If you believe that weight loss is dependent solely on your caloric balance, then you would have lauded the latest study by George Bray, et. al., fresh off the presses at JAMA – get it while you can!: http://jama.ama-assn.org/content/307/1/47.full (PDF here)

Most mainstream media outlets are taking this study as confirmation of the “calories in/calories out” theory – that weight gain/loss is totally dependent on the difference between the calories you eat and the calories you expend each day – and it’s hard to imagine why they wouldn’t.  Let’s take a quick look at the parameters of the study:

• 25 people were overfed for 8 weeks to the tune of roughly 40% over their baseline consumption.  Meaning, they ate an extra 954 calories each day.
• There were 3 groups: A 6% (low) protein group; a 15% (normal) protein group; and a 25% (high) protein group.
• All groups gained different amounts of weight, but similar amounts of body fat (about 7.7lbs in each group).

Seems pretty cut and dried – despite the amount of protein the groups ate, they ended up gaining the same amount of weight.  Let’s pack up for home, right?  Wrong. Let’s take a closer look at the data.

One necessary aside: The subjects were overfed for 8 weeks in a metabolic ward (Warning: PDF), which is about as a controlled, lab-rat environment that you can put people participating in a nutrition study in.  For those of you unaware of what metabolic ward testing entails, it’s like sleep-a-way camp: There are organized times for data collection and feeding; all you can eat is what the research facility provides; and you get to enjoy all the fun of being cooped up in a “controlled environment“.  What this implies is that we can assume the data in this study is legit.  No misreporting, no sneaking in a Snickers bar after lights out, no bad food surveys or faulty recall (”What did I have for breakfast yesterday?”) – all their food was measured and prepared in the metabolic unit kitchen.

I’ll save you a whole lot of reading and reprint the Table from the study:

As reported, all three groups had nearly the same amount of gain in Fat Mass (3.66kg, 3.45kg, and 3.44kg) at the end of the study.  But look at the differences between groups.  The low-protein group lost Lean Mass (read: muscle) and correspondingly impaired their metabolisms, but not by much (see Resting Energy Expenditure, -86.1 kJ/day, which is about 21 calories, if you’re keeping score) whereas the normal and high-protein groups both raised their lean body mass (2.87kg and 3.16kg; 6.3lbs and 7lbs respectively).   So even though all groups were consistently overfed by about 1000 calories a day, very different outcomes resulted (and personally I wouldn’t be too happy if I were in the low-protein arm.  Gaining fat, losing muscle, and lowering my metabolism are not high priorities on my health watch-list).  Since all groups were overeating by the same amount (roughly 954 calories), then according to the calories in/calories out model, shouldn’t they have gained the same amount of weight?  If all the surplus calories they ate went to fat storage, then where the heck did all that new muscle come from in the normal and high protein groups?

But wait, there’s more!  Check out line item Non-Resting Energy Expenditure.  The normal protein nearly doubled their expenditure from a baseline level of 1979 kJ/day (that’s 473 cal/day) to 3275 kJ/day (1979+1296; that’s 782 cal/day).  The high protein group also increased their expenditure, by 181 cal/day.  The low protein group decided it would be better to kick back a little, raising expenditure by a paltry 59 cal/day (maybe they were tired from the loss of muscle).  Now, one wonders what could possibly account for such wild variance.  Well, the table has an answer for you: Physical Activity.  Although the lead researcher has stated that there was no formalized exercise during the 10-12 week trial, it’s well established that energy expenditure can increase significantly through NEAT (warning: PDF). If the calories in/calories out model held true, wouldn’t the normal and high protein groups have gained less fat than the low protein group, since all 3 groups were eating roughly the same amount of calories, but were burning significantly different amounts of calories?

Is there any way to reconcile the fact that all of the groups gained roughly the same amount of fat? Aside from calories, was there anything else held constant in all three groups?  Quoted from the study:

Absolute carbohydrate intake was kept constant throughout the study.

All groups consumed 41% of their calories from carbs – that’s about about 250 grams of carbs per day.  And they were exactly the kinds of carbs you’d expect; foods that drive up insulin and promote fat storage:

The eating plans that Bray and his colleagues used included food you’d find in the typical American diet: eggs, bacon, biscuits or cereal for breakfast, for instance; tuna salad, turkey sandwiches and chips for lunch; pasta, rice, pork chops or casserole for dinner, accompanied by salads and fruit; and plenty of baked goods, candy and other processed sweets for snacks and dessert.

