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  #16   ^
Old Fri, Mar-10-17, 17:19
WereBear's Avatar
WereBear WereBear is offline
Posts: 10,558
 
Plan: Epi-Paleo/IF
Stats: 220/161/150 Female 67
BF:
Progress: 84%
Location: USA
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I think the quote you started with is describing the Pit of Moderation. HFLC or LWHC will work (with, as you noticed, varying degrees of satiety) for weight loss.

The famous Rice diet was almost pure carbs (my pancreas is screaming just thinking about it) but for a hefty percentage of diabetics, it worked. But not for all.

That's why we are all about the N=1.
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  #17   ^
Old Fri, Mar-10-17, 19:50
rconn2 rconn2 is offline
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Posts: 7
 
Plan: none
Stats: 179/179/160 Male 70 inches
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Progress: 0%
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I plan on experimenting as an N=1... just bought a BG testing kit incl. one for cholesterol. Time to see what's what.

btw, I'm planning on trying the Fasting Mimicking Diet (FMD) the week of the 20th. And, taking readings. That should be interesting.
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  #18   ^
Old Fri, Mar-10-17, 22:46
mike_d's Avatar
mike_d mike_d is offline
Grease is the word!
Posts: 8,361
 
Plan: PSMF/IF
Stats: 236/181/180 Male 72 inches
BF:disappearing!
Progress: 98%
Location: Alamo city, Texas
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Not sure about FMD nutrient wise, but PSMF is designed to burn fat and spare muscle unlike plain water fasting.
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  #19   ^
Old Sun, Mar-12-17, 13:23
dan_rose dan_rose is offline
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Posts: 138
 
Plan: None
Stats: 161/140/140 Male 5'10"
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Progress: 100%
Location: Loughborough, UK
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Seems like mixing carbs with fat is unhealthy (but tasty e.g. junk food).

The question I'm interested in: Does the mixing apply per meal, per day or longer term? From what teaser says, I'd guess it's per meal.

(In terms of increasing food choices / enjoyment, it would be nice to be able to up my carbs if it could be done in an healthy way)
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  #20   ^
Old Sun, Mar-12-17, 19:07
Justin Jor Justin Jor is offline
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Posts: 183
 
Plan: Bernsteinish
Stats: 314/231/199 Male 6'1
BF:
Progress: 72%
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By the way, protein remaining the same isn't really true. Your actual protein needs fluctuate based on what your diet is and what you're doing.

Carbs are, for instance, protein sparing. This isn't a real concern if you're not training fairly hard, but if you ARE training hard, and you reduce carbs, you might need to kick up the protein.

And so on. You need a certain amount of glucose for your brain, for instance. Your body will produce this, mostly from protein, so if you're at like zero carbs and trying to, for instance, gain muscle, you'd need more protein to do it than you might if you were eating more carbs.

For the average person, a ballpark protein is probably fine, but that's not quite the same as protein needs being static.
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  #21   ^
Old Sat, Mar-25-17, 15:59
M Levac M Levac is offline
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Posts: 6,451
 
Plan: VLC, mostly meat
Stats: 202/200/165 Male 5' 7"
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Progress: 5%
Location: Montreal, Quebec, Canada
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Quote:
Originally Posted by rconn2
I just read the book: "Volek & Phinney's Art & Science of LC". Fascinating, but then it raised a serious question that undermined my understanding:

page 86: "pretty consistently, as dietary fat percent is increased from 30% to 60% in animals and in humans, insulin sensitivity does get worse. But once above 60% of energy as fat, which typically translates to less than 20% of energy as carbohydrates (assuming 15-20% from protein), insulin resistance turns around and starts to improve."

"does get worse"?! They did describe an "island effect" where going half-way low carb might not get you there (better insulin sensitivity and other beneficial effects). But, that both duration of diet (at least 2 weeks long) and degree of carb restriction were important.

This is very confusing and yet is very important to understand. So, cutting out that baked potato might be making matters worse for someone w/ IR or T2D? That is, unless they're willing to go full ketogenic?

