If saturasted fats were so bad for us then why does our body choose to use it as storage? - the fat we're all trying to get rid of is saturated - our bodies turn our eccess energy and food intake into saturated fat and distributes it around our bodies!

jo

Mcsblues,
I hope you don't mind my questioning your theory (that protein is not a problem for blood-sugar sensitive as it does not affect blood glucose & insulin levels adversely). I'm trying to sort this out myself. Personally, I feel that I react very similar to a high consumption of many proteins (particularly leaner meats) that I would eating too many carbs. Not all protein sources are a problem, just some, which makes things confusing. For example, processed protein in the form of carb countdown milk, yogurts, bars & shakes are as if I were eating something like eggs or avocado (extremely satisfying). But often times leaner meats in large quantities with insufficient fat will set me off.

So I'm curious about all of this, for personal reasons...

Note that the author specifies that insulin can cancel glucagon in the non-diabetic state. To my understanding this is basically code for "people who's insulin signaling work's right have no problem with gluconeogenesis; people who have insufficient insulin OR cannot effectively perceive insulin (insulin resistant) will have problems with gluconeogenesis".

As we all know, the conventional way of looking at blood sugar problems is incorrect. Doctors recognize "non-diabetic" and they recognize "diabetic". The truth is, it's a gradient. Before one becomes diabetic, they were pre-diabetic, and before they were pre-diabetic they were insulin resistant.

If it is a truth that gluconeogenesis is heavily insulin-dependent (for several reasons), and it is a truth that diabetics have trouble controlling blood sugar from gluconeogenesis because of this...
...doesn't it stand to reason that those of us who are avoiding carbs, should also be trying to reduce gluconeogenesis, too? If both cause problems for people with insulin issues (diabetics), and if we feel ourselves to have "minor" forms of these same issues (pre-diabetic/ir/whatever), shouldn't eating tons of protein indifferently be unwise?

Again, wouldn't this be happening - albeit on a smaller scale - for people with impaired glucose tolerance & other problems with insulin? Insufficient insulin (or a body that is deaf to it) is the reason behind all of this carb control stuff. We all know carb control is important for the same reason it is for diabetics, to some non-diabetic individuals who are sugar sensitive.

If these (blood sugar/insulin) protein problems happen to diabetics specifically because of insufficient insulin/poor insulin sensitivity, wouldn't the sugar-sensitive individual also have a bit of an issue too, just as we do with carbs?

Speaking personally, I know that if I eat too much proteins, especially proteins from certain sources, I feel similarly as I do if I over did it with carbs. It's not quite as bad or as dramatic but it's definitely there. Who knows, maybe it's all in my head. I am a salt & fat & meat craver, after all. But if it's true, why don't I have the same problems with roasted flavored salted nuts? Those make me want to eat more, but I don't feel that same insatiability, I don't feel the physical symptoms that I do sometimes with proteins.

I find it interesting that not all protein sources are equal in their effects on glucagon & insulin. Makes sense after all, some are more gluconeogenic others ketogenic right?

If true, it would explain why I feel very "stable" on some proteins but not others.

The very simple answer is no - having insufficient insulin and being insulin resistant are two very different states - because it is the insulin:glucagon ratio which is paramount, and this will decide the fate of dietary protein. This can be seen in the studies that I mentioned in my post, most of which looked at type 2 diabetics (ie highly insulin resistant individuals) or a ‘normal’ and a diabetic group – hence in the Nuttall and Gannon 2004 paper;

“Seven subjects with type 2 diabetes [5], and 8 subjects without diabetes [6] ingested 50 g of protein in the form of very lean beef. In the non-diabetic subjects, there was no change in blood glucose concentration over the 4 hours of the study, as had been noted previously. However, in the subjects with type 2 diabetes, the glucose concentration actually decreased over the 5 hours of that study”

The lower BG in the diabetic group is because there appears to be a stronger insulin response from diabetics as a result of protein intake (compared to a ‘normal’ response which sees an equal rise in insulin and glucagon) – and this higher level of insulin for the highly insulin resistant subjects means that far from promoting more gluconeogenesis – this remains firmly suppressed, and even in the face of insulin resistance, the higher insulin will have the effect of lowering BG over time. The opposite would be true for poorly controlled type 1 or insulin dependant type 2s.

Your question about different perceived satiety levels for different protein sources would also probably be a no – if you wanted to you could do an analysis of the amino acids contained in each source and the proportions of each that individual foods supply, and then look at the amount of glucogenic and ketogenic amino acids you wer consuming … but I doubt it would get you very far – because first of all, the insulin glucagon ratio will still decide their fate (as just because a particular amino acid is glucogenic - doesn't mean that it will be converted to glucose - in fact to confuse matters further, some are both glucogenic and ketogenic!), and, as you know, there are so many variables when it comes to satiety including the combination of nutrients in each protein source, the foods that you eat with that protein source, and all the other non physiological factors which influence how we respond to different foods. And generally when I talk about satiety it is a question of how long a particular meal will satisfy me – but as you know, others confuse this concept with whether or not a particular food provides its own ‘off switch’ to stop you eating in the first place – which is a whole different ball game. If that was the guide, I can think of quite a few high carb foods that have high ‘immediate satiety’ but cause major hunger pains not long after (the Chinese meal syndrome springs to mind).

