S.P.E.E.D. - Evidence Based Weight Loss

I Wish I Had Your Metabolism

2012-01-30T20:37:22Z

A friend of mine brought up a good topic on Facebook the other day, something I’ve had to deal with quite a bit over the years. I guess it’s mostly been because I haven’t reached a ripe old age yet, unlike my distinguished colleague Mr. Thiboutot. The issue is this: while a client is discussing their poor state of health accompanied by an extra X0 lbs, they say “I wish I had your metabolism.” I’ve always dodged the statement by moving the focus to something more productive, like a good coach, by saying “well, you just have to do what works for where you’re at now” which of course is true.

But what I really wanted to say is “How dare you write off all the hard work I’ve put in at the gym and the restraint I’ve shown at the feeding trough by claiming it’s my metabolism! Do you have any idea how insulting that is? I started lifting weights when I was 12 in my hometown’s YMCA and except for a few months here or there I’ve never stopped exercising. I also started reading about nutrition soon thereafter, even though I wish I hadn’t ever read some of it now that I look back on it.”

“Right now, I’m 31 and I’m as lean as I have been in years, getting older be damned. At what point will I be old enough where you can’t use that excuse? What about a guy like Randy Couture? Is he old enough to shut you up?”

Okay, enough of my being as bitter as raw kale. As we’ve discussed before, the metabolic slowdown associated with aging, after adjusting for body composition differences, equates to a change of 1-2% per decade. (Roberts) Crunch the numbers, if your average caloric burn is 2000 calories/day when you’re 20, it will be 1900 calories/day at 70. The important point here is that these figures are adjusted for changes in body composition. What does this mean? Well, as we age we tend to lose some muscle and gain some fat, the former being more metabolically active than the latter, especially if you use it. These figures take that into account and establish the estimated metabolic slowdown due to other, less controllable factors like a decrease in brain glucose utilization.

Roberts and Rosenberg also discuss evidence of an attenuated adaptive increase or decrease in thermogenesis in response to overfeeding or underfeeding with age. What does this mean? The older you get, the less your metabolism responds to overeating or undereating by speeding up or slowing down, respectively. This would lead to older people gaining more weight as a result of overeating than their younger counterparts. But, before you go feeling vindicated for your flabby waistline, it also means older people will lose more weight as a result of undereating compared to their younger counterparts, given the same degree of deficit. Shut it.

It should be noted that this attenuation in adaptive thermogenesis is tied to lean tissue – just one more reason to keep the muscle you have and maybe add some.

“But, maybe I have a slow thyroid… so there”

What if you have a slow thyroid? Well, researchers investigating sublclinical hypothyroidism (SH) had to split the SH group into upper and lower halves to discover a difference in resting energy expenditure per kilogram of fat free mass. No differences were found in various energy expenditure measurements between the entire SH group and healthy controls. (Tagliaferri) In thyroidectomized patients, basal energy expenditure was about 300 calories/day lower than healthy controls before thyrotrophine-suppresive thyroxine therapy. (Wolf) A deficit of 300 calories/day will put a nice dent in your ability to eat without paying much attention and maintain your body weight, but please understand that this is in thyroidectomized patients. This is severe and if you’re reading this wondering “Hey, I wonder if I have that” you probably don’t. My guess is you’d know.

By all means, if you feel you might be suffering as a result of an underactive thyroid, go to the doctor. Have them run an extensive test and try to help you figure it out because it’s a serious issue. But don’t go crying hypothyroid simply because you “can’t loose [sic] weight, no matter what” you try.

The BBC Tells you to STFU about It

Remember this post? I talked about the BBC documentary “10 Things You Need to Know About Losing Weight“…

The most exciting part, in my opinion, starts at about 8:30 into this video and continues into this video where Debbie gets her metabolic rate tested and finds that her metabolism is spot-on average and she can no longer blame her weight problem on a slow metabolism. Then they have her keep a food diary for nine days, first by video at the end of the day and then by journaling throughout the day. At the same time, they use the doubly-labelled water method to calculate the amount of calories she takes in and expends. When comparing her video and journal food diaries to the doubly-labelled water calculations, they find Debbie failed to report 60 and 43 percent of her calories, respectively.

Debbie, like many others, claims a slow metabolism is to blame for her life-long weight problem. A lack of control at the plate is really the problem, and I’m not talking about swinging a bat.

It all ends in the end

Look, we’re all going to die and chances are unless you really screw things up you’ll live about as long as me. You have every right to spend those years however you want. If you’re comfortable with 30 extra lbs hanging off your ass, who am I to tell you not to keep it there? But if you’re not happy with that extra 30, do what you need to do to get it off (WARNING! MAY REQUIRE EFFORT) and don’t you dare say “I wish I had your metabolism” to anyone who has been putting in the effort all along.

Weight Loss is NOT Simple!!

2012-02-02T13:36:25Z

Weight management is often presented in the following way;

Intake of calories – energy expenditure = X (maintain, gain, or lose weight)

Based on this equation, to lose weight you need to decrease intake and/or increase expenditure.

Let me illustrate the point;

2,000 intake – 2,000 expenditure (BMR + activity) = no change in weight

1,500 intake – 2,500 expenditure (BMR + More activity) = decrease in weight, if this is maintained, then a person would lose 2 lbs a week (there would be a potential 7,000 calorie deficit accrued during the week and each pound of fat = 3,500 calories, it is usually not that simple or linear, but for now let’s go with it)

This basic, or simple equation of weight regulation is TRUE. No doubt about it. If the balance of the equation is positive then weight will be gained, if it is negative weight will be lost. This is weight management 101 and most of you are saying “No shit!”. Anyway, this simple view is the basis for the typical recommendation to just “Eat less and move more”, again, most everyone will say “Thank you Captain Obvious!”.

