Good Reads

apparently I cant escape the knee thing...it's officially everywhere
 
Why women shouldn't run
Thanks for the article Steve. Made sense to me because my wife just keeps having pain when she runs. new shoes helped for a while but now she is having more problems. I found another article by a female runner on the subject
 
Comment: Obesity is a disorder of excess fat accumulation, not overeating,
and not sedentary behaviour.
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Then how does fat accumulate?

Comment: Consuming excess calories does not cause us to grow fatter any
more than it causes a child to grow taller. Expending more energy
than we consume does not lead to long-term weight loss; it leads to
hunger.

Response: Consuming excess calories routinely produces obesity, and consuming
fewer calories than your body needs produces weight loss.
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Ok clearly the coffee hasn't kicked in...

Must read again
 
The comments are from Thaubes or whatever his stupid name is.

The responses are from the reviewer.
 
Here's a great blog entry by Lyle, and it seems like it's going to be a long series... so if I don't post all of them be sure to follow along in his blog found at if you're interested.

Set points, Settling points, and Bodyweight regulation Part 1


Following up on the , I want to discuss quickly some of the physiology behind diet failures. This is a topic that I discuss in detail in nearly all of my recent books and I’m not going to spend endless time on it here (trying to eventually get back to the psychological factors behind diet failures).

A long standing debate in the world of obesity research revolves around the idea that bodyweight (or perhaps body fat) is regulated. What does that mean exactly?

Think about your thermostat (yes, this is the example I always use): you set it to keep the house at 80 degrees and it continually senses the temperature (via a thermometer). If the temperature goes above 80 degrees, the air conditioning comes on; if it drops below 80, the heat comes on. This is a regulated system. Your cruise control in the car works the same way: you set the speed you want to maintain and it either gives more or less gas to the engine in an attempt to maintain that level.

For some 50 odd years, it’s been thought that bodyweight/bodyfat are regulated similarly; that is the body is attempting to maintain some set level (called the set point) and is adjusting things like appetite, behavior, movement, etc. to do so.

A great deal of animal research supports this model: starve a rat and its metabolic rate slows, it moves around less (conserving energy), it’s appetite goes up such that when you give it free access to food again it will eat until it reaches its starting weight at which point things go back to normal. The same occurs when you fatten it up, metabolic rate goes up, activity goes up, appetite/hunger go down and it rapidly returns to its starting weight when you stop force feeding it. The rat is, somehow, trying to maintain weight at a set level.

Quick note: and this ties into that a few weeks back: exposed to certain types of diets (in rat lingo, this is called a cafeteria diet and consists of calorically dense tasty foods), most rats will readily maintain a weight that is above their set point (when exposed to a more typical rat diet). That is, the tastiness of the food can overcome any homeostatic attempts to prevent weight gain. This is important and something I’ll come back to later in this series.

Some research has found a similar effect in humans although the studies tend to be very mixed on this (I’ll address why in a later blog post): when you diet down a human being, often you see metabolic rate decreasing far more than you’d expect based on the loss of body weight alone. That is, based on the weight loss, say you expected metabolic rate to drop by 200 calories; but when you measure it it really drops by 300. That extra 100 calories is more than predicted and suggests that the body is ‘adapting’ to the weight loss in an attempt to not only slow further fat loss but also to get bodyweight/body fat back up when food becomes available again.

There are other adaptations, folks often decrease their activity levels (conserving energy), fat burning goes down and fat storage goes up, appetite often goes up so that people eat more when food is made available. In common parlance, this is often referred to as the ’starvation response’ and, yes, there is something to it. Unfortunately, it’s basically the price that has to be paid for losing body fat to any significant level. People talk constantly about avoiding the starvation response and things of that nature but the only way to avoid it completely is to never lose fat.

In any case, perhaps the classic study in this regards is the Minnesota semi-starvation study, a 6 month study undertaken during the mid 20th century where a number of lean male war objectors were placed on 50% of their maintenance calories for the entire time while forced to engage in quite a bit of daily activity (5-6 miles walking per day).

In that study, after reaching the lower limits of human body fat levels (about 5%) and showing a host of adaptations (including an obsession with food), the men showed uncontrolled hunger when food was made available and rapidly ate themselves back up beyond their initial body fat level.

