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  #1   ^
Old Mon, Sep-09-13, 16:32
zmktwzrd zmktwzrd is offline
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Default Insulin's Role in Fat Storage Questioned

Some researchers question if insulin plays as big a role in fat storage as many members of the low-carb community think.....

"Is it time to stop blaming insulin for "fat storage"?

Thoughts?

Last edited by zmktwzrd : Mon, Sep-09-13 at 18:33.
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  #2   ^
Old Mon, Sep-09-13, 16:37
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WereBear WereBear is offline
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Good luck with that one.
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  #3   ^
Old Mon, Sep-09-13, 19:06
M Levac M Levac is offline
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I wrote a long post, but I gave up. Too many ad hominems. So I'll start again but try to stick to the topic as best I can.
Quote:
Because of this well-known role of insulin, one of the more puzzling explanations offered by some – including a few respected scientists and medical professionals — for weight gain is that elevated insulin is to blame because of its involvement in “fat storage”. In addition, they argue that the reason why a diet lower in carbohydrates works for weight loss is because of reduced levels of the peptide hormone.

It’s an easy conclusion to make. The logic goes that carbohydrates through their stimulation of insulin are fattening beyond their contribution of energy as kilocalories. It doesn’t matter how much you eat, so long as you avoid carbs to lose weight.

It can't be puzzling if it's an easy conclusion to make.
Quote:
Another growing belief floating mainly around fitness circles is that it’s best to forego foods containing carbs when heading to the gym. It’s for fear that the carbs’ action on insulin will squash fat burning stimulated by exercise. Then again, some low-carb proponents have also argued, physical activity as a means to expend energy for weight management is pointless altogether. Again, carbs are really all that matter because of their action on insulin.

There's various reasons for this belief. The main reason is the effect of carbs on insulin sensitivity. As glycogen is depleted, cells becomes insulin sensitive. As cells are insulin sensitive, blood insulin level drops. As insulin level drops, its effect on fat tissue is thus less. Eating carbs would replete glycogen, causing cells to shut down insulin receptors, in turn causing blood insulin level to rise again, on top of the insulin spike we get just from eating carbs, with the ultimate greater effect on fat tissue. Makes sense to me.

Exercise makes us hungry, so we eat more. No exercise, less food intake, more weight lost. Also, since the goal is to lose weight, this means we're fat, and exercise is just harder to do when you're fat. Better to wait until we get leaner through low-carb, then do exercise at this point since it's now much easier. I see no problem with any of this.
Quote:
Where does all the extra energy from excess protein and fat go when overconsumed? And what about protein’s own effects in stimulating insulin or insulin’s role in promoting satiety? These questions are often overlooked or not easily answered by those that promote the “insulin is a fat storage hormone” proposition.

No, they are just overlooked by you, so you can make a point that we're not that smart. What extra energy are you talking about? As far as I know, low-carb blunts hunger, so we eat less. If anything, we undereat. So your argument of "when they are overconsumed" is a red herring just to make a point. But to please the audience, we have a few experiments of overeating on low-carb, the latest I found is this: http://www.dietdoctor.com/what-happ...on-an-lchf-diet

As he noted, his waist shrunk. So whatever excess he ate, most certainly did not go to belly fat. That should answer your red herring, Mr Science Writer.
Quote:
Out to help repair insulin’s reputation is obesity researcher Stephan Guyenet

I'll pretend I didn't read that bit.
Quote:
Exercise researcher John Ivy, Ph.D., of the University of Texas, is in agreement that insulin is an often-misunderstood hormone and also makes the point that insulin’s specific action following meals does not relate to long-term fat storage. “The most important thing is calories burned in a day,” he comments.

That's just not true. The nature of insulin does not change just because we're eating or we're fasting. To borrow a phrase from our CICO proponents, insulin is insulin is insulin. When insulin is high, the effect on fat tissue is the same regardless.
Quote:
As previously shared on this blog, Ivy emphasizes that understanding how to make the best use of insulin and carbohydrate can be critical for long-term weight management. The main reason is because of their support to muscle maintenance and growth. Ivy reminds that insulin’s role extends well beyond its action on promoting fatty acid synthesis. The hormone also both prevents protein breakdown and boosts protein synthesis in muscle. Although protein by itself promotes insulin’s release (again, often overlooked by low-carb proponents), carbohydrates can boost both these effects.