So, mystery solved: You could posit that the reason the three groups all gained the same amount of fat is that they were all eating enough carbohydrate to cause high levels of insulin, which would promote fat storage, particularly if you were, say, eating an extra thousand calories a day (which all three groups were).  This would neatly explain why the higher protein groups gained muscle while the low protein group lost muscle (and slowed down their metabolisms in the process) and would explain the thorny issue of different energy expenditure (and consequently, different caloric balances) between the three groups.

So we arrive at three conclusions based on Bray’s research:

1) Low intake of protein while overeating seems to have compound negative effects.  It slows metabolism and results in loss of lean tissue.  So despite what your latest cleanse guru told you, there is a minimum amount of protein intake necessary to “run the ship”, and that minimum is probably higher than the official government recommendations.

2) It’s unlikely that caloric balance was responsible for the similar fat gain between the low, normal, and high protein groups, since the three groups exhibited big differences in expenditure.  In other words, the math doesn’t work out.  What’s more likely is that similarities in the diet composition (the carb intake, in other words) caused the fat gains to be equal across the groups.

and

3) Always check the data.  It’ll tell you what the real story is.

Single progression is the gradual addition of weights over time.  Yep – that’s about as sexy as it gets.  In a single progression model, you select a fixed number of reps (or time) – say, 5 reps (or 60 seconds).  Select a weight.  Lift it.  If you can successfully lift that weight for the target number of reps or the target time, then add a little bit of weight to the bar.  You can use percentages (1% per workout, for example) or fixed weight increments (2.5 pounds), but what’s important is the gradual increase of weight over time.

What happens when you can’t increase the weight?  You get stuck at 175 lbs for 4 reps, and you can’t seem to get that fifth one? First, determine if you’re really stuck.  If you’re not making progress weight-wise after three consecutive workouts, then on the fourth, it’s time to decrease the weights slightly.  In an exercise involving multiple muscle groups (e.g., squat, pulldown, deadlift), take the weight down by 20%*.  Then work your way back up.  What should happen is that you’ll squeak a little bit past your previous plateau point, then reach a higher plateau.  At that point, you’d repeat the process (known as “cycling” the weights).

Single progression is the simplest method of improving strength and muscle.  Combining single progression and cycling will probably net you as much strength and muscle gain as you can get, provided you use a sensible program.

Single progression is largely poo-pooed by the strength sub-culture as being too simplistic:  “Only beginners use it”, “It doesn’t work”,”You plateau too quickly”, and the like.  Try it.  Worry about the plateaus when they come.

P.S. – Quitting because the weights feel too heavy to lift isn’t plateauing.

*It doesn’t have to be 20%.  I will typically lower clients’ weights by 10% first and see if that does the trick.

If you’re like most people, when it comes to exercise, you use the terms “program” and “workout” interchangeably.  But they are completely different things.

Individual workouts are important, as they’re the building blocks upon which real results are made.  But what ultimately gets you the results you want is not a single monumental workout, but a series of consistently done workouts, arranged intelligently, will. And that intelligent arrangement of workouts?  That’s a program.

Here’s a missive to you:  Stop thinking of your fitness journey in terms of individual workouts.  No, I’m not asking you to stop giving it your all during each and every exercise bout.  What I’m asking you to do is abandon the search for the miracle workout that will transform you from a milquetoast to brick house.  Get on a solid program.  Embrace single progression (the steady but gradual addition of weights over a period of time) and settle in for the long haul.  Commit to improving your lifts a pound at a time, consistently, over the course of , say, a year.  Then get back to me.

“Spend most of your time on squats; spend pretty much your balance of time on bench presses. Every now and then see what you can do on the deadlift.”  – Bradley J. Steiner.

Sounds about right to me.  How about you?  What are your thoughts?  Post to comments.

From CNN.com.

It should surprise no one in the health or medical field that the diabetes drug Avandia is linked to an increased risk of heart attacks (at least, not after Steven Nissen’s 2007 study of Avandia).  Unfortunately, for most doctors, Plan B is to simply prescribe another drug.

“Don’t worry about the Avandia scare, Mrs. Jones; here, just take Actos or Glynase instead.”