This has been termed (a technical word that means overeating). Of course, it’s crucial to realize just how lean these men got; the response to less severe diets or fat loss is exactly that: less severe. A lot of this also depends on the nature of the intervention (e.g. type of diet) and the population studied. Initial body fat percentage plays a huge role here for reasons you’ll learn about in future blog posts.

Unlike in rats however, in humans, overfeeding doesn’t have nearly as reliable an impact in terms of increasing metabolic rate and it looks increasingly like any bodyweight regulation system present in humans is : that is it protects against weight loss far more so than it protects against weight gain.

Put a bit differently and most realize this on some level: for most it’s far harder to lose weight than it is to gain it.

The reasons for this are a bit obscure but it’s thought that since humans never had any real evolutionary pressure to not get fat (e.g. we had no real predators and, during evolution, few could have gotten or stayed fat for extended periods), the body never had to develop defenses against weight gain. In contrast, starving to death was a very real reality in our evolutionary past and the body developed a number of ways of ‘defending’ against weight loss.

Moved into modern times (where food is readily available and activity levels continue to drop), this is a bad bad thing.

For completeness, I should note that there are exceptions, some people appear to show a pronounced response to overfeeding which is now being called (non-exercise activity thermogenesis) or SPA (spontaneous physical activity); some folks ramp these up to high levels when subjected to increased caloric intakes, burning off the excess calories instead of storing them as fat.

These are the people for whom gaining weight is often difficult: invariably when they try to increase food intake, not only do they subconciously start moving around more (burning off the excess calories), their hunger shuts off. You probably had one of these guys in your high school, the one who was always fidgeting and bouncing his leg and all of that; it turns out that the caloric expenditure from that type of activity adds up significantly over a day.

Hunger also seems to shut off more rapidly in these folks as well. They are often the folks who also claim “I eat a ton and can’t gain weight” but when you look at their food intake, they either aren’t eating much at all or they eat a single big meal and get so full that they don’t eat much else for the rest of the day (or next day).

Unfortunately, NEAT seems to be quite genetic and researchers still haven’t really figured out the exact causes or if this can be applied to help in any practical way. It probably has to do with not only the various hormones involved in all of this (which I’ll discuss in a later blog post) but how the brain responds to them.

In any case, all of the above supports the basic idea of a setpoint in humans: human metabolic rate, etc. clearly adapts (and does so more than weight loss alone would predict) to caloric restriction and weight/fat loss.

Unfortunately, it doesn’t appear to adapt nearly as well to overfeeding and weight gain.

Even more unfortunately, this isn’t the end of the story and determining exactly what sets the setpoint or whether or not it can change in the long-term is an area of continuing debate. Most of what I’ve seen suggests that, if setpoint can change, it only goes up. I’ve seen nothing to suggest that it ever comes back down, even over years of maintaining a lowered body weight.

Additionally, not everyone agrees with the idea of a . And that’s the topic for the next post.
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Excellent bit on IR from Lyle McD

I received this email at my bodyrecomp adress and the sender said he didn't mind (and sort of wanted me to) if I adressed it in the forum so here goes.

***


I was extremely shocked to see you writing that during dieting, it would be actually GOOD to be insulin resistant. You argued that Clen/ephedrin actually cause insulin resistance (IR), sort of implying that that's one of the mechanisms via which they work whereas I always thought that they worked DESPITE that effect.
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The thing to realize is what insulin resistance actually implies. Insulin is a storage hormone, stimulating nutrient uptake in many tissues (including liver, muscle, and fat cells). This is especially true for glucose.

So what happens when fat cells are insulin resistant? It means that insulin can't inhibit lipolysis (fat breakdown). Nor can it activate nutrient storage. This is part of why severely insulin resistannt individuals get increased blood levels of glucose, fatty acids and cholesterol, insulin is unable to either limit release from the cell or stimulate uptake. Since muscle is full (see below), they either get stored in inappropriate places (beta-cells of the liver) or float around in the bloodstream.

What about in muscle? An insulin resistant muscle cell is unable to uptake glucose. Without glucose to use for fuel, the cell has to find an alternative source. In this case, that alternative source is fatty acids.

So when fat cell insulin resistance is high, fatty acids are easier to mobilze. When muscle cell insulin resistance is high, glucose isn't used for fuel and fatty acids are. So in a caloric deficit, this means you use more fat for fuel b/c they are coming out of fat cells more easily and muscle is usingg them preferentially for fuel.