That's so true. The functions of insulin go well beyond promoting fatty acid synthesis. Let's see, from http://en.wikipedia.org/wiki/Insuli...ogical_effects:
Quote:
Physiological effects

The actions of insulin on the global human metabolism level include:

-Control of cellular intake of certain substances, most prominently glucose in muscle and adipose tissue (about two-thirds of body cells)
-Increase of DNA replication and protein synthesis via control of amino acid uptake
-Modification of the activity of numerous enzymes.

The actions of insulin (indirect and direct) on cells include:

-Increased glycogen synthesis – insulin forces storage of glucose in liver (and muscle) cells in the form of glycogen; lowered levels of insulin cause liver cells to convert glycogen to glucose and excrete it into the blood. This is the clinical action of insulin, which is directly useful in reducing high blood glucose levels as in diabetes.
-Increased lipid synthesis – insulin forces fat cells to take in blood lipids, which are converted to triglycerides; lack of insulin causes the reverse.[clarification needed (see talk)]
-Increased esterification of fatty acids – forces adipose tissue to make fats (i.e., triglycerides) from fatty acid esters; lack of insulin causes the reverse.
-Decreased proteolysis – decreasing the breakdown of protein
-Decreased lipolysis – forces reduction in conversion of fat cell lipid stores into blood fatty acids; lack of insulin causes the reverse.
-Decreased gluconeogenesis – decreases production of glucose from nonsugar substrates, primarily in the liver (the vast majority of endogenous insulin arriving at the liver never leaves the liver); lack of insulin causes glucose production from assorted substrates in the liver and elsewhere.
-Decreased autophagy - decreased level of degradation of damaged organelles. Postprandial levels inhibit autophagy completely.[30]
-Increased amino acid uptake – forces cells to absorb circulating amino acids; lack of insulin inhibits absorption.
-Increased potassium uptake – forces cells to absorb serum potassium; lack of insulin inhibits absorption. Insulin's increase in cellular potassium uptake lowers potassium levels in blood. This possibly occurs via insulin-induced translocation of the Na+/K+-ATPase to the surface of skeletal muscle cells.[31][32]
-Arterial muscle tone – forces arterial wall muscle to relax, increasing blood flow, especially in microarteries; lack of insulin reduces flow by allowing these muscles to contract.
-Increase in the secretion of hydrochloric acid by parietal cells in the stomach
-Decreased renal sodium excretion.

Bolded the pertinent parts. Let's analyze this stuff. Basically, fuel and protein. What happens to all fuels? They all get stored. Glycogenesis, lipogenesis. Their release is inhibited. Glycogenolysis, lipolysis. Sure, protein synthesis and proteolysis are affected, which suggests we'll end up with bigger muscles. But here's the problem. All cellular functions require fuel, and all the fuels are being stored and their release is being inhibited. Nothing left for normal functions, like protein synthesis. What we really end up with is emaciation of lean tissue, and hypertrophy of fat tissue, all due to fuel partitioning from the global actions of insulin. And I'm not even a science writer.

There's one bit in there that struck me. It's "decreased autophagy". I've read that word before. Chaperone-mediated autophagy. That's the recycling of glycated protein inside cells, due to the action of ketones. And this means there's a bit missing in the Wikipedia list of things insulin does: Inhibition of ketogenesis at the liver and other cells capable of it. Ya, insulin inhibits the recycling of glycated protein inside cells (through its inhibition of ketogenesis at the liver), protein which could otherwise be used elsewhere, but ultimately end up gunking up the works inside cells.
Quote:
Diabetes researcher Joseph Henson, Ph.D., of University of Leicester, affirms that physical activity’s powerful effects on promoting insulin sensitivity makes it the “first line” of defense for prevention and treatment of insulin resistance. But while perhaps timing nutrients for after exercise may be best, he says that just getting any activity is what counts most. “A single bout of exercise can increase insulin sensitivity for at least 16 hours post exercise in healthy people as well as people with type 2 diabetes,” Henson comments.

Ya, if you eat high-carb. But if you eat low-carb, low-carb is the first line of offense. As we restrict dietary carbohydrates, glycogen is depleted all the time, relatively speaking. This means all cells are insulin sensitive all the time. Exercise is just overkill at this point.
Quote:
On the other hand, the lack of activity, or general muscle contraction, Henson argues, can exacerbate insulin resistance and decrease insulin sensitivity, which are prerequisites for type 2 diabetes. Henson’s recent research suggests that probably more important than exercising regularly is simply avoiding staying sedentary for too long for cardiovascular health.