But, there is a BIG problem with this simple view/approach to weight regulation. The problem comes from the fact that there is a whole lot of shit going on under the surface. This simple view is like the tip of an iceberg, doesn’t look so bad, but the big part is found under the water. Under the surface there are many physiological, social, and psychological variables that influence the in and out parts of the equation. The “eat less and move more”, which is true, is too simple and I think leaving it at that level would be similar to saying to someone with an alcohol or drug problem, “Just stop drinking or using drugs”. Well, obviously, but there are often a number of real reasons that a person is struggling with alcohol or drugs and stating the obvious is not likely to be beneficial. The thing is our eating behavior is actually more complex and likely more challenging because eating is a biological necessity. We can’t stop eating forever whereas we can stop drinking alcohol or taking drugs forever.

The basic in and out equation

The “eat less and move more ” recommendation

The MANY biological, social, and psychological variables that strongly influence our ability to modify the in and out aspects of the equation. These variables must be addressed if long-term changes in behavior and weight are to be accomplished.

Here are a few more illustrations to highlight my point. These are from the paper;

Zheng, H. & Berthoud, H. (2008). Neural systems controlling the drive to eat: Mind versus metabolism. Physiology; 23: 75-83

Here is the abstract from the paper mentioned above;

“With the bleak outlook that 75% of Americans will be overweight or obese in 10 years, it is essential to find efficient help very soon. Knowledge of the powerful and complex neural systems conferring the basic drive to eat is a prerequisite for designing efficient therapies. Recent studies suggest that the cross talk between brain areas involved in cognitive, emotional, and metabolic-regulatory functions may explain why energy homeostasis breaks down for many predisposed individuals in our modern environment.” (p.75)

Yes, many people need to eat less and move more. But, HOW is that accomplished (not the point of this post so you will have to read the book or other posts to find out)? Well, it seems self-evident that the simple recommendations are not working, at least not for a lot of people. Which leads to the point of this post, which is to highlight the fact that weight regulation is actually very complex and for the millions of people who struggle with maintaining a healthy weight a simple recommendation of “eat less and move more” is NOT likely to lead to any real change. Due to this fact a comprehensive approach to the problem must be used if the problem is to be remedied.

You can find EVIDENCE to support ANY view?

2012-01-26T02:05:02Z

There seems to be a fairly common view that virtually any idea or concept can be supported with “evidence”. I have had a couple of recent comments that have highlight this view.

One of the recent comments was;

“All scientific research is based on controlled studies, all of which can be arranged to “prove” any outcome that you want. I can setup a viable study to have it demonstrate that protein is bad and whole grains is good, even if that is not the case.”

I also think that these types of statements are used by people who feel that their view on a subject is challenged. They use this position as some type of argument.

Is this true, can we prove anything we want and find research to back up anything? On the surface there may be some truth to these statements. However, when you look behind the curtain you really CAN’T prove everything or find research to back up anything, IF, and this is a big IF, you play by the “rules”. Let me explain.

When it comes to research and doing studies there are many variables that will determine the internal and external validity of it. Basically, the type of research and how the studies are done will determine how well it can demonstrate a CAUSE and effect relationship. There are many aspects that help us determine the “quality” of the research and therefore, how much emphasis we can put on it. Some of the variables include (this is not an exhaustive list);

Sample size
Sample type
Randomization
Length of intervention
Blinded or not
Type of statistical analysis
How well variables were controlled (i.e., metabolic ward versus free-living)
Type of study (randomized controlled trials, cohort, case-controlled, cross-section survey, etc)

These variables will determine if the study actually demonstrates some kind of effect and if we can determine WHAT actually CAUSED the effect.

Before making any conclusive judgments, it is generally recommended that a similar effect has been produced more than once.

These would be the “rules” of research and if they are followed it is NOT likely that anything can be supported. I think anyone familiar with the many aspect of research would agree. You just CAN’T prove anything, just like you CAN’T say that left is right, up is down, or that researchers always follow the rules.

This last point also relates to the view that “anything” can be supported or there is more uncertainty than there is on a topic. Researchers are human, therefore, like us mortals, they to do NOT always follow the rules. This means that the conclusions from a study may actually have little or no validity. This can be due to weaknesses in the above “rules”. However, the problem can actually be with how the authors state the results in the conclusion of the paper which is the part that is included in the abstract, which often translates into a misleading title of a paper (due to the the peer-review process this should really not happen, but it does). These latter points are what are often publicized and contribute to the confusion. However, if someone were to look at the meat of the paper, the boring information explaining the “rules” of the study and the actual results, a different conclusion may be more likely or at least a less “definitive” conclusion would be warranted. I am not saying that this happens all the time, but it happens enough to muddy the waters and leads to the impression that “anything” can be supported with evidence.

This problem also stems from biases (often we are not conscious of) and a lack or lapse of critical thinking (it is very demanding) that happens to researchers, writers, and practitioners. We WANT to believe certain things, therefore we can easily focus on what seems to support our current beliefs and miss the information that may challenge our current beliefs.

On a superficial level, there is certainly an impression that most anything can be supported with evidence. But, when a deeper perspective is taken, this view loses its validity. I am NOT saying that things are black and white, there is definitely a lot of grey. But, the grey area is often more like nuances of a topic rather than a complete divergence from what the “quality” evidence actually demonstrates. With that said, I don’t think that the argument that anything can be supported with evidence or any study can be manipulated to show any result are valid IF the rules are followed. When the rules are followed and we become aware of our biases and implement critical thinking skills there is often a rather small range of possible conclusions that can be supported by evidence.

Your Protein Shake is No Longer a Protein Shake

2012-01-18T21:15:15Z

Client: I started drinking a protein shake to get a little more protein in my diet.

Me: Cool! Are you using a pre-made shake or making your own?

Client: Making my own. I use 1 scoop of protein, a banana, 2 tbs peanut butter

Me: That’s not a protein shake.

Client: It has protein in it.

Me: So does a Double Quarter Pounder With Cheese.

413 calories, 17 grams of fat, 36 grams of carbohydrate, and 33 grams of protein does not equal a protein shake.

The take-home lesson here is be careful that your protein shake isn’t turning into a meal replacement shake. There’s nothing wrong with meal replacement shakes, except when they’re not replacing but instead adding a meal, know what I mean? Know which one you need and know how to make it.

By the way, the shake above is actually pretty damn good with chocolate protein powder and ice

Carbs & Exercise?