The book is acknowledging that increasing fat does cause a worsening of IR. Can anyone provide any insights?

I recently developed a hypothesis to explain the need for low-carbers to eat some carbs to prepare to pass a OGTT. This hypothesis happens to be quite pertinent to your questions as well, because it basically explains what insulin resistance really is. I wanted to make a blog post about it, but a comment in your thread is as good a place as any to post.

First, insulin resistance does not exist, at least not as it is popularly described, i.e. cells do not respond to insulin, therefore blood glucose remains higher than otherwise. Fact is, cells respond exquisitely to insulin - the liver takes up the bulk of dietary glucose as can be seen by a proportionately small amount of lingering blood glucose after a meal. Consider that in a OGTT for example, it's a bolus of 75 grams of glucose, while the entire bloodstream contains about 5 grams, and this bolus will cause BG to rise only about 3-fold (from 100mg/dl to 300mg/dl), rather than a mathematically expected 15-fold (75 / 5 = 15, or 1,500mg/dl, but at this BG level, we're dying or dead). Even if we test positive for insulin resistance, BG will never rise anywhere near that. Maybe it will go up to 350mg/dl, maybe 400, but not at a level where we're literally dying on the spot. In fact, the BG level for a diagnosis of insulin resistance is between 120 and 140 - 2 hours after a OGTT. As we can see, there is no such thing as insulin resistance.

So, the reason low-carbers need to eat carbs to prepare to pass a OGTT is the enzyme called insulin-degrading enzyme (IDE). This enzyme is mostly located/produced/active in the liver and the brain. The liver is most pertinent for our purpose. Unlike hormones such as insulin for example, IDE cannot be produced in huge relative quantities. With insulin for example, blood level can rise several-fold, while IDE can only rise a small amount. That's because IDE stays within the cells, it doesn't get out of the cells and in the bloodstream - there's only so much space inside cells.

While IDE can't be produced in large quantities, its total quantity can be lowered, that's how eating carbs allows low-carbers to pass a OGTT. If IDE is lower than otherwise, insulin in the blood stays higher than otherwise. As simple as that. IDE level in the liver cells drop because IDE also gets degraded as it performs its various function, i.e. inhibiting ketogenesis, inhibiting glycogenolysis, and finally degrading insulin. In the last step, that's when IDE also gets degraded, thus lowering its total quantity inside the cell. This is completely normal and in fact it's essential, there must be a way to lower insulin once insulin has done its various jobs, but there must also be a way to shut down this mechanism once we lowered insulin back to normal level.

In low-carbers, there's little carbs, so there's little insulin being secreted, so there's little IDE needed to degrade this insulin. But in a sort of contradictory way, there's more IDE in a low-carber than a high-carber, because more IDE is needed to keep insulin lower. Or if we prefer, there's more IDE because there's less insulin to degrade, and the production of IDE is mostly constant independent of external stimuli. As a low-carber eats more carbs, there's more insulin being secreted, there's more IDE being degraded, there's less IDE in the end, blood insulin stays higher than otherwise, insulin can now handle a bolus of 75 grams of glucose, without any significant portion of this bolus lingering in the blood long enough to cause the doc to diagnose insulin resistance, i.e. to diagnose diabetes type 2.

In a way, it must absolutely work this way. Otherwise, a tiny amount of dietary glucose will cause very serious problems. IDE inside the liver would stay higher than otherwise, insulin would get degraded too much, there would not be enough insulin in the blood to deal with excess dietary carbs, we would suffer the symptoms of diabetes type 2 almost instantly at every meal. Or, the pancreas would need to produce more insulin than otherwise to compensate the excess IDE.

Granted, it's just an idea, not a fact, but it's quite plausible that it works exactly as I described above, so in a way it predicts a drop of IDE in the liver when we eat carbs, which should be detectable in the lab by some genuise scientist. And if it's already been detected through experiment and a paper has already been written about it, then that's all it takes to confirm or refute the hypothesis.