Ya, that's true. But the primary prerequisite of diabetes type 2 is hyperglycemia. And the primary effect of dietary carbohydrates is hyperglycemia. Did somebody say "puzzling" earlier?
Quote:
In a review paper last year, Westerterp-Plantega (along with colleagues Sofie Lemmens and Klaas Westerterp) wrote that controlled trials have shown that the answer is that it is the relatively higher protein of the diets including Atkins, South Beach Diet, Paleo, etc., and not the relatively lower carbohydrate content that has led to the success of these approaches for weight loss. The reason is that dietary protein acts on three “metabolic targets”: it increases satiety, stimulates energy expenditure, and spares fat-free muscle (helping to maintain resting energy expenditure).

How much more protein, exactly? The A-TO-Z study shows protein intake was the same in all diets tested. The bolded part, the same is true of dietary fat. It increases satiety due to its action on speed of digestion, stimulates energy expenditure due to its action on ketogenesis, and spares fat-free muscle due to its action on chaperone-mediated autophagy. Low-carb is inherently high-fat.
Quote:
Westerterp-Plantenga’s hypotheses are now supported further by a new study of which she was the lead author published earlier this year. The study compared two energy-restricted diets, one normal in protein (0.8g/kg/d) and one higher in protein (1.2g/kg/d) on 72 overweight and obese men and women. While both groups lost weight, as expected, the group that consumed more protein retained more muscle and had a higher resting metabolism (this was independent of physical activity).

Low-carb is typically ad libitum. In spite of unrestricted caloric intake, low-carb produces better weight loss. How can we explain this by testing energy-restricted diets? In another study we discussed here (I forget which one exactly), Eout was higher with low-carb than with high-carb, with protein intake presumably remaining constant. Even with the A-TO-Z study, which didn't measure Eout, we must conclude that Eout was higher on Atkins, because it produced the greatest weight loss.

Last edited by M Levac : Mon, Sep-09-13 at 19:12.
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  #4   ^
Old Mon, Sep-09-13, 19:29
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teaser teaser is offline
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Quote:
If not because of reduced insulin, how then does a lower-carb diet really work for weight loss? Professor of regulation of food intake Margriet Westerterp-Plantenga, Ph.D., of Maastricht University Medical Centre, suggests that the reason low-carb works has nothing to do with carbohydrates at all, but everything to do with protein and its role on energy balance.


Problem here, low carb isn't always higher protein. Sometimes it's the same protein, and carbs are replaced instead with fat.

Here's what we know; restrict carbohydrates, and a lot of people end up leaner. We can lay insulin aside for the moment. Maybe it's not what causes weight loss on low carb. But any theory of weight loss we have will be just that, theory; and secondary to the direct observation of reduced carbohydrates leading to weight loss.

Also "reason low-carb works" is loaded. What do we mean by "works?" Lowering triglycerides? That's from the reduced carbs. No question. Better blood sugar control? That's from the reduced carbs. No question. Protein has a role there, for some, slow source of glucose made from the protein. Increased HDL? Some of that's from the reduced carbs. Some of it's the benefit of increasing saturated fat in the diet.

Bodybuilding boards are full of people eating lots of protein. Sometimes that isn't enough. Some of them turn to low carb.

Lowered blood pressure?

I ate meat plus fruit for a while, inspired by Art Devaney's site. I probably ate it wrong. But high protein, high fruit. I didn't lose weight. My blood pressure was high. It sucked. It ain't just the high protein. Whatever it is, it ain't just that.

I don't think it's just the effects of carb on insulin at work. But it's not not the insulin, either.

It's hard to prove it's not the insulin.

Insulin injected into the brain can make rodents slim... so it's a slimming hormone. But insulin injected into the brain can also make 'em fat. Depends on how you go about it.

Various insulin mimetics can cause weight loss. But they aren't insulin. Fulfilling some functions of insulin, but not others, reducing the body's requirement for insulin--slimming.

Really too big a subject. The proper reply to this question would be a research paper in itself.

Quote:
carbohydrates through their stimulation of insulin are fattening beyond their contribution of energy as kilocalories.


What if we reword part of this?