2012-01-27T23:45:54Z

First, a bit of background information is needed, so that certain aspects of this post make sense. This information was presented to other fitness professionals so there is a bit more jargon than usual and there will be wording that depicts a “trainers” point of view.

It is a common belief that lower carbohydrate (CHO) diets, (usually considered less than 50% of calories), will not supply enough CHO to fuel exercise, particularly intense exercise, sufficiently and, in general, will lead to a reduced “energy” level or general fatigue. The reasoning behind this view goes something like this;

“The muscles primary fuel is CHO, therefore a low CHO diet will not supply enough “energy” to fuel your workouts or general activities”

This criticism of low CHO diets is common. A recently comment about the “Zone” diet;

“The 30/40/30 percentage is too high in protein and too low in carbs for a healthy eating plan. Extra protein will not help you build lean body mass but instead will stress your system and drain your glycogen stores—the muscle’s primary fuel” and “I do not see the “moderation” part of the Zone diet but instead view the Zone diet as a similar type of fad low-carb diet, far too low in carbs to fuel hard workouts and better health.”

Is this true? Do we need at least 50% of our calories to come from CHO in order to fuel our workouts and to be able to have the energy to do daily activities? I think this view is almost completely false.

This statement is likely to sound very heretical to many of you reading this. Therefore, I better back this up with some solid evidence.

The first place to start is a brief review of anaerobic and aerobic metabolism. I won’t go into much detail here, but I would strongly suggest to anyone who wants to really understand this topic to go read through your Bio-chem, Exercise Phys or other textbook that covers the subject matter. There are usually some great diagrams, which for me, makes it easier to understand the processes involved.

When talking about energy production I think stating that we need carbs or fats or proteins to make energy is a bit misleading. It’s true, but what we are really talking about is making ATP. ATP is the real energy molecule, so any discussion about energy really needs to revolve around ATP production.

Aerobic (with oxygen) Metabolism (AM) is the system of energy production we use for making almost ALL of our energy. In AM a key ingredient is Acetyl-CoA, as this is the molecule that enters the Citric Acid Cycle and pops out a bunch of ATP. Want to guess which macronutrient supplies the majority of this molecule at rest and low intensity activities? It’s not carbs. The fuel that runs the AM is fat.

“Skeletal muscle cells also oxidize lipids. Indeed, fatty acids are the main source of energy in skeletal muscle during rest and mild-intensity exercise.” (El Bacha)

“Other organs that use primarily fatty acid oxidation are the kidney and the liver” (El Bacha)

Interesting aspect about the heart

“Cardiac muscle is unlike smooth or skeletal muscle in that it cannot rely on anaerobic metabolic pathways to provide its energy” Retrieved from http://www.biog1105-1106.org/demos/105/unit10/muscles.html

“Between meals, cardiac muscle cells meet 90% of their ATP demands by oxidizing fatty acids. Although these proportions may fall to about 60% depending on the nutritional status and the intensity of contractions, fatty acids may be considered the major fuel consumed by cardiac muscle” (El Bacha et al)

Therefore, most of the day we are running on mostly fat (dietary or body fat).

Anaerobic (without oxygen) Metabolism (AnM) is run by the ATP/CP system and glycolysis. These systems are mainly fueled by CHO. So we do need some CHO for this, although it can actually be from a very limited amount of dietary CHO along with protein (gluconeogenesis), glycerol from fatty acids and ketones, which is what the metabolism does when a very low amount of dietary CHO are ingested (that is for another day). However, the amount of time spent in this system is relatively small. Using our typical client who works out for 3 to 5 hours a week (not all of it is actually in the AnM system), that would only account for about 3% (based on the full 5 hours) of our weekly hours. This leaves 97% of our time in the AM system. Therefore, for the typical client, the amount of CHO to fuel this is relatively low.

When it comes to exercise the type of fuel used is on a sliding scale, low intensity mostly fat, very high intensity virtually only CHO. However, there is the potential to modify what is used by dietary changes and training adaptations. For now I will not consider those aspects. Our typical client working out 3 to 5 hours a week is likely to only be in AnM for ½ the time and the AM system for the other half. How many CHO would this person likely burn?

“Exercise, an acute bout of muscular activity, requires an expenditure of energy above resting levels. This required mechanical energy is provided through the conversion of metabolic fuels into ATP, the base currency of chemical energy. Once produced, ATP is the only direct form of energy that is transferred and utilized by the contractile apparatus within the muscle. Fats are the predominant fuel source of resting skeletal muscle and during exercise, there is a complex interaction between skeletal muscle fat and carbohydrate (CHO) metabolism (see [1] for review). When evaluating the effects of exercise on skeletal muscle fuel utilization, there are many facets that must be taken into consideration. These include intensity and duration of the bout of exercise and the training status of the subjects. During low intensity physical activity (25% maximal oxygen uptake (VO2max)), fat supplies the majority of metabolic fuel to exercising skeletal muscle [2]. As physical activity increases to moderate levels (65–70% VO2max), there is a shift to more reliance on CHO, specifically muscle glycogen [2]. However, at this level of physical activity, fat oxidation becomes increasingly important as the duration of exercise increases [2] or as training status improves [3].” (Peters et al p.1)

“During exercise, the primary nutrients used for energy are fats and carbohydrates, with protein contributing a small amount [2-15% (p.40] of the total energy used” (Powers et al p.31)

“Approximately 50% to 60% of energy during 1 to 4 hours of continuous exercise at 70% of maximal oxygen capacity is derived from carbohydrates and the rest from free fatty acid oxidation” (Position of the ADA…p.511)

“Long-chain fatty acids derived from stored muscle triglycerides are the preferred fuel for aerobic exercise for individuals involved in mild- to moderate-intensity exercise” (Position of the ADA…p.512)

“As a result of aerobic training, the energy derived from fat increases and from carbohydrates decreases. A trained individual uses a greater percentage of fat than an untrained person does at the same workload” (Position of the ADA…p.512)

For simplicity sake we can conclude that 50% of the aerobic exercise will use CHO and 90% of the AnM will use CHO. So for an hour of exercise (30 min walking @ 4mph and 30 min intense resistance training) a person (female, 160lbs) will likely burn a total of 400 calories (182 cal and 218 cal, respectively,(http://www.webmd.com/diet/healthtool-fitness-calorie-counter).