For our purpose however, we're talking about dietary fat causing insulin resistance. Dietary fat cannot cause insulin resistance, it does not have the physiological means to do so. However, it does have the means to activate the PPAR-x pathways in the liver, which also happens to be the same way we activate IDE in the liver. Well, if we activate IDE, there's more IDE, we degrade more insulin. And if we degrade more insulin, blood glucose is now allowed to linger higher and longer than otherwise, thus giving the appearance of insulin resistance, i.e. cells do not respond to insulin, therefore blood glucose lingers higher than otherwise. But as I explained, insulin resistance does not exist, so the appearance of insulin resistance is an illusion created by our misunderstanding of the actual mechanisms, which my hypothesis above should help explain more correctly.

This is just how I see it, not necessarily how it actually works.
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  #22   ^
Old Sat, Mar-25-17, 16:42
M Levac M Levac is offline
Senior Member
Posts: 6,451
 
Plan: VLC, mostly meat
Stats: 202/200/165 Male 5' 7"
BF:
Progress: 5%
Location: Montreal, Quebec, Canada
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Quote:
Originally Posted by Justin Jor
Carbs are, for instance, protein sparing. This isn't a real concern if you're not training fairly hard, but if you ARE training hard, and you reduce carbs, you might need to kick up the protein.

And so on. You need a certain amount of glucose for your brain, for instance. Your body will produce this, mostly from protein, so if you're at like zero carbs and trying to, for instance, gain muscle, you'd need more protein to do it than you might if you were eating more carbs.

Without going on a tangent, I feel I have to correct these two points based on how I see it.

More appropriately, carbs are believed to be protein-sparing, but with little evidence to confirm the belief. This belief is due to the fact that insulin stimulates proteosynthesis (creation of new protein), and also inhibits proteolysis (destruction of existing protein), therefore more insulin should do more of that. However, carbs also cause glycation - the creation of advanced glycation end-products (AGE's) - which is the binding of glucose to protein, thus rendering these protein inert or making them work differently than normal.

By comparison, ketones stimulate a different process called chaperone-mediated autophagy (CMA) which is the degradation of AGE's, so that the useless protein that's bound to glucose is now released, free to be used where needed, thus genuinely sparing existing protein, and in effect reducing one's dietary protein requirement.

Furthermore, hyperglycemia inhibits growth hormone, which is the single most powerful growth factor for muscle, therefore carbs stifle muscle growth through this inhibition mechanism rather than stimulate growth through insulin/proteosynthesis/proteolysis. Fat doesn't do that, growth hormone works normally.

Finally, protein stimulates insulin, in exactly the amount required to stimulate the exact amount of proteosynthesis and the exact amount of inhibition of proteolysis. Excess insulin (from dietary carbs) is superfluous, it will not cause any more muscle growth than already caused by the protein itself. However, excess insulin will cause growth - in fat tissue. This is helped by the fact that glucose is converted to glycerol in fat cells, thereby giving fat cells the ability to create triglycerides for storage, so the more carbs, the more glycerol, the more triglycerides, the more fat inside fat cells.

For the glucose-from-protein point, that's mostly incorrect for our purpose. Fat is made from fatty acids and glycerol, and glycerol is used to make glucose, and we have a huge amount of fat reserve so we have a huge glycerol reserve too. In order for glucose-from-protein to be true, there's gotta be no fat left, i.e. we'd have to be literally starving and emaciated. Incidentally, fasting causes insulin to drop to its lowest level, and ketogenesis to increase to its highest possible level, thus stimulating CMA to a higher degree, thus sparing existing protein to a higher degree as well. Granted, if we fast for a significant amount of time, then we get into losing protein due to lack of dietary protein itself, but that's a different cause of protein loss altogether.

As for dietary protein requirement depending on training level, I agree, but not to the point about a different protein requirement depending on carbs intake level. Muscle is made of protein, not glucose, therefore protein requirement does not change just because we eat more or less carbs. However, based on what I wrote above especially with regards to AGE/CMA, we could argue that protein requirement would actually drop as we eat less carbs, because less of it would end up glycated/useless so more of it would be used for growth.

Again, this is just how I see it, not necessarily how it actually works.
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