This is part of how things like clen, EC and GH work. By mobilizing fatty acids at a high rate and making the muscle cell insulin resistant, muscle has to forego glucose for fuel and use the mobilized fatty acids instead (note: this also spares protein in a carb insufficient state). A recent study on GH found that the fatty acid mobilizing effect of GH was THE key to its protein sparing effects: block the increase in fatty acids and you get the same amount of protein loss.

On that note, you should realize that studies examining predisoposition to obesity (for example, in the Pima indians) find that insulin sensitivity predicts weight gain and insulin resistance predicts weight loss or stability.

Insulin resistance develops with obesity and can be thought of as a way for the body trying to prevent further weight gain. Note that this is different in growing individuals such as children or pregnant women. More below.

Well I always thought IR was extremely bad in all situations (gaining weight, losing weight, fat guy, skinny guy).
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To be even more accurate to what I wrote above you need to differentiate muscle insulin resistance from whole body insulin resistance. In general, the body will develop insulin resistance in this order:

liver then muscle then fat cell

There are some weird genetic exceptions but the above would be a typical progression with diet induced insulin resistance.

Now, when muscle becomes insulin resistant, this shuttles more calories to the fat cells preferentially. In that sense, localized (muscular) insulin resistance causes more fat to be gained for a given caloric load. It's negative calorie partitioning. Note that this isn't only local, there are central (brain effects) controlling these processes as well.

This makes perfect sense: if the muscle is plenty full of nutrients and there is still a surplus, they should get pushed into storage as effectively as possible. So the msucle stops accepting nutrients and the rest go to the fat cells. The best way to prevent this is not to overeat and to deplete muscular fuel stores with exercise. In modern society, we do both: eat too much and don't exercise often enough. So muscle gets full of nutrients, becomes insulin resistant, and the excess calroeis go to fat cells post haste.

But as fat cells get filled up, problems start. The fat cell starts releasing a lot of hormones such as leptin, TNf-alpha, resistin (may only be relevant in rats) and others that prevent further nutrient storage (you can also get an increase in fat cell number). Now you're developing full body insulin resistance.

Once full body insulin resistance develops (with obesity), this acts to LIMIT further weight gain. Note that insulin resistance also means higher basal levels of insulin (there are also higher levlels of leptin as you get this fat). Both insulin and leptin *should* act to signal the brain to make you stop eating but the system isn't very sensitive to that. Additionally, it serves to push nutrients towards oxidation when you diet for the reasons above.

It's interesting to note that individuals without fat cells (lipodystrophy), which mimicks full body insulin resistance are protected against weight gain. First their muscles and liver fill up with nutrients, then they develop severe hyperglycemia, hypercholesterolemia and all the rest. Individuals with severe genetic insulin resistance have the same effect occur: they don't gain weight. They get a bunch of other health problems if you overfeed them but the severe genetic insulin resistance makes it so tnutrients can't be stored in their cells.

Also consider that insulin sensitivity improves as you lose weight. And the single time you are most prone to gain wight is at the end of the diet: when you are most insulin SENSITIVE.

As above, insulin sensitivity predicts weight gain, insulin resistance (full body) weight/fat loss.

Basically insulin resistance isn't always BAD. Quite in fact, it can be adaptive.

Now, in the context of excess calories/carbs and no activity (i.e. weight gain), insulin resistance is a bad thing to have. If you have muscular insulin resistance, more calories go to fat cells. If you have ful lbody insulin resistance, excess calories either sit in the bloodsream or get stored in the wrong spots, causing cell death.

Actually, if the goal is muscle gain with limited fat gain, it'd be wonderful to have fat cells resistant to nutrient storage and locally increase muscular insulin sensitivity. This would cause preferential nutrient partitioning to muscle. The question is how to do it. I have an idea but it's not fully fleshed out. For fatter individuals who begin an exercise program, this occurs naturally which is (IMO) one reason they can lose fat and gain muscle at the same time. The exercise preferentially improves muscular insulin sensitivity, the fat cells are releasing fat like nobody's business and you get calorie partitioning until the point that it all starts to balance out.

When you're dieting and not eating enough carbs (by definition, on a diet, carbs are reduced), insulin resistance is adaptive. By making muscle rely on fatty acids for fuel, glucose is spared for the brain and other tissues which require it.