Until some “rogue independent researcher” publishes a meta-analysis showing those drugs will kill you as well, that is.

There is an alternative solution to this problem.  Beware: It’ll require some critical thinking on your part.

1) Understand and acknowledge the role insulin resistance has in diabetes.

2) Understand which foods and foodstuffs raise insulin levels.

3) Avoid eating said foods and foodstuffs.

4) Move around a little bit.  It’d be better if you exercised. It’d be even better if you strength trained.

There you have it.  No 342 page report or dubious drug prescriptions required.

Every so often I’ll get in a client who was a jock of some sort in a former life.  Either they played ball in high school or college, or they had some experience on a professional or semi-professional level.  But the story is nearly the same in every case: Through accumulated or acute injury or life circumstance, they stopped playing and gained a ton of weight.

Being a former fit person, they attack the weights with unusual vigor.  The second workout finds them considerably more gun-shy than the first, due to crippling soreness.  “What happened?”, they ask.  “I used to lift twice as much as this.  I used to work out 20 times harder and still made every late-night party on campus.”

My typical advice:  Forget “used to.”  But this doesn’t just follow for former athletes.  This applies to trainees across the board.

It applies to you if you obsess about the size of jeans you wore back in high school (that, sadly, you’ll never fit in again).

It applies to you if you stubbornly chase a poundage you used to lift last year, back before you sustained injuries to both your shoulders and left wrist.

It applies to you if you complain that every time you used to get a little too fat all you needed to do was run a couple of times a week without changing your diet.

Maybe that’s the way things used to be.  But they aren’t that way now.

“Used to” is self-limiting because it keeps you from the difficult but necessary work of addressing reality.  Maybe things aren’t as they used to be, but that doesn’t change the fact that right now you’re not where you want to be.  Worse, getting stuck in “used to” blinds you to the actions that you need to take right now, when the rules of the game have changed.

Forget “used to.”  Focus on “need to”, right now.

I recently sustained injuries to both my shoulders, probably as a result of overuse and chronic trauma (apparently, throwing someone on top of you instead of over you via Morote Seoi hurts your shoulders).  Over the past couple of months, I’ve managed to nurse at least one shoulder back to health, with the other well on the way.

Some of my classmates and clients are amazed that I’ve been able to do this without going to physical therapy.  But it’s really not a mystery.  What did I do?  Liberal application of ice, heat, and meaningful (read: heavy enough to challenge) exercise for the support muscles of the shoulder.

When you sustain an injury, the first impulse you have is to rest it.  You’d avoid movements that hurt in attempts to give the injury enough time to get better, hoping that things will work out at some point.  Well, while it’s important to manage pain, decrease swelling, and allow enough time for your body to repair itself, the reality is that you can’t avoid usage of your joints (at least, not unless you plan on consigning yourself to complete bed rest).

Problem #1: By avoiding usage of the joint, you impair the joint’s function.

Problem #2: By impairing the joint’s function, you allow the joint to get weaker.

Problem #3:  A weaker joint is less capable.  So you end up either using it less (see problem #1) or continuing on as if nothing happened and risking further damage to the joint (see problem #2).

In physical therapy literature, this sequence is referred to as “the downward spiral of pain” – by limiting function as a response to pain, a patient gets worse and worse until he’s virtually non-functionally.  Interestingly enough, the only way to interrupt this cycle is to perform corrective exercise to strengthen the muscles surrounding the injury site.

The true role of PT in rehab is to strengthen the muscles that support the damaged joint. All the bells and whistles that are done to you as a patient (modalities) serve to decrease inflammation and pain, either pre-emptively (so you can exercise) or post-emptively (so as to control additional pain and swelling resulting from exercising the injured area).  You can see the sense in this – without icing a swollen joint, for example, you’d have very little active motion in the joint (not to mention tons of pain when you do try to move it).  Bring down the swelling, turn the volume down on the pain, and you can meaningfully exercise.

Unfortunately, this isn’t what most people go to PT for.  They’re in it for the modalities: A little stim to ease lower back pain; an ice massage for patellofemoral syndrome; some wet heat for a sore neck.  There’s nothing wrong in seeking relief from pain.  What ultimately matters, however, is obtaining pain relief for the long-term, and that’s only going to happen if you progressively improve strength.

