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  #196   ^
Old Mon, Feb-02-15, 11:02
teaser's Avatar
teaser teaser is offline
Senior Member
Posts: 15,075
 
Plan: mostly milkfat
Stats: 190/152.4/154 Male 67inches
BF:
Progress: 104%
Location: Ontario
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Another thing that's been covered in Peter's blog, there are some studies showing that animals put on a diet higher in polyunsaturated fat vs. saturated fat have a higher fasting ketosis. They also had less body fat when calories were controlled Peter looks at this as bad--failure of polyunsaturated fat to induce physiological insulin resistance, leading to threats of hypoglycemia, forcing higher ketone production, he suggests that the animals are probably hungrier, based on this. I'm not sure what to make of that. If he's right, it might depend on context. Without a trial, I couldn't really guess whether the ketosis-guys would be more prone to hypoglycemia, or less.


At any rate, what this suggests is that the animals probably burned more carbohydrate in the fed state, on the omega 6 fatty acid diet vs. the saturated fat diet, so were forced to burn more fat when fasted.

This abstract is in humans;

Quote:
Differential metabolic effects of saturated versus polyunsaturated fats in ketogenic diets.
Fuehrlein BS1, Rutenberg MS, Silver JN, Warren MW, Theriaque DW, Duncan GE, Stacpoole PW, Brantly ML.
Author information
Abstract
Ketogenic diets (KDs) are used for treatment of refractory epilepsy and metabolic disorders. The classic saturated fatty acid-enriched (SAT) KD has a fat:carbohydrate plus protein ratio of 4:1, in which the predominant fats are saturated. We hypothesized that a polyunsaturated fat-enriched (POLY) KD would induce a similar degree of ketosis with less detrimental effects on carbohydrate and lipid metabolism. Twenty healthy adults were randomized to two different weight-maintaining KDs for 5 d. Diets were 70% fat, 15% carbohydrate, and 15% protein. The fat contents were 60 or 15% saturated, 15 or 60% polyunsaturated, and 25% monounsaturated for SAT and POLY, respectively. Changes in serum beta-hydroxybutyrate, insulin sensitivity (S(I)), and lipid profiles were measured. Mean circulating beta-hydroxybutyrate levels increased 8.4 mg/dl in the POLY group (P = 0.0004), compared with 3.1 mg/dl in the SAT group (P = 0.07). S(I) increased significantly in the POLY group (P = 0.02), whereas total and low-density lipoprotein cholesterol increased significantly in the SAT group (both P = 0.002). These data demonstrate that a short-term POLY KD induces a greater level of ketosis and improves S(I), without adversely affecting total and low-density lipoprotein cholesterol, compared with a traditional SAT KD. Thus, a POLY KD may be superior to a classical SAT KD for chronic administration.


Short term study, mildly ketogenic diet.

http://press.endocrine.org/doi/full.../jc.2003-031796


Quote:
10 mg/dL (0.96 mmol/L)


So the 8.4 mg/dl betahydroxybutyrate at least approaches the level of 1 mmol/l, which is where I've seen Jeff Volek suggest that as much as 1/2 of the brain's energy supplies could come from ketones.


So I'm not totally keto-jacking this thread--if you look at figure 1, blood glucose decreases mirror the ketone increases, down about 10 mg/dl in the polyunsaturated group, down 3 mg/dl in the saturated group. Insulin up slightly in the saturated fat group, down slightly in the polyunsaturated fat group.


Personally, I'd rather eat a higher ratio keto diet with heavy cream, than a lower ratio one with corn oil. Yech. I guess if we were talking sunflower seeds, walnuts etc., that might be different.
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  #197   ^
Old Mon, Feb-02-15, 11:05
Liz53's Avatar
Liz53 Liz53 is offline
Senior Member
Posts: 6,140
 
Plan: Mostly Fung/IDM
Stats: 165/138.4/135 Female 63
BF:???/better/???
Progress: 89%
Location: Washington state
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Teaser, thanks for the detailed explanation. I've spent a fair amount of time at Hyperlipid reading his posts on PIR, taking in what I can. However, I think your more user friendly explanation will make it possible for me to drill a level deeper with his writing. Thanks so much.

