High protein diet = High sugar diet? Dr. Fung's latest IDM post

#22

If I recall correctly Dr. Bikman’s talk was about protein and glucagon.

(Nigel Williams) #23

Yes that was it sorry ignore me

(Banting & Yudkin & Atkins & Eadeses & Cordain & Taubes & Volek & Naiman & Bikman ) #24

Protein’s effect on insulin and glucagon. Dr. Bikman’s work is highly focused on insulin.

As I said, context matters. In fasted state, protein stimulates glucagon way more than insulin. In a low carb ketogenic state, keeps the ratio the same. In a SAD state, insulin much higher and glucagon not much. Context matters more than a lot of folks care to admit.

The difference between Fung and Naiman is one of context as well. Fung’s patients are largely different from Naiman’s. The other anti-protein guy, Rosenstein is concerned with longevity and mTOR obsessed (and my reading suggests that he’s wrong there, too).

(Omar) #25

I am assuming that in healthy indivduals ( not t2d) the level of blood glucose will be the same wether on hi protin or hi fat ( low or no carbs)

if individuall 1 has 30 units delta of bg( hi protin vs hi fat diet ) and individual 2 has 70 units as delta then would not that point in a relative manner to insulin resistance?

the answer maybe no maybe yes. I dont know. I am engineer with no medical background so the point I am trying to make maybe foolish and I will accept that.

(karen) #27

But that’s the whole question, isn’t it? I think what we’re trying to figure out is whether a healthy individual’s blood glucose is affected by high protein. It may be that as a T2D your data doesn’t tell us what happens in healthy individuals, but it certainly doesn’t lead me away from the idea that protein has an effect on BG. And yes, I have some biochemical education but not enough to be fluent about this. I just feel like a lot of people here are pooh-poohing this concept because they’re very fond of bacon. :wink:

ETA: when I think about it, your data might be even more telling. You can’t metabolize glucose properly. So perhaps you are the perfect candidate here: your glucose, whether it’s produced by carbs or protein, stays in the blood where it can be easily measured, and you’re measuring a lot more of it when you eat a high protein diet.

(bulkbiker) #28

That may be what the study (done on people with Type 2 by the way)was trying to uncover. But as it was composed of 2 relatively high carb diets then it would be impossible to draw any conclusions as to the effect of protein on blood glucose from it. In other words it was a waste of time.

(Justin Jordan) #29

In a diet as close to zero carbs as I can get it (so whatever carbs exist in beef, chicken and eggs) protein intakes absolutely does affect my blood sugar.

I’m a T2 diabetic, and if I restrict my protein (restrict, here, is somewhere around 50 grams a day - my LBM is approximately 160 pounds) I can get my blood sugar to true normal (so around 80 fasting). If I go higher than that, the best I can do is a blood glucose of around 100.

In my case, this doesn’t really scale. Eating 75 grams consistently will get my BS up about 20 points, but doing 125 doesn’t seem to cause it to get any higher.

In my case, months of ‘restricted’ protein hasn’t caused any notable loss of muscle mass and I’ve gotten stronger. And I’ve been lifting weights for close to 30 years.

#30

excellent high level conjecture from Peter (hyperlipid) possibly explaining what happens with very high protein intake in the absence of carbs

(karen) #31

Love your kitty, he looks like a lion. Very interesting that your protein to glucose conversion has a cutoff. I wonder if that’s as much glucose as your body wants, so once you reach that point the process stops …

(Banting & Yudkin & Atkins & Eadeses & Cordain & Taubes & Volek & Naiman & Bikman ) #32

Given that gluconeogensis is demand driven, not supply driven, Justin’s experience is about what one should expect.

(Candy Lind) #33

No, what you do is make some cheese crisps and get out the guacamole and set up your easy chair front and center! :smiling_imp:

(Banting & Yudkin & Atkins & Eadeses & Cordain & Taubes & Volek & Naiman & Bikman ) #34

[quote=“Justin_Jordan, post:29, topic:40746”]
Eating 75 grams consistently will get my BS up about 20 points, but doing 125 doesn’t seem to cause it to get any higher.
[/quote] supports demand driven gluconeogensis.

Additionally, you’re only measuring BS, not insulin and certainly not glucagon. So, maybe you have enough information to make informed decisions for T2, maybe not for optimal health.

(Justin Jordan) #35

Nor did I claim to.