Am I saying to eschew the services of a professional when you’re hurt?  To take matters into your own hands and treat yourself?  No.  But what I hope to point out (to those of you who are engaged in some sort of rehab program, anyway) is that the yardstick for improvement is still the same – if you’re not getting stronger, you’re not improving.  Do what’s necessary to make it possible for you to strengthen the injured area via corrective exercise, but remember that the corrective exercise is the keystone your recovery hinges upon.

One prominent  and controversial question in strength training circles: Is training strength and demonstrating strength the same thing or different things?  In other words, what’s the best way to build strength – by “demonstrating” it through heavy maximal lifts, explosive movements, and plain-ol’ ‘lifting stuff‘, or by ‘training it’ through more measured and precise means?

This is a huge waste of mental energy (better directed towards actually exercising).

To clarify what I mean, take a look at my foster kids’ handstand form:

For my convenience’s sake (l.-r.): Max, Shirley, Santa

Who would you say is the strongest?  Why?

Note the following observations:

• Santa has near perfect form (it’s only imperfect because she’d been holding the handstand for a minute waiting for her siblings to get into their handstands).  It’s safe to say she’s not only well-practiced at handstands, she’s strong for her size.
• Upper body wise, Shirley is the weakest in the upper body – you can see her arms beginning to give way to the weight of her torso and legs (alas, her leg falling forward makes this obvious).
• Max fell over a split second after this picture was taken.  And yet, he’d be the first one of the three I’d enlist to help me carry a Murphy bed up three flights of stairs.

Of course, it’s a trick question.  You can probably see what I’m getting at here.  Strength can be demonstrated.  But in order to be demonstrated:

1) You have to be able to demonstrate it (skill).

2) You need to have strength to demonstrate.

Pick a different skill (say, carrying a Murphy bed up three flights of stairs with a partner) and the evaluation changes.  Now, it’s clear who’s “strongest” – the only one capable of performing the task at all.

All this is mental piffle.  For actual exercise purposes, here’s what it boils down to:

The muscular/joint system has one global job: To move your body through space.  There is a near-infinite number of potential movements in which your body can be propelled (an infinite number of “skills”).  To effect the greatest change, choose those movements that are most global in scope (that effectively work the most muscle) and most applicable to your goals (after all,  a ballet dancer and your bocce ball-playing grandfather probably have markedly differing fitness goals) and apply measured, precise doses of exercise to improve the capacity of that muscle.

So it doesn’t matter if you lift a sandbag or a chrome-plated machine handle.  Work hard at increasing your ability; make it so that you can do more today than you could yesterday or yesteryear.  You’ll never master every skill known to man.  But you can make yourself a better version of yourself by mastering a few skills.  You even get to choose which skills they are.

Last night my foster son picked my brain regarding diabetes (his birth father is a Type 2 diabetic). While the entire car-ride conversation was ripe fodder for a blog post, what I’m going to recount here is our discussion on fatty liver, fructose, and diabetes.

What is fatty liver?

Fatty liver is an excess buildup of fat cells in your liver. When the liver becomes too fatty, inflammation occurs and liver function is compromised.

What does fatty liver have to do with diabetes?

They both are diseases of sugar metabolism. In Type 2 diabetes, your cells are insulin-resistant – they no longer respond to insulin’s attempts to pull sugar out of your bloodstream. In development of fatty liver, chronic high intake of fructose causes fatty deposits to develop in the liver.

Fructose?

Fructose is a type of sugar found in fruit (and in high fructose corn syrup, but we’ll get to this later). Chemically, it’s a simple sugar just like glucose but is metabolized differently. Glucose (and other sugars) are metabolized like this (courtesy University of Miami):

Fructose, however, follows a much shorter route:

Fructose—->Liver—->Fatty Acids

Ok, I’m dramatically oversimplifying the fructose pathway, but I want you to understand the “big picture” concept here. What happens with excess consumption of all carbohydrates is that they get repackaged as fat through a process called de novo lipogenesis.   However, there’s a limit to how much and how quickly sugar gets repackaged as fat – a rate-limiting step.