I'm looking forward to the christening of my first Great Nephew in April. How did THAT happen? Yikes!
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  #198   ^
Old Mon, Feb-02-15, 13:25
WereBear's Avatar
WereBear WereBear is offline
Senior Member
Posts: 14,675
 
Plan: EpiPaleo/Primal/LowOx
Stats: 220/130/150 Female 67
BF:
Progress: 129%
Location: USA
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Now I'm wondering if it's just an aging function, and low carb actually makes it a better situation that the SAD would. Remember, type II diabetes used to be called Adult Onset.
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  #199   ^
Old Tue, Feb-03-15, 08:10
synger synger is offline
Senior Member
Posts: 146
 
Plan: IR Diet framework, LC
Stats: 310/288/150 Female 64 inches
BF:
Progress: 14%
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Quote:
Originally Posted by coachjeff
But then again, I would also question if LC really and truly does raise the absolute amount of palmitic acid. I mean how much butter would one really eat without bread to put it on? How much cheese, without pizza? How much sour cream without nachos?
(emphasis mine)

I had to blink at that. I always keep sour cream in my fridge, and I never have nachos. Maybe it's the German/Eastern European heritage I come from, but I mix sour cream with mustard and eat it with sausages. Or put a dollop of sour cream atop soups or stews or in creamy sauces I use over meat or veg.

Yes, I use it atop taco salads and chili. But I use it much more widely than that.

Last edited by synger : Tue, Feb-03-15 at 08:17.
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  #200   ^
Old Tue, Feb-03-15, 08:20
synger synger is offline
Senior Member
Posts: 146
 
Plan: IR Diet framework, LC
Stats: 310/288/150 Female 64 inches
BF:
Progress: 14%
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My FBG is seldom lower than 115, no matter what I eat or don't eat. My PP numbers are usually pretty good so long as I stay on-plan with my eating.

But I've been IR for YEARS. Looking back at my medical history, I realize that when I was diagnosed as "hypoglycemic" in the 80s, and having "PCOS" in the 2000s, and "pre-diabetic" today is pretty much all the same thing. I'm a metabolic nightmare of insulin resistance, at 50 years old and 300 pounds.

So at this point, my FBG does not bother me so much as my A1C. I can control my PP numbers by what I eat. I can't control my FBG.
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  #201   ^
Old Wed, Feb-04-15, 05:52
JEY100's Avatar
JEY100 JEY100 is offline
Posts: 13,433
 
Plan: P:E/DDF
Stats: 225/150/169 Female 5' 9"
BF:45%/28%/25%
Progress: 134%
Location: NC
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Going back to my post #6, my Hba1c is even worse. It climbed to 5.9 from 5.7' both pre-diabetic, and I am at my wits end. My blood sugars have been coming down again with IF (FBG was 94 and 81) but only started it Jan 5. Maybe this picked up off plan Christmas eating. Maybe the more I keep BG low, the longer lived my red blood cells are (the Chris Kresser argument why a1c is not the best test for diabetes). Whatever, my oncologist bought the glycated red cells not always accurate for LCers excuse, and we moved on the good news.
He is rearranging his practice to separate the survivors clinic from the treatment area and offer more lifestyle management help with a focus on nutrition. He wants me to help with weight loss and I am thrilled with the chance to help others. He is looking into some of the studies on lifestyle and impact on recurrence/survivorship. This is something I have wanted to do for years, and already do informally with many neighbors and at the Y...but this may be the platform where I can make a difference in my community. So my enthusiasm over this opportunity has overshadowed my being pissed off about my a1c...for now.
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  #202   ^
Old Wed, Feb-04-15, 06:22
Benay's Avatar
Benay Benay is offline
Senior Member
Posts: 876
 
Plan: Protein Power/Atkins
Stats: 250/167/175 Female 5 feet 6 inches
BF:
Progress: 111%
Location: Prescott, Arizona, USA
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Janet, I am so very pleased to hear about you being asked to help at the clinic. My teaching attempts have all fallen on deaf ears, so when I hear your story, I am thrilled. Wonderful!