(Matthew) #36

3/4 of what Peter writes goes over my head, but this stuck out:

“Dr Shawn Baker who eats an all meat, very high protein diet, maybe over 400g/d protein intake. His HbA1c is reported as 6.3%”

Above 6 and below 6.5% is prediabetic. I would guess the glucose is being generated from the protein slowly over time, so wouldn’t be as toxic as ingested sugars, but above 5.6% means his pancreas is slowly dying through glucose toxicity. I would think Peter would know about this, as knowledgeable as he is, but doesn’t mention it.

http://phlaunt.com/diabetes/14045678.php

I would consider this another datapoint against high protein diets.

(Banting & Yudkin & Atkins & Eadeses & Cordain & Taubes & Volek & Naiman & Bikman ) #37

I don’t think Dr. Shawn Baker is the best example as he’s not just a carnivore, he’s a multiple world record holder and can deadlift a small automobile.

He doesn’t have spikes above 135, and there are several reasons to believe that he’s not diabetic based on the larger picture. He’s certainly not TOFI.

(Justin Jordan) #38

Maybe.

For one thing, I’m not sure glucotoxicity to beta cells has actually been proved. Fung makes a pretty good argument as to that not being what’s happening.

Beyond that, and this is dealing with Type 1 diabetics so applicability to normal people is suspect, but Fung talks about looking at type 1 diabetics who avoided complications well into their seniors years and they found that, on average, their glucose wasn’t actually super low or even normal. They were averaging (and I’d need to look this up so take this number with some tasty salt) an HA1C of around 7.

But they were all using really low doses of insulin.

So what’s healthy in low insulin environment may not be the same as what would be healthy in a higher insulin environment.

(Justin Jordan) #39

Looking up the relevant bits:

The Golden Age Cohort. That had an average A1C of 7.6, and according to Fung, none of the diseases associated with glucotoxicity.

Which seems to be what the abstract implies.

"Abstract
BACKGROUND:

Type 1 diabetes mellitus is associated with high levels of premature morbidity and mortality. Prolonged survival is possible, however, and some patients appear to be protected from the long-term complications of this condition.
METHODS:

Diabetes UK awards medals to patients who have had Type 1 diabetes for 50 years or more. By examining medal-holders, we have established the clinical and biochemical features of a group of 400 subjects (54% male) with Type 1 diabetes of long duration.
RESULTS:

Mean age of the subjects was 68.9 years and mean age-at-onset of diabetes 13.7 years. Features of long duration diabetes in this cohort include normal body mass (mean BMI 25.0 kg m-2), low insulin dose (mean 0.52 units kg-2) and greatly elevated HDL-cholesterol (mean 1.84 mmol/l). Mean HbA1c was 7.6% (normal range 3.8-5.0%) and no patient had a normal HbA1c at the time of venesection. As a group, they have long-lived parents and consume moderate amounts of alcohol. Medical contact has often been sporadic. A significant proportion (29%) were taking anti-hypertensive medication. Screening for micro- and macroalbuminuria was positive in 35.7%.
CONCLUSIONS:

Patients with long-duration (> 50 years) Type 1 diabetes are relatively protected from clinical diabetic nephropathy and large vessel disease; our data are consistent with protection possibly being genetically determined in part via elevated HDL-cholesterol levels. An abnormal urinary albumin/creatinine ratio is common in these patients, despite their low risk of significant renal deterioration; this may have implications for microalbuminuria screening programmes."

(Banting & Yudkin & Atkins & Eadeses & Cordain & Taubes & Volek & Naiman & Bikman ) #40

I don’t see any discussion of lifestyle in there, which suggests either:
A: The researchers didn’t ask
Or
B: The researchers didn’t like the answer.

Given the low dose of insulin, one might assume these folks keep it LC. Or, maybe they have a type of T1 that is inherently mild.

(Justin Jordan) #41

Given that they averaged a normal BMI (which, really, is fairly thin by modern standards) it’s probably likely they weren’t eating a lot of carbs as an absolute number, compared to the average person. But yeah, my instinct is that they were likely doing some kind of low carb.

It’s also possible they were people who were naturally more sensitive than normal. The fact that they had long lived parents might be a sign of this - there’s some correlation between long lived folks and insulin sensitivities.

And there’s survivor bias here - these may be the people who were resistant to glucotoxicity.

That said, my overall point was, there’s stuff we just don’t really know. High glucose levels and high insulin levels in most people go together, so what is a bad level of A1C in someone (like Shawn Baker) we know has low insulin is not well established.

The Golden Years Cohort suggests some things, but doesn’t prove much.

(Banting & Yudkin & Atkins & Eadeses & Cordain & Taubes & Volek & Naiman & Bikman ) #42

Every study of any value suggests a minimum of three more studies to expand the knowledge. I think this one suggests lots of other ways to look at the Golden Years Cohort… Some that DiabetesUK might not be interested in…