An analogy:  Imagine a FedEx shipping plant with a huge fleet of trucks and piles and piles of boxes to be shipped.  How quickly can you ship the packages?  The number of workers packing the trucks would be your rate-limiting step.  The boxes can only be delivered as quickly as the trucks are filled.  It doesn’t matter how large a fleet you have to deliver boxes with, without workers to pack them, the packages can only drip-drip-drip out of the plant.

The rate of sugar metabolism (see above complicated diagram) is bottlenecked by the regulatory enzyme phosphofructokinase.  Consume a ton of glucose, and what will eventually happen is that insulin rates rise, causing levels of leptin to rise, which limits your appetite.  No appetite = you stop flooding the system with sugar (but not before the damage is done).

Not so with fructose.  Fructose, that lucky dog, gets to skip that step.  Instead of having to be shuttled via the insulin pathway, fructose directly enters the liver and gets metabolized without this rate-limiting step.  So if you consume a lot of excess fructose, your liver synthesizes a lot of triglyceride (fat).  In fact, there’s practically no limit since insulin isn’t involved and thus your appetite won’t be blunted (recent research indicates that fructose effectively “shuts off” your appetite regulation).  So what happens?  Fatty deposits begin to show up in the liver (undelivered “packages” sitting around in the plant warehouse) – and over time, inflammation and liver cell damage occurs.  Continue this over time, and you’ve got the fertile breeding grounds for obesity and diabetes.

So does that mean if I eat fruit I’ll get diabetes?

It’s unlikely.  Remember, we’re talking about excess consumption of fructose.  Eat a bunch of fresh fruit, and you’re likely to consume 15-20 grams of fructose, tops.  But with industrialization of food and the addition of high fructose corn syrup as the primary sweetener used in food manufacturing, daily intake of fructose is nearly 4 times higher.  Think about all the possible sources of fructose – it’s in just about every sweetened drink you can think of: soda; fruit juices, iced tea, etc.  Moreover, sucrose (table sugar) is 50% fructose.  All that adds up to a considerable intake.

What it boils down to is that it’s easy to develop fatty liver (and diabetes) if you’re indiscriminate about what you eat and drink.  Avoid sweetened drinks high in high fructose corn syrup, stay away from sugar, and you’ll likely be fine.

Let’s offer a Cliffs Notes version of the above:

This great diagram from the American Liver Foundation (via msnbc.com) says it all:

As a general rule, sugar is bad for you.  But fructose is particularly bad.  So disregard what the food companies tell you and stay away.

Chris points us to an interesting study involving circadian rhythm and weight gain (to be fair, Melissa sent it to me first, but she doesn’t have a blog).  In the study, nocturnal rats fed during what would have been their sleeping hours gained more weight than rats fed during their waking hours, despite the same overall intake and energy expenditure.

(BTW, if any of you have the full text of the study, might I request a copy?  Pretty please?)

What’s interesting to me is not just the physiological implications of the study (that there might be some unique mechanism that causes animals to store fat more effectively during their snoozing hours), but the statements the obesity experts were quoted as saying:

“How or why a person gains weight is very complicated, but it is clearly not just calories in and calories out,” said Fred Turek, from the Northwestern’s Center for Sleep and Circadian Biology, where the research took place.  “Better timing of meals could be a critical element in slowing the ever-increasing incidence of obesity.”

and

Tam Fry, from the National Obesity Forum, agreed. He said: “It is groundbreaking. It really gets you thinking why this has not been done before.  It could be very dramatic if it affects whether you are going to get fat or not.”

Are you kidding me?

“Better timing of meals?”

“Groundbreaking?”

“Affects whether you are going to get fat or not?”

The study looked at rats that were eating during their sleeping hours.  While I don’t doubt there are some overfat folks eating during the hours they should be sleeping, I highly doubt that 64% of Americans are waking up in the middle of the night and chowing down.  Or perhaps they’re suggesting we’re all operating on schedules that run counter to our normal Circadian rhythms? And these guys are supposed to be experts?

What these folks do is what clients and trainees often do – they lose the forest for the trees.  It’s all too easy to get bogged down in the myriad details of the (admittedly) complex picture of fat loss and lose sight of the one or two most important things which, if done consistently, would yield you 80% or more of the results you’re looking for.  Believe me, if you’re having trouble losing weight, it isn’t because you should be on vampire hours.

There’s nothing wrong with seeking new information or looking to add to your understanding.  But figure out how it falls into the larger picture.