Synger, I wish there was something I could offer you that would help. Perhaps prayer. It's all I can think of.
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  #203   ^
Old Wed, Feb-04-15, 08:41
Liz53's Avatar
Liz53 Liz53 is offline
Senior Member
Posts: 6,140
 
Plan: Mostly Fung/IDM
Stats: 165/138.4/135 Female 63
BF:???/better/???
Progress: 89%
Location: Washington state
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Janet, that is really exciting news that your doctor wants you to help counsel other cancer survivors. You will be so good at that and so helpful to othersA friend of mine is currently undergoing chemo and was telling me that she has days where she eats no carbs and then worries that her diet is not balanced (according to her daughter the vet and the literature she's been given). I'm enough of a food nazi that I don't want to annoy her by supplying her with alternate info, but it is so astonishing to me that more clinics and patients will not investigate alternative eating plans for endocrine-based cancers.

I'm truly sorry to hear about your HgbA1c going up. That's exactly where mine was 8 months ago when last checked, after staying at 5.6-5.8 for several years. My FBS had always been low and has gradually been creeping the more compliant I am with low carb.

As luck would have it, I'm going to see my GP today, armed with reams of paper showing weight loss (progress) and glucose readings (the opposite of progress over the past 8 months). I expect to have glucose, A1c and insulin tested while there. I floated Chris Kresser's theory to her last time but she didn't buy it. I'm taking my glucose meter to calibrate (informal analysis shows many many more high fasting glucose readings after switching to new meter last fall) and expect to repeat these tests in May at my yearly checkup especially if I do not like the results.

It makes no sense that glucose readings go UP with greater compliance unless Turtle was right a few pages back when she says that maybe we are lucky to have dodged the bullet of full blown diabetes. Still I don't see how those diagnosed with diabetes can see glucose drop so much, while those of us with normal levels inch up into the pre-diabetic range with LC eating. It just doesn't make sense!
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  #204   ^
Old Wed, Feb-04-15, 10:10
WereBear's Avatar
WereBear WereBear is offline
Senior Member
Posts: 14,675
 
Plan: EpiPaleo/Primal/LowOx
Stats: 220/130/150 Female 67
BF:
Progress: 129%
Location: USA
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Quote:
Originally Posted by JEY100
This is something I have wanted to do for years, and already do informally with many neighbors and at the Y...but this may be the platform where I can make a difference in my community. So my enthusiasm over this opportunity has overshadowed my being pissed off about my a1c...for now.


This is awesome news!
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  #205   ^
Old Wed, Feb-04-15, 11:00
synger synger is offline
Senior Member
Posts: 146
 
Plan: IR Diet framework, LC
Stats: 310/288/150 Female 64 inches
BF:
Progress: 14%
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Quote:
Originally Posted by Benay

Synger, I wish there was something I could offer you that would help. Perhaps prayer. It's all I can think of.


THank you so much. All the support here is extremely helpful. I come here when I feel like giving up. It always cheers me.
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  #206   ^
Old Thu, Feb-05-15, 04:25
gotsomeold gotsomeold is offline
Senior Member
Posts: 112
 
Plan: IF, LCHF
Stats: 175/110/125 Female 5'4"
BF:
Progress: 130%
Location: Asheville,NC Marietta,GA
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Janet! What exciting and wonderful news! Happy Dance all over the room.

Synger, I believe you are right to concentrate on PP and health overall. The subtle damage that happens at the mitochondrial and cellular levels.....well, it seems to take a lot of time to heal. I believe you are on the right - if frustrating - track.
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  #207   ^
Old Fri, Feb-06-15, 08:27
coachjeff's Avatar
coachjeff coachjeff is offline
Senior Member
Posts: 635
 
Plan: Very Low Carb
Stats: 211/212/210 Male 72
BF:
Progress: -100%
Location: Shreveport, LA
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Quote:
Originally Posted by synger
My FBG is seldom lower than 115, no matter what I eat or don't eat. My PP numbers are usually pretty good so long as I stay on-plan with my eating.

But I've been IR for YEARS. Looking back at my medical history, I realize that when I was diagnosed as "hypoglycemic" in the 80s, and having "PCOS" in the 2000s, and "pre-diabetic" today is pretty much all the same thing. I'm a metabolic nightmare of insulin resistance, at 50 years old and 300 pounds.