Sooo, I don’t think abnormal gluconeogenesis is a likely answer to your query – but if you are not convinced, grab yourself a BG meter and do some tests!

Cheers,

Malcolm

I am probably getting into this conversation way to late and haven't read through the whole thing. For me an easy way to think of the difference in Insulin Resistance and not having enough insulin is a very easy thing. Insulin Resistance, a person produces enough insulin for the BS but the cells are so saturated that the BS can't be stored, in not having enough Insulin either the pancreas can't produce it, or the hormone to trigger it is not working. I get gestational diabetes, and IR is increased because the placenta produces a hormone that blocks the action of insulin, There fore BS goes up. I have a hard time getting my father to understand that GD is a different animal from most diagnosis, because you can have a normal insulin level and response and not be able to utilize the insulin properly. Hope this makes sense.
Tanya

Almost, Tanya.

In Insulin resistance, the pancreas is actually producing far more insulin than a normal person would need for the amount of blood sugar present, but the insulin receptors ignore it and do not allow the glucose to enter the cell. Kind of like a mom tuning out her kids when they're noisy; she knows they're there but she's not paying attention to them. With blood sugar not dropping, the pancreas produces still more insulin until the cell receptors finally get the message and let the glucose in (think again of one of your kids standing there tugging on your sleeve saying, "mom....mom....MOM!!!! until they get your attention). One of the defining markers for IR is high circulating levels of insulin in the bloodstream. The cycle repeats itself over and over until eventually, the cells in the pancreas that produce insulin (the beta cells) start wearing out.
In diabetes (Type 1 and later stages of Type 2) the pancreas either is producing no insulin at all or can't produce enough to keep blood sugar levels at normal levels.

if this were the case, it only would be half as bad as it is. instead of finally getting the message and letting in glucose, the unreceived glucose is converted and stored as fat. this is what atkins was referring to when he said your body becomes a fat-making machine.

Some of it is, yes, but most of it does eventually get inside the cells to be used for energy as well. If it didn't, your body would be forced to burn fat and muscle for energy instead of storing fat since the cells have to have some source of energy. This situation (no or little glucose getting into the cells for energy, blood glucose levels high, body burning fat and muscle for energy) describes what happens in diabetic ketoacidosis.

Well no, that is not what he meant at all. Unless you are a type 1 diabetic (or insulin dependant type 2) the "unreceived glucose" is eventually absorbed by the cells - but as Lisa says, as you get more and more insulin resistant this takes more and more insulin to acheive. It is only after the glucose is absorbed by the cells that it is converted to fat (yes some carbs are converted to triglycerides in the liver - but that is another story)

You become a fat making (and fat storing) machine because the insulin glucagon ratio is almost continually weighted on the insulin side - and with high insulin you will store more fat when you have a dietary energy excess and fatty acids will not be made available for energy requirements when a deficit occurs.

Cheers,

Malcolm

from DANDR (p.52):

epobee, the way I understand it, glucose is transported into the cells and converted into energy and fat whether one is insulin resistant or not. In the case of insulin resistance (high insulin:glucagon), fat is not mobilized out of the fat cells for use by the other cells as energy.

Wyv

Well yes, but as I was saying is that this is just the half of it. Insulin resistance is much worse than just that. When the cells become less sensitive to insulin, and blood sugar rises after a carbohydrate meal, excessive amounts of insulin are released to clear the high BS. One way is that the liver converts some into tryglycerides (fats) but insulin also directs both the tryglycerides and the excess blood sugar into the cells (eventually) where both tend to be stored as fat - ie. you have become both a fat producing and fat storing "machine".

The other side of the coin is that with prolonged periods of insulin dominant metabolism (where insulin overides the effect of glucagon) you are inhibited from using stored fat or dietary fat for energy - for stored fat, there are two enzymes which control this - the first, lipoprotein lipase [LPL], transports fatty acids into the fat cell and keeps them there.... The other, hormone-sensitive lipase [HSL], does just the opposite - it releases the fat from fat cells into the blood [where it is then transported to other cells to be "burned" as fuel. Insulin promotes LPL and inhibits HSL - glucagon works the other way round. Insulin also suppresses carnitine, which is needed to shuttle free fatty acids into the mitachondria (the fat burning 'furnaces' in most cells).

So insulin resistance means you not only become a "fat producing" (and storing) machine, but also are less able to use fat from you body or diet as a source of energy.

As Atkins describes elsewhere in his book (yes, its not very well written, but it is there!) this is the basis of the success of a low carb approach - lowering carbs, means lowering and keeping more stable blood glucose, which in turn means lower basal insulin - which changes the hormonal balance - which not only stops you from being a fat producing/storing machine - but it turns you into a fat burning machine!

Cheers,

Malcolm

Or, if you're up for a more detailed explanation of the effects of insulin and glucagon on hormones and metabolism, the Eades in Protein Power do an excellent job of explaining the whole relationship.

Weel yes - is my bias showing?

But even i would have to say that Protein Power is not well put together. If you want even more detail, in a much better written book, Protein Power Lifeplan is the best low carb book by far IMHO .

Cheers,

Malcolm

yep. that's what i originally tried to say. lisa wrote that glucose continually circulates (stimulating more insulin) until it is finally taken up by the cells' worn out receptors, and i commented that fat storage was also a problem associated with insulin resistance.