Never mind insulin, lets say "Carbohydrates are not fattening beyond their contribution of energy as kilocalories." That is... the effect of carbs on bodyweight is unidimensional, having only to do with the calories they contain. This is an unsupportable statement. Or we can put insulin back in. "The fattening effect of carbohydrates does not involve insulin." Equally silly. The question is the extent of insulin's involvement, not whether it's involved.
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  #5   ^
Old Mon, Sep-09-13, 19:34
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teaser teaser is offline
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I should point out that leptin, ghrelin, growth hormone, adiponectin, glucagon--every hormone besides insulin, in short, involved in fat storage and appetite homeostasis--is also involved in the regulation of glucose. We have a choice of two major fuel depots to draw from--glycogen or fat. Of course regulation of glucose is involved in fat storage. It must be.
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  #6   ^
Old Mon, Sep-09-13, 19:35
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Quote:
Originally Posted by WereBear
Good luck with that one.


All respects, Martin--WereBear "wins" the thread.
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  #7   ^
Old Mon, Sep-09-13, 20:09
s-piper s-piper is offline
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Quote:
Originally Posted by M Levac

No, they are just overlooked by you, so you can make a point that we're not that smart. What extra energy are you talking about? As far as I know, low-carb blunts hunger, so we eat less. If anything, we undereat. So your argument of "when they are overconsumed" is a red herring just to make a point. But to please the audience, we have a few experiments of overeating on low-carb, the latest I found is this: http://www.dietdoctor.com/what-happ...on-an-lchf-diet


My favorite part of your post. Really more diet writers should internalize this message "Just because I overlooked it doesn't mean everyone has"

The thing about when protein and fat are over-consumed, I think, really depends on the person.
Most LCer women will tell you that calories do still matter, but, as you mentioned, LC food is more satisfying so you don't get hungry, and ketosis tends to blunt hunger/appetite so you don't want to overeat.
However, yeah there are also people (men and women) who can eat large amounts of calories and still gain weight if they keep their carbs very low.
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  #8   ^
Old Tue, Sep-10-13, 03:43
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WereBear WereBear is offline
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Quote:
Originally Posted by teaser
All respects, Martin--WereBear "wins" the thread.


Appreciated, but I just didn't have the patience for what M Levac did so well.

Because I knew it would be a whole bunch of idiocy just to try and support the conclusion that "it's not the carbs!"

But it is. It is so undeniably the carbs that watching so-called scientists jump through their own behinds is just too sickening to read.

If it is only the calories, then why does a fat fast work so well? Sure, come up with another hormone we can give to diabetics so they don't die; and explain how they get those fat deposits around the injection site if they don't rotate. Explain why diet regimens which are 700 calories of mostly sugar don't work!

They don't want it to be the insulin because they don't want it to be the carbohydrates.
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  #9   ^
Old Tue, Sep-10-13, 05:57
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teaser teaser is offline
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Yeah, Martin did good. But still, congratulations for having the wisdom to not want to get involved in what could easily turn into a total crapfest.


I think my biggest problem with Dr Guyunet isn't with the idea that reward/palatability etc. is involved with fat regulation. That's fine, there's room for all sorts of things to contribute to the problem--and for different people to have different underlying problems. (Though I suspect much of the problem with palatability is which foods are made more palatable--even with something like MSG, I'd bet effects on weight gain would be different using it to make doughnuts and potato chips taste good, then to make porkchops taste good, for example). But when you get away from the most direct observations possible--Joe went low carb. Joe lost twenty pounds. Joe got good blood pressure. Joe's body spent the next decade no longer trying to become obese, any time he stopped paying attention. Then there's danger of doing real damage. You can theorize that a diet of fatty pork chops, fried onions, and sour cream worked for Joe because of its obvious low palatability rather than some effect of carbohydrate restriction itself, and switch him to a diet of bland carbs, or add boring carbs to his diet, but you'd be risking his health doing that. This is why we can't just shrug and say "maybe it's not the carbs." Maybe it isn't. But the most direct observation is, Joe reduced carbs, Joe lost weight, Joe is healthier.

Ps in case it isn't obvious, I am that Joe.

Quote:
Where does all the extra energy from excess protein and fat go when overconsumed? And what about protein’s own effects in stimulating insulin or insulin’s role in promoting satiety? These questions are often overlooked or not easily answered by those that promote the “insulin is a fat storage hormone” proposition.


So, do we ignore Jimmy Moore's experiment with nutritional ketosis? Do we ignore Nora Gedgaudas, Ron Rosedale, Dr Bernstein, Drs. Phinney and Volek, Dr Kwasnieski, etc? Not to mention Dr Robert Atkins, for flipping sake--and accept that effects of protein in stimulating insulin haven't been considered as a possible factor working against fat loss, at least in some people? Because we do have anecdotal evidence, and some clinical evidence, that sometimes even protein reduction, once carbs have been reduced, is necessary and helpful for further fat loss. (Or at least helpful, leaving open the possibility that there are other things that might have worked).