So at this point, my FBG does not bother me so much as my A1C. I can control my PP numbers by what I eat. I can't control my FBG.


Am not really overweight by medical standards, but I seem to be like you. Maybe not as bad off, but still. There were indications of my insulin resistance in my teens (Near sighted, acne, hypo attacks).

I find LC does a great job of controlling my post meal BG's. But no matter what I do, I have high FBG's ranging from about 100 to as high as 125.

I suspect my A1C is decent though.

I feel like I'm actually healthy on LC, despite the high FBG's.

But I am VERY concerned that when I apply for health insurance shortly, they will test my FBG's, and that a bad number is going to cause me problems.

Of course I could try to explain to them that "hey, but my PP's and A1C look great!"

But if they are fixated on FBG's, it'll fall on deaf ears. Much the same way as trying to help a doctor understand that a sort-of high total cholesterol number is NOT unhealthy if the ratios and triglyceride levels are good. They just myopically fixate on the toal number.
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  #208   ^
Old Fri, Feb-06-15, 10:25
Liz53's Avatar
Liz53 Liz53 is offline
Senior Member
Posts: 6,140
 
Plan: Mostly Fung/IDM
Stats: 165/138.4/135 Female 63
BF:???/better/???
Progress: 89%
Location: Washington state
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I understand your concern about the insurance, Jeff. My husband has had a consulting job since he retired 3 years ago and it has provided insurance. That deal may terminate in May and he has 1.5 years till Medicare, I will have 3. I'm hoping we just roll over into a new plan, but not sure about how exactly it works and whether we will have to have tests...

The reason that most diabetes Dx is by fasting glucose is that for the ordinary diabetic fasting glucose is the last to go up, long after PPs. They won't be given an A1c until the FBG is in diabetic range and by that time the A1c will be well into the diabetic range.

What makes your case different (and mine) is the high FBS in the context of low PPs. It's non-sensical from the perspective of how diabetes is said to progress.

Did you ever do an A1c test? Apparently you can get home kits at the drugstore.

Also, have you calibrated your meter? I took mine to my doctors this week and discovered mine was reading 20 pts higher than their meter - certainly enough to push my readings from normal to pre-diabetic. I've ordered a new meter and look forward to seeing if the results are any different.
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  #209   ^
Old Fri, Feb-06-15, 12:33
WereBear's Avatar
WereBear WereBear is offline
Senior Member
Posts: 14,675
 
Plan: EpiPaleo/Primal/LowOx
Stats: 220/130/150 Female 67
BF:
Progress: 129%
Location: USA
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  #210   ^
Old Fri, Feb-06-15, 13:00
Turtle2003's Avatar
Turtle2003 Turtle2003 is offline
Senior Member
Posts: 1,449
 
Plan: Atkins, Newcastle
Stats: 260/221.8/165 Female 5'3"
BF:Highest weight 260
Progress: 40%
Location: Northern California
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I’m really bugged by this thing where long term low carbers/paleo eaters wind up with higher than ideal fasting BG numbers. Everything I’ve read tells me that this is a good, healthy way to eat, and yet there’s those damned BG numbers. Why won’t my FBG go down into the 80s?

Of course, it could be that the researchers are all wrong about the effects of low carb eating, and maybe we are as well, but what are my choices? If I continue to eat low carb, I will have to just ignore those FBG numbers, unless they get truly crazy, which may indicate I need to use metformin (I certainly don’t want to use exogenous insulin. I know one thing for sure, if I eat more carbs, my FBG gets even worse, and my post-prandial readings go nuts. That just can’t be a better choice than what I’m doing now.

For now, I’ve decided that what I’m doing is the right way to eat, and there is something going on with the fasting glucose readings that nobody completely understands at this point. Which brings me to this paper, which indicates that maybe, just maybe, this matter of IR caused higher FBG can be a good thing, even a life extending thing. The authors suspect that the IR and higher BG numbers which are caused by severe CR diets and mimicked by intake of rapamycin, are a natural result of reducing the mTOR nutrient signalling pathway. Could it be that long term low carb eating has the same effect?