So 50% of 182 = 91 calories and 90% of 218 = 196 calories for a total of calories that would likely need to be supplied by CHO as 287 calories, divide that by 4 = 72 grams of CHO

So based on these calculations, the person would need 72 grams of CHO to fuel this hour workout. However, the following data actually shows that 60grams per hour may be the maximum amount of CHO used per hour.

“The general consensus in the scientific literature is the body can oxidize 1 – 1.1 gram of carbohydrate per minute or about 60 grams per hour” (Krieger, p.8)

Here is what I posted earlier for a fictional, although very likely, client regarding a lower CHO diet

-Female
-Age: 40
-Weight; 160lbs
-Height; 5-5
-BMI: 27
-Goal: lose 20lbs

Total Energy Expenditure (TEE) = 2,274

Because weight (fat) loss is her main goal, her calorie intake should be reduced. The usual recommendation is to reduce calorie intake by 500 calories a day

The result of the reduction would be1,774 cal/day to induce fat loss

Protein intake based on 1.5g/kg = 110g = 440 calories = 25%
Fat intake @ 30% of calories = 58g = 523 calories
Carb intake @ 45% would account for the remainder of calories (811) = 202 g

Carbs intake = 202g, carbs used for the workout 72g

One more scenario for this client using a protein intake of 2g/kg/day, a potentially useful amount during a weight loss phase

Protein @ 2g/kg = 146g = 584 calories = 33%
Fat @ 30% = 58g = 523 calories
Carb intake @ 38% would account for the balance of calories (667) = 167 grams

Carb intake = 167g, carbs used for the workout 72g

Based on how the body makes energy for daily activities and exercise it is very likely that there is enough CHO to fuel the workout and fuel certain tissues that require CHO as the source for energy (ATP) production. Now all of this has been a theoretical case, based on basic biochemistry/physiology. What would be nice is to have some studies that have addressed the exercise and lower CHO intake question. Well, lucky for us, there are a number of studies that have done just that. We can see if the theoretical assumptions actually pan out.

The following studies use participants that are similar to our typical client.

Kerksick, C et al (2009). Effects of a popular exercise and weight loss program on weight loss, body composition, energy expenditure and health in obese women. Nutrition & Metabolism; 6:23.

“Methods: Participants were assigned to either a no exercise + no diet control (CON), a no diet + exercise group (ND), or one of four diet + exercise groups (presented as kcals; % carbohydrate: protein: fat): 1) a high energy, high carbohydrate, low protein diet (HED) [2,600; 55:15:30%], 2) a very low carbohydrate, high protein diet (VLCHP) [1,200 kcals; 7:63:30%], 3) a low carbohydrate, moderate protein diet (LCMP) [1,200 kcals; 20:50:30%] and 4) a high carbohydrate, low protein diet (HCLP) [1,200 kcals; 55:15:30%]. Participants in exercise groups (all but CON) performed a pneumatic resistance-based, circuit training program under supervision three times per week.” (p.3)

Interesting is the fact that they 3 of the diets were only eating 1,200 cal/day. The overall carb intake for the 3 diets where all relatively low;

VLCHP: 21 grams/day
LCMP: 60 grams/day
HCLP: 165 grams/day

“Cardiovascular and Muscular Fitness Changes

At baseline and after 14 weeks of following the diet and exercise programs, all participants completed maximal strength and muscular endurance assessments (Table 3). As expected, exercise training significantly increased relative peak oxygen uptake in VLCHP (P < 0.001), LCMP (P < 0.01) and HCLP (P < 0.001) while mean reductions in resting heart rate (-3.3 ± 16.5%; P = 0.01), systolic blood pressure (-2.8 ± 12.5%; P = 0.02), mean arterial pressure (-3.4 ± 10%) and rate pressure product (-5.8 ± 20%) occurred in these groups (data not shown). No significant group × time interaction effect was found for bench press (P = 0.44) or leg press 1 RM (P = 0.38), although those groups that participated in the exercise program did achieve significant increases (P < 0.05–0.001) in relative bench press and leg press 1 RM while CON did not experience changes in either bench press (P = 0.59) or leg press 1 RM (P = 0.54), respectively. No significant differences were observed among those groups that exercised for 14 weeks suggesting that all dietary regimens equally impacted adaptations to exercise training.” (p.8, emphasis added)

“Conclusion

In summary, results of this study indicate that combining a diet that restricts caloric intake in combination with a resistance-based circuit exercise program stimulates the greatest amount of weight loss and improvements in measures of body composition (e.g. waist circumference, DXA, etc.). When carbohydrate is replaced with protein while keeping fat intake at recommended levels (VLCHP and LCMP), larger decreases in waist circumference, body mass, fat mass and fat free mass when compared to a diet that has a higher proportion of carbohydrate (HCLP) in addition to greater decreases in fasting insulin levels… These findings suggest that replacing carbohydrate with protein can be an effective strategy to improve body composition and reduce cardiovascular disease markers while participating in a resistance-based circuit exercise program in sedentary overweight women. (pp.13-14, emphasis added)

Another recent study

Brinkwork, G. et al (2009). Effects of a Low Carbohydrate Weight Loss Diet on Exercise Capacity and Tolerance in Obese Subjects. Obesity; 17

Before getting into the specifics of this study and the conclusions, I am posting some of the author’s introduction as they give a good overview of the low CHO and exercise situation.

“However, concern surrounds the potential for LC diets to deplete muscle and liver glycogen stores (6,7), leading to symptomatic side-effects of tiredness, weakness, or fatigue (8,9). These effects may reduce muscle performance, increase muscle fatigue, and adversely affect physical function and exercise tolerance that may compromise an individual’s capacity to adhere to an exercise regime and reducing the usefulness of LC diets as part of a comprehensive weight loss program. However, the effect of an energy reduced, LC diet on exercise capacity and physical performance in sedentary, obese individuals has been poorly studied.