Note that most of the current insulin sensitizing medications (especially the TZD drugs) cause further weight gain. Obesity docs don't care becuse they just want to see blood glucose and the rest levels go down.

As above, whole body insulin resistance develops in an effort to both limit further fat/weight gain and ensure that the body burns the fat off (sparing muscle) when you diet. This would have been adaptive in the context of our evolutionary dieting pattern, it's maladptive in our current environment.

I've been avoiding caffeine like the plague since I read it causes IR - should I now start getting in massive amounts again? And acquire ephedrine which I haven't used in years?
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ONLY if you're going to diet.

Should I also NOT get my fish oil in?
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Fish oils are interesting, in rats at least (I have yet to see this studied in humans and I don't consider the rat research conclusive except for the fact taht humans demonstrate similar end effects) they decrease fat cell insulin sensitivity and improve muscle cell insulin sensitivity. They also improve fat oxidation and a host of other stuff but the net results is nutrient partitioning aways fomr fat cells and towards muscle cells.

And should I NOT try to acquire Glugophage from the doc? If I should try to get a prescription for something, what would you recommend?? . I am 29yrs old, 5' 11", weight around 300 lbs with fat% around 32%.
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Riht before his death, Dan Duchaine commented that adding insulin sensitizersr to a diet seemed to increase muscle loss.

However, if you're at the point medically that you need to control blood glucose, you need to listen to your doctor, not me. Getting your diet and exercise program in order and losing bodyfat should be your primary goal as that alone will improve insulin sensitivity.

Lyle
 
same convo cont'd from above

Lyle, a heartfelt thanks for your time and detailed answer. I learned SO MUCH from this! First of all, interesting to note the concept of "full body IR" and how it actually makes 100% beautiful sense from evolutionary perspective - it's hard to hunt if you're fat as a house.
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Looking over what I wrote, I dropped the ball on one part. I mentioned our evolutionary eating pattern but didn't go into much detail. In most cultures, it was common to have great food availability for part of the year and poor or no food availability the rest (winter). So you would fatten up and get good and insulin resistant when food was available. But during the winter times, the goal was to survive in the face of nearly no food (and certainly not much carbohydrate, fruits and naturally occuring carbs not being present during the cold winter months). Hence the adaptations I talked about: preferential shuttling of stored bodyfat to muscle for energy, sparing of glucose for the brain.

In modern times, we lack the famine each year so people get and stay fat and insulin resistant. And that's when it becomes maladatptive and unhealthy as hell. A good paper on this is



I also forgot to mention the fact that obese individuals (who are usually insulin resistant) lose more fat and less muscle when they diet compared to lean and all of this is surely the reason (there are others such as hormones: leptin and the rest). They mobilize fat more effectively and since muscle isn't using glucose well, it gets burned. The more fat you can burn, the less your body needs to use glucose (and by extension muscle protein) for fuel.

Are you Lyle by the way aware of the study of fish oil done on humans which showed that by substituting 6 grams of "normal" fat with 6 grams of fish oil in an otherwise identical diet produced almost a pound's fat loss in 3 weeks? That's at least what they claimed in T-mag a while back, I can dig you guys the link if you want to see it.
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It's to the point that I don't even bother reading new fish oil research. They do everything and that's only mild hyperbole.

Seriously, if I didn't know that the research was there and had read a summary of their effects, I'd think someone was bullshitting me.

So did I get this right? I should start again the good old EC stack and keep the fish oil and only take glucophage or something else if the doc thinks it's a medical necessity? IR (both in muscles and fat) is good in my case IF I am dieting (ie negative calorie balance/reduced carbs), because of the increased fat burning and decreased use of glucose. If and when I have a refeed day(s) during my diet I should do everything in my power to decrease my IR and improve the IS of my muscles so I should not use EC on those days but mayby double the dosage of Fish oil?
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Fish oils don't really work that acutely, they are long term (since they affect membrane permeability and gene expression). Doubling them over a day or two refeed won't do much. But you got the general concept just fine.

During refeeds, high insulin sensitivity (again, ideally you want local muscular insulin sensitivity moreso than whole body), dieting, insulin resistance to shuttle fat calories from fat cells to muscle for burning.

Lyle
 
Here's a short but sweet Q&A from Cressey in his blog:
 
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