Insulin's role in satiety is very often answered, and I think perfectly well. Taubes suggested early on that a mechanism was needed to counter insulin itself--we can't just get hungrier after a meal because of an increase in insulin, without limit. So we have a signal in the brain, that eventually works to shut down the effects of insulin to increase appetite throughout the body and in the brain itself. Obviously, this is necessary, or we'd all eat until we burst.

Unlike carefully administered central insulin, peripherally administered insulin seems to be fattening. It's staggering trying to understand why people who want to admit something as unnatural as injecting insulin directly into the brain think injections at other sites, or insulinomas, don't deserve to be included as evidence.

I think things get messy with insulin. While we're getting fat, insulin isn't necessarily elevated--we're insulin sensitive, because we're below our body fat potential, so it's easy for insulin to do it's job. Later, insulin is high, we're insulin resistant--and it's harder for us to get fat. Yes, the high insulin might be failing to make us fat (at least subcutaneous fat, visceral and liver fat is another story), but this isn't because insulin isn't fattening, it's because we're resistant to its effect. It's the insulin signalling that matters, not actual levels of insulin in the body.
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  #10   ^
Old Tue, Sep-10-13, 12:39
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ojoj ojoj is offline
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I always point out that during my weight loss phase, I was doing around 4000 calories a day, it was mainly made up of fat and protein - but I wasnt hungry, lost alot of ailments (IBS, arthritis, eczema...) and lost the weight....... and no I didnt exercise!

These days I dont know how many calories I consume...? I'll see if I can find an app and work out what I've eaten today. But it doesnt matter to me. I've lost the weight, I've gained back my health and alertness and I'm not climbing the walls with cravings for junk food - I personally dont care what the so called "experts" try to work out. But they need to do something about the obesity epidemic that coincided with the "fat is bad" campaign!

Jo xx
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  #11   ^
Old Tue, Sep-10-13, 16:53
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WereBear WereBear is offline
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Quote:
Originally Posted by ojoj
But they need to do something about the obesity epidemic that coincided with the "fat is bad" campaign!


They STILL have not taken responsibility for that!
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  #12   ^
Old Wed, Sep-11-13, 20:58
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mike_d mike_d is offline
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That's probably why an old USDA study found carbohydrates to be 6 times more fattening than either fats or proteins. Even though nutrition 'experts' like to parrot "well fat has 9 calories per gram ..."

I don't have a link for the study, ill keep looking ...
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  #13   ^
Old Thu, Sep-12-13, 04:16
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WereBear WereBear is offline
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Quote:
Originally Posted by mike_d
That's probably why an old USDA study found carbohydrates to be 6 times more fattening than either fats or proteins. Even though nutrition 'experts' like to parrot "well fat has 9 calories per gram ..."

I don't have a link for the study, ill keep looking ...


Sure enough, carnivorous animals never grow fat (consider wolves, jackals, birds of prey, crows, etc.). Herbivorous animals do not grow fat easily, at least until age has reduced them to a state of inactivity; but they fatten very quickly as soon as they begin to be fed on potatoes, grain, or any kind of flour. ... The second of the chief causes of obesity is the floury and starchy substances which man makes the prime ingredients of his daily nourishment. As we have said already, all animals that live on farinaceous food grow fat willy-nilly; and man is no exception to the universal law. Brillat-Savarin, Jean Anthelme, The Physiology of Taste

In 1825.
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  #14   ^
Old Thu, Sep-12-13, 08:15
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Seejay Seejay is offline
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I ran across this one from George Washington Carver where he talks about carbs as fat formers. In a bulletin about sweet potatoes, 1936.

Quote:
A glance at the table below will convince the most skeptical of its superiority over many of the standard foodstuffs.
Code:
AVERAGE COMPOSITION Food Material Protein or Muscle Builders Carbohydrates or Fat Formers Mangel Beet 1.4 per cent 26.4 per cent Turnip 1.1 per cent 11.4 per cent Rutabaga 1.2 per cent 9.3 per cent Carrot 1.1 per cent 9.0 per cent Parsnip 1.6 per cent 7.6 per cent Sweet Potato 1.5 per cent 7.6 per cent
We readily see that the potato contains practically as much muscle-building material as any, and more than double that of the fat formers.
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  #15   ^
Old Thu, Sep-12-13, 08:31
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wheeler wheeler is offline
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"And I'm not even a science writer," says Martin.

Oh yes, you are.
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