciences like science simple (and to avoid any pedantic writing).
Sugars in their simplest forms can be classified as the monosaccharides. We’ll stick to three of them: glucose, fructose, and galactose. Combining them together into disaccharides such as glucose + fructose gives you sucrose (table sugar) or glucose + galactose gives you lactose (what is found in milk). Each have different properties and their own role in metabolism. I’ve included a figure on the breakdown of carbohydrates and the absorption of these three monosaccharides.
The history of increases in sugar consumption began during the period of the Crusades when it was considered white gold. As you can see in the second figure, there was a large increase in sugar around 1850 which corresponds to an eventual (100 year) subsequent increase in obesity (the black dots) up until present day. This leads scientists to attribute increases in sugar as one of the main factors for the increase in obesity. However, is this really the sole cause?
The third figure shows the increase in sugar consumption per capita since 1986. It is important to note that this does not include consumption of the less expensive sweetener, high fructose corn syrup (more on this tomorrow). Finally, if we focus just on the U.S. you can clearly see in the last figure the trend of an increase in sugar consumption and a switch from ingesting sucrose to more high fructose corn syrup. Is this cheaper alternative really that bad for your health?
What I hope for you to take away from this month is the pathophysiological effects of a diet containing high amounts of sugar, specifically fructose, and how this potentially could have lead to the obesity epidemic and the relationships with diabetes.
So do you feel your body is stubborn when it comes to weight loss? In many animal studies, scientists induce obesity just by supplementing the animal’s drinking water with sucrose. Think about that next time you want that soda or other sugary drink. Nothing bothers me more than seeing someone consume Gatorade just for the flavor.