Early studies showed that maximal aerobic capacity ( O2max) was not impaired in obese patients following very low energy ( 3.5 MJ/day), carbohydrate restricted, ketogenic diets of relatively short duration (between 4 and 6 weeks) (10,11,12). However, effects on the capacity to perform submaximal aerobic exercise to exhaustion are equivocal, with enhancements (11), impairments (10), or no effect (13,14) being reported. The discrepant findings may reflect differences in several important aspects of study design, including the type and intensity of aerobic exercise investigated and varying macronutrient contents of the dietary interventions. These previous studies (10,11,12,13) were also limited by small sample sizes, in some cases lacked an appropriate control group (11,12), the use of relatively short intervention periods, and very low energy intakes ( 3.5 MJ/day) whereas moderate dietary restriction (4.2–6.2 MJ/day) is recommended for weight management (4,5). Therefore, the data presently available do not allow for conclusive interpretation of the chronic effects of an LC dietary pattern on the ability to undertake concurrent exercise as part of a comprehensive weight loss program in sedentary obese individuals, indicating the need for further research to substantiate previous findings.

In addition to aerobic fitness, muscle strength is important for maintaining physical function and is an independent predictor of all-cause mortality (3), but the effects of LC diets on muscle strength in obese subjects is poorly understood.” (p1916)

“The aim of this study was to compare the effects of a moderate energy restricted, LC diet with an isocaloric high carbohydrate, low fat (HC) diet on aerobic exercise capacity, muscle strength, and metabolic adaptations to exercise in a large group of sedentary, overweight, and obese subjects.” (p.1917)

“The planned macronutrient profiles of the dietary interventions were: LC, 35% of energy as protein, 61% as fat, 4% as carbohydrate; HC, 24% of energy as protein, 30% as fat, and 46% as carbohydrate. The diets were designed to be isocaloric with a moderate energy restriction of ~30% of energy (providing ~6,000 kJ for women and ~7,000 kJ for men) for 8 weeks.” (p.1918)

LC diet with only 4% CHO provided about 14 or 17 grams of CHO/day (women/men respectively)

HC diet with 46% CHO provided about 165 or 192 grams of CHO/day (women/men respectively)

“In the present study, no differences were found in the effects of isocaloric LC and HC weight loss diets on exercise function or perceptions of fatigue and exertion in a group of overweight and obese subjects. Diet composition altered fuel partitioning during exercise, with an increase in fat oxidation during submaximal aerobic exercise in the LC group.” (p.1920, emphasis added)

Conclusion

“In conclusion the current data suggest that in untrained, overweight individuals, the consumption of an LC weight loss diet for 8 weeks, does not adversely affect physical function or exercise tolerance compared with an HC diet. This suggests that, at least over the short-term, an LC weight loss diet is unlikely to limit an individual’s ability or desire to participate in concomitant exercise which is unequivocally recognized as an important adjunct to diet for obesity treatment. Indeed, metabolic adaptations occur that elicit greater fat oxidation during submaximal exercise” (p.1922).

Now this study used a very low CHO intake, much lower than a 30-40% intake, but still it did not find any detrimental effects on exercise ability or general energy.

One more study for now, but there are many others.

Brehm, B et al (2005). The Role of Energy Expenditure in the Differential Weight Loss in Obese Women on Low-Fat and Low-Carbohydrate Diets. J Clin Endocrinol Metab; 90

“Nutrient intake

Subjects randomized to the low-fat (n = 20) and the low-carbohydrate (n = 20) groups reported similar energy intake at the initiation of the diets, 2176 ± 118 kcal and 2166 ± 128 kcal (9111 ± 494 and 9069 ± 536 kJ), respectively, per day, with comparable distributions of macronutrients (Figs. 1⇓ and 2⇓). During the first 2-month phase of the study, subjects complied with their assigned diets as reflected on their 3-d food records. At 2 months, both diet groups reported similar decreases in energy intake of approximately 850 kcal (3559 kJ) per day compared with baseline. Although energy intake in the two groups was similar in the low-fat and low-carbohydrate groups (1339 ± 72 and 1288 ± 104 kcal/d, respectively; 5606 ± 301 vs. 5393 ± 435 kJ/d, respectively; Fig. 1⇓), the proportion of carbohydrate, protein, and fat consumed differed dramatically. Compared with baseline, the low-carbohydrate group decreased their carbohydrate intake from 48 to 15% of total energy and increased their fat intake from 36 to 57% of total energy at 2 months. In the low-fat group, the distribution of macronutrients as a percentage of total energy was relatively unchanged from baseline to 2 months (Fig. 2⇓). At 2 months, the low-carbohydrate group consumed significantly less carbohydrate, vitamin C, and fiber and significantly more total fat, saturated fat, monounsaturated fat, polyunsaturated fat, and cholesterol than the low-fat group (P < 0.05 for all comparisons; data not shown). At 4 months, the two groups still differed significantly for most of these measures but continued to report similar levels of energy intake (low-fat, 1422 ± 73 kcal/d, and low-carbohydrate, 1531 ± 102 kcal/d; low-fat, 5954 ± 306 kJ/d, and low-carbohydrate, 6410 ± 427 kJ/d; Fig. 2⇓).” (p.1477).

For clarity, the subjects ingested about 1,300 calories a day and the low CHO diet had about 15% CHO intake and the high CHO group had about 55% CHO intake

“Physical activity.