Quote:
Once again on rapamycin-induced insulin resistance and longevity: despite of or owing to

Mikhail V. Blagosklonny
Author information ► Article notes ► Copyright and License information ►
This article has been cited by other articles in PMC.

http://www.ncbi.nlm.nih.gov/pubmed/22683661

Some extracts:

Abstract

Calorie restriction (CR), which deactivates the nutrient-sensing mTOR pathway, slows down aging and prevents age-related diseases such as type II diabetes. Compared with CR, rapamycin more efficiently inhibits mTOR. Noteworthy, severe CR and starvation cause a reversible condition known as “starvation diabetes.” As was already discussed, chronic administration of rapamycin can cause a similar condition in some animal models. A recent paper published in Science reported that chronic treatment with rapamycin causes a diabetes-like condition in mice by indirectly inhibiting mTOR complex 2. Here I introduce the notion of benevolent diabetes and discuss whether starvation-like effects of chronic high dose treatment with rapamycin are an obstacle for its use as an anti-aging drug.
---------------------------------------------------------------------------

Starvation diabetes-like condition with low mTOR activity

If you read the Abstract, you might wonder whether rapamycin extends lifespan despite or because of “starvation-like diabetes”. As described by Lamming et al [1, 2] extending several previous observations [3-6], chronic administration of high doses of rapamycin causes insulin resistance in mice. Yet, at similar doses, rapamycin prolongs life span in mice [7, 8]. Moreover, in several studies, rapamycin prevented complications of diabetes such as nephropathy [9-14]. Also, theoretical considerations indicate rapamycin for retinopathy [15], which was recently confirmed in an animal model [16]. Rapamycin prevents atherosclerosis in rodents [17-20] and coronary re-stenosis in humans [21, 22]. In contrast, diabetes promotes nephropathy, retinopathy, atherosclerosis and coronary disease. How could this be reconciled? mTOR is a part of a nutrient-sensing pathway [23-27]. Nutrients and insulin activate mTOR. Rapamycin, which inhibits mTOR, is a “starvation-mimetic”, making the organism “think” that food is in a short supply. The most starvation-sensitive organ is the brain. The brain consumes only glucose and ketones. Therefore, to feed the brain during starvation, the liver produces glucose from amino acids (gluconeogenesis) and ketones from fatty acids (ketogenesis). Since insulin blocks both processes, the liver needs to become resistant to insulin. Also secretion of insulin by beta-cells is decreased. And adipocytes release fatty acids (lipolysis) to fuel ketogenesis by the liver. Thus, there are five noticeable metabolic alterations of starvation: gluconeogenesis, ketogenesis, insulin resistance, low insulin levels and increased lipolysis. This metabolic switch is known as starvation diabetes, a reversible condition, described 160 years ago (see for references [28]). Starvation diabetes could be explained by deactivation of mTOR, which otherwise is activated by nutrients. In theory, rapamycin can cause similar symptoms in the presence of nutrients.
--------------------------------------------------------------------------------
The two opposite conditions?

Type II diabetes and starvation diabetes seem to be the two opposite conditions: the first is associated with activation of nutrient-sensing pathways, whereas the second is associated with deactivation of nutrient sensing pathways such as mTOR. Type II diabetes is dangerous by its complications such as retinopathy, neuropathy and accelerated atherosclerosis and cancer. Long-term effects of prolonged “starvation diabetes” is not known of course: it could not last for a long time, otherwise an animal (or human) would die from starvation. Or would not? An outstanding study by Fontana et al provides some answers [55]. Among individuals who had been practicing sever CR for an average of 7 years, 40% of CR individuals exhibited “diabetic-like” glucose intolerance, despite low levels of fasting glucose, insulin and inflammatory cytokines as well as excellent other metabolic profiles. In comparison with the rest CR individuals, they had lower BMI, leptin, circulating IGF-I, testosterone, and high levels of adiponectin, which are key adoptations to CR in rodents, suggesting severe CR [55]. The authors speculated that the “insulin resistance” in this severe CR group might have the effect of slowing aging, also based on the finding that a number of insulin-resistant strains of mice are long-lived [55]. The same conclusion could be reached from the mTOR perspective (Appendix 1).
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