Mean pedometer readings for the low-fat group and the low-carbohydrate group were similar at baseline, 6786 ± 811 and 6327 ± 686 steps per day, respectively. Physical activity as estimated by pedometer readings did not change significantly over time or between groups (P < 0.9992; Fig. 4⇓). These data indicate that both groups maintained their baseline level of physical activity, as instructed at the initiation of the study.” (p.1477)

“Weight and body composition

Body weight and body fat in the low-fat and low-carbohydrate groups were similar at baseline (Table 1⇑). The women in the low-carbohydrate group lost an average of 6.69 ± 0.50 kg after 2 months and 9.79 ± 0.71 kg after 4 months of diet. Women following the low-fat diet lost 4.79 ± 0.58 kg and 6.14 ± 0.91 kg at two and four months, respectively (Fig. 3⇓). Both fat mass and fat-free mass decreased significantly in the two groups over the course of the trial (P < 0.001; Table 2⇓). However, fat mass decreased significantly more in the low-carbohydrate group compared with the low-fat group at 4 months (P < 0.001). There were no significant changes in bone mineral content noted in either diet group over the course of the study.” (p.1477)

“Blood pressure and plasma lipids

Blood pressure and plasma lipids were normal at the outset of the study. Significant time effects (P < 0.05) were noted, indicating small improvements in systolic blood pressure, total cholesterol, triglycerides, and HDL-cholesterol over the 4 months (Table 4⇓). Differences between the groups were not detected in total cholesterol, LDL-cholesterol, and triglycerides at the 2- or 4-month assessments. However, similar to the findings of other researchers (6), HDL-cholesterol increased significantly more in the low-carbohydrate group compared with the low-fat group at 2 months and 4 months (P < 0.001).” (p.1479)

The participants were in the very low CHO group were able to maintain the same amount of activity as the high CHO group. But, as highlighted above, the low CHO lost more fat mass, there were no negative effects on lipids and, in fact, the low CHO group, had a greater increase in HDL than the high CHO group.

What about athletes?

Even in athletes there is the potential for low CHO, high fat diets to produce high levels of exercise capacity. I don’t think they produce better results than high CHO diets, they are certainly not ergogenic, but the difference between a high fat and high CHO diet can be minimal. My point with this; if athletes can perform at a very high level with a low CHO diet then it is likely that our typical client can function very well on a lower CHO diet. To be clear, I do think that a high CHO diet is likely the best type of diets for most athletes as pointed out in a number of recent reviews (Erlrnbusch et al; Krieder et al; Position of the ADA…; ). But, the evidence is not completely definitive as highlighted in a recent meta-analysis on the subject.

Effect of High-Fat or High-Carbohydrate Diets on Endurance Exercise: A Meta-Analysis

“…a conclusive endorsement of a high-carbohydrate diet based on the literature is difficult to make…” (Erlrnbusch et al, p.1)

For those of you interested in this topic I would recommend reading the paper mentioned above as well as the Burke et al; Peters et al, Pendergast et al, and Phinney papers. But for fun, here is one recent study on the subject (Case & Haub);

Higher-protein diets do not hinder athletic perform in male fighters (2010)

Design

US Army soldiers (n=13, age=24±4yr, weight=75±13kg, body fat=14±7%) in the Combatives training program were recruited for this study. Prior to the start of the 6-week training program participants were prescribed one of three diets: PRO (40% carbohydrate, 30% protein, 30% fat), CHO (65% carbohydrate, 15% protein, 20% fat) and control (no dietary restrictions). Pre-test and post-test assessments of vertical jump height, explosive leg power index (LPI), 600m shuttle and 1.5 mile run were completed during the first and last week of the 6-week program.

Results

Control group consumed 16.49±4.8 MJ daily, 41±10% carbohydrates, 23±2% protein and 33±9% fat. PRO consumed 8.34±2.2 MJ, 36±10% carbohydrates, 30±10% protein and 35±8% fat. CHO group consumed 14.54± 6.9 MJ, 58±10% carbohydrates, 17±2% protein and 26±10% fat. Control group significantly decreased their 1.5 mile time, significantly increased highest power factor and significantly increased VO2max. There were no significant differences in the changes in performance variables between groups, except for the LPI. The CHO had a significantly different change in the average power factor and highest power factor compared to the control group, but not compared to the PRO group.

Two main points; First the low CHO diet was 40% CHO, 30% PRO, and 30% FAT and second, there was NO significant differences between the low CHO and high CHO groups.

A final line of evidence to support the view that a low CHO will support the ability to exercise and have energy comes from cultures that typically eat a low CHO diet. Two well know cultures are the Inuit in Canada and Alaska, and the Masai tribe of Africa. The Inuit typically eat a very low CHO, high fat diet and are able to function very well physically, not to mention that they are typically very healthy (Phinney). The Masai tribe of Africa often eat a lower CHO diet, in particular

“At approximately 14 years old, Masai men are inducted into the warrior class, and are called Muran. For the next 15-20 years, tradition dictates that they eat a diet composed exclusively of cow’s milk, meat and blood. Milk is the primary food. Masai cows are not like wimpy American cows, however. Their milk contains almost twice the fat of American cows, more protein, more cholesterol and less lactose. Thus, Muran eat an estimated 3,000 calories per day, 2/3 of which comes from fat.” (Guyenet)

The Masai are very active and a recent paper on the topic stated;

“The most conspicuous finding for the Masai was the extremely high energy expenditure, corresponding to 2565 kcal/day over basal requirements” (Mbalilaki, J et al; p.121)

When worldwide hunter-gather societies have been studied the “percentages of total energy from macronutrients would be 19-35% for protein, 22-40% for carbohydrate, and 28-58% for fat” (Cordain et al; p.689). The authors conclude;

“Anthropological and medical studies of hunter-gatherer societies indicate that these people were relatively free of many of the chronic degenerative diseases and disease symptoms that plague modern societies and that this freedom from disease was attributable in part to their diet. Therefore, macronutrient characteristics of hunter-gatherer diets may provide insight into potentially therapeutic dietary recommendations for contemporary populations” (Cordain et al p.691).

Again, the point here is to highlight the fact that a lower CHO diet can and does have the ability to support plenty of exercise and general vigor.

Conclusion

The fact is skeletal muscle as well as our vital organs are mostly fueled by fats for 95%+ of the time for most people including our typical clients. CHO are useful for higher exercise intensities often producing the best outcomes. However, there is enough evidence that a high level of exercise intensity can be achieved with a very low CHO intake. To be clear, I am not suggesting that a high CHO diet is inherently unhealthy or should not be followed by some people. But, it is not the only way to fuel the body.

Finally, there is no quality evidence that lower CHO diets will cause a decrease in exercise capacity for the typical person doing 3 to 5 hours of exercise a week. Therefore, the use of this argument to oppose the use of lower CHO diets, which have the ability to cause significant improvements in many metabolic aberrations, typically more so than high CHO diets, is without merit. The argument that a high CHO intake is necessary to fuel daily muscle function and exercise ability is not supported by the current evidence.

References;

Brehm, B et al (2005). The Role of Energy Expenditure in the Differential Weight Loss in Obese Women on Low-Fat and Low-Carbohydrate Diets. J Clin Endocrinol Metab; 90

Brinkwork, G. et al. (2009). Effects of a Low Carbohydrate Weight Loss Diet on Exercise Capacity and Tolerance in Obese Subjects. Obesity; 17

Burke, L. & Kiens, B. (2006). “Fat adaptation” for athletic performance: the nail in the coffin? J Apply Physiol; 100

Case, J. & Haub, M. (2010). Higher-protein diets do not hinder athletic perform in male fighters. J Inter Society Sports Nutr; 7 (suppl 1): P4

Cordain, L. et al (2000). Plant-animal substance ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. Am J Clin Nutr; 71

El Bacha, T., et al. (2010). Dynamic Adaptation of Nutrient Utilization in Humans. Nature Education 3(9):8

Erlrnbush, M. et al (2005). Effect of High-Fat or High-Carbohydrate Diets on Endurance Exercise: A Meta-Analysis. Inter J Sport Nutr Exerc Metab; 15(1).

Kerksick, C. et al (2009). Effects of a popular exercise and weight loss program on weight loss, body composition, energy expenditure and health in obese women. Nutrition & Metabolism; 6:23.

Kreider, R. et al (2010). ISSN exercise & sport nutrition review: research & recommendations. J Inter Society Sports Nutr; 7:7

Guyenet, S. (2008, June 11). Masai & Atherosclerosis. Retrieved from http://wholehealthsource.blogspot.com/2008/06/masai-and-atherosclerosis.html

Mbalilaki, J et al (2010). Daily energy expenditure and cardiovascular risk in Masai, rural and urban Bantu Tanzanians. Br J Sports Med; 44: 121-126.

Pendergast, D. et al (2000). A Perspective on Fat Intake in Athletes. J Amer Coll Nutr; 19(3).

Peters, J. et al (2004). Metabolic aspects of low carbohydrate diets and exercise. Nutrition & Metabolism; 1:7.

Phinney, S. (2004). Ketogenic diets and physical performance. Nutrition & Metabolism; 1:2

Position of the American Dietetic Association, Dietitians of Canada, and the American College of Sports Medicine: Nutrition and Athletic Performance (2009). J Amer Diet Assoc; 109(3)

Powers, S. et al (2007). Exercise physiology. Boston. McGraw Hill.

Saks, V. et al (2006). Molecular system bioenergetics: regulation of substrate supply in response to heart energy demands. J Physiol 577.3: 769–777

Scrapple – It’s just so damn tasty.

2012-01-15T15:45:17Z

Growing up in Lehigh Valley area of Pennsylvania exposed me to cool things that other parts of the country have never heard of, like quoits and Yuengling Lager. Quoits is a lawn game. It isn’t horseshoes. Don’t say that it is or you’ll likely get a 1 lbs rubber washer hurled at you. There are variations, but ours goes like this:

This is a popular outdoor variation played principally in and around Pennsylvania, USA. This game uses two one-pound rubber quoits per player, which are pitched at a short metal pin mounted on a heavy 24x24x1 inch slab of slate.

Players take turns throwing a quoit at the pin. The quoit nearest the pin gets one point. If one player has two quoits nearer the pin than either of his opponent’s quoits, he gets two points. A quoit that encircles the pin (called a ringer) gets three points. If all four quoits are ringers, the player who threw the last ringer wins the game; otherwise, the first player to make 21 points wins the game.

From Wikipedia: http://en.wikipedia.org/wiki/Quoits#Slate-board_quoits

Here’s an action shot taken by Bruce Winter: (I swear it’s coincidence I’m wearing a SPEED shirt)

Perfect form, including Yuengling Lager in non-throwing hand

Okay, enough about all that. Here’s what I really wanted to talk about – Scrapple. It’s a food and you might guess what some of its ingredients are. Yup, scraps. The scrapple I’m cooking in the pictures below is from Schreiner’s Sausage here in Phoenix and it’s pretty good stuff. The best scrapple I’ve had, by far, is from R&R Provisions. The difference? Buckwheat vs cornmeal. Buckwheat wins every time.

Scrapple is typically sliced from a loaf and fried until it’s brown on the edges. You’ll see that in my kitchen slices weren’t exactly achieved and the reason for this is that it was frozen before I made it. Once thawed, scrapple has a tendency to fall apart when being sliced. It still browned up nicely so all was not lost. Here it is being fried with 3 eggs in bacon grease. The bacon was also from Schreiner’s and was the best I’ve had since being in the Lehigh Valley. The first sign of great bacon is that it’s being sliced to your liking right in front of you.

3 eggs and Schreiner's Scrapple

The ingredients of Schreiner’s scrapple are as follows: pork snouts, pork tongue, corn meal, bacon ends, ham ends, water, onions, salt, spices, sugar, sodium nitrite. I have no idea what the calorie or macronutrient content of this meal is, nor do I care. Here it is on the plate with bacon and eggs:

Breakfast on a Saturday Morning

I’m no food artist, that’s for sure. In fact my pictures probably make all this look completely unappetizing. Good, more for me.

Quick, Light, Low-Carb Meal – RO*TEL Rescue

2012-01-11T15:11:00Z

I bought some thinly sliced steak over the weekend from the “manager’s special” section of the butcher counter. It is, after all, my favorite section of the store. For various reasons I didn’t get around to using the steak until last night and when I opened the package it smelled kind of funky. There I stood, in my girlfriend’s kitchen with no steak and a pretty empty kitchen.

RO*TEL, tuna and cheese to the rescue!

1 can RO*TEL diced tomatoes and jalepenos

1 can tuna

1 oz colby jack cheese

microwave for 1 minute

Calories – 305
Protein – 33g
Carbs – 15g (12 net)
Fat – 10g

When I sat down to eat, my girlfriend said “that looks disgusting.” I just shrugged and started shoveling. It was heavenly.

RO*TEL Rescue

Out of My Inbox: Vitamins

2012-01-06T23:34:27Z

Sometimes we get email from our coaching clients that could help the rest of you out. So, with their permission, they get put on the blog for all to enjoy. This one happens to be about how a multivitamin fits into a paleo-style, SPEED enhanced, fat loss plan.

Chris writes:

On a different note, I wanted to ask you guys if you had read any of the stuff from gnolls.org. (http://www.gnolls.org/2304/why-are-we-hungry-part-1-what-is-hunger-liking-vs-wanting-satiation-vs-satiety/) Very intriguing stuff. In the series on hunger, satiety, satiation, etc. in particular he mentioned this study he sites…http://www.nutraingredients.com/Research/Multivitamins-may-help-weight-loss-in-obese-women and also in part IV of his series on Why are we hungry, he talks about this inability of obese and formerly obese to garner nutrition from their energy stores.

All in all it looks like a very well researched set of articles, and it makes me wonder if I should be taking some sort of a multi-vitamin/mineral supplement. Then if so, how the heck do you know which one? I do take 2,000iu daily of D3, most days, as I have been tested and show low stores of that, and it was prescribed in 10,000iu a week dosage. But beyond that I am hesitant to start playing with supplements in general because of the importance of the interplay of nutrients, and the general lack of understanding (mine and the science community’s) about the details of nutrients, and the possibility that if they really do what they say could I make matters worse. I have IBD, in remission right now, don’t wanna rock the boat!

I write back:

J. Stanton’s series on hunger is something I’ll admit I’ve only skimmed, mostly because its conclusions don’t seem to disagree with our recommendations: Eat a whole food, low carb/medium protein/high fat diet, take a multi-vitamin and all the mental trickery found in our Psych and Environment chapters to help control over-eating.

The multivitamin study referenced in the series is interesting, with supplement users losing an average of about 8 lbs over 26 weeks with no dietary modification. (Li 2010) However, in a study when multivitamin use is paired with dietary restriction, no additional weight loss effect is seen. (Major 2008) This means that the vitamin alone in Li did seem to have some effect on weight loss, but good ol’ dietary restriction unsurprisingly trumps this effect. Why did the vitamin in the Li study show a positive effect? The researchers state “possibly through increased energy expenditure and fat oxidation.” With the astounding dietary control (food frequency questionnaire) – yes, that’s sarcasm – we can’t really say. Maybe the vitamin caused the subjects to eat less. Yes, their RQ dropped significantly (P < .01 – yawn), but that also would happen with calorie restriction. I’m not willing to draw any firm conclusions about why the multivitamin caused a slow decrease in body weight in the Li study.

As to whether or not you should take a multivitamin, that’s entirely your choice, of course. Many consider a multivitamin like nutritional insurance. The evidence for multivitamin use having a positive effect on our health is slim, which I don’t find surprising. Having more of a good thing you already have enough of might not be beneficial, know what I mean? The evidence for multivitamin use causing adverse effects is equally slim, so no harm no foul there. The fact that supplementation with certain antioxidants (vitamin A, beta carotene, vitamin E) may increase mortality leads me to think supplementing with a variety of vitamins and minerals may be more beneficial than going bananas with just a few. (Bjelakovic 2008)

Of course, there is always the possibility that you are deficient in a certain vitamin, at which point you might garner a benefit from supplementation with that vitamin alone or from a multi which includes that specific vitamin. This might be one reason vitamin trials show no benefit; they give a generic multi to a large population and nothing happens on average. What if you’re the one person who was deficient in something important and the multi was sufficient to bring you up to acceptable levels? You don’t care about the average at that point. Of course, you’d never know anyway because you can’t know that you would have suffered. There is no placebo you.

Two things popped into my head as I was mulling this over: First, I’m not sure what we all expect to find one day while studying large populations with vitamin use. “Hey, we gave these people a vitamin and nobody ever died! We’re all living forever!!!” Second, some of the vitamin trials base their outcomes on how people feel or function. That’s great, but doesn’t point to whether the multi is causing cancer to grow more rapidly at the same time. Heroine makes you feel pretty good, right? Third, because I can’t count, if you spend $20/month on a multivitamin, you’ll spend $7,200 over 20 years. Is that worth it? Does the “nutritional insurance” a multi may provide justify its cost? Since you’re already spending money on food, could you just make your best effort to get a wide array of vitamins and minerals through diet? Will I just keep asking questions? Is this starting to remind of you a commercial lead-in on Batman? BAM! KAPOW! SPLOOSH!

References:

Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C. Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases (Review). Cochrane Collaboration. 2008; Issue 3

Li Y, Wang C, Zhu K, Feng RN, Sun CH. Effects of multivitamin and mineral supplementation on adiposity, energy expenditure and lipid profiles in obese Chinese women. Int J Obes. 2010;34:1070–1077

Major GC, Doucet E, Jacqmain M, St-Onge M, Bouchard C, Tremblay A. Multivitamin and dietary supplements, body weight and appetite: results from a cross-sectional and a randomized double-blind placebo-controlled study. Br J Nutr 2008; 99: 1157–1167.

In Case Your Hatred of Ancel Keys Keeps You Up At Night

2012-01-04T02:55:31Z

Denise Minger has a nice little (that’s not true) summary (not true either) of Ancel Keys’ early work and some arguments that have been levied against him and it.

It’s long, but the take home message I’ll quote here:

Correlation isn’t causation. Correlation isn’t causation. Correlation isn’t causation. Correlation isn’t causation. Correlation isn’t causation. Correlation isn’t causation. Correlation isn’t causation. Correlation isn’t causation. Correlation isn’t causation. Correlation isn’t causation. Correlation isn’t causation. Correlation isn’t causation. Correlation isn’t a cucumber.

Have fun reading!

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2012-01-04T14:35:04Z

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