las

Welcome all seeking refuge from low carb dogma!

“To kill an error is as good a service as, and sometimes even better than, the establishing of a new truth or fact”
~ Charles Darwin (it's evolutionary baybeee!)

Wednesday, October 26, 2011

Some Spiked Leptinade with My Science Krispies Please!

Well, Jimmy Moore is out with another installment of his crusade against "safe starches".  Yeah, I know, I know.  He's all about learning and helping people get to the truth, moving the debate forward constructively, and above all else protecting people from potentially bad advice such as that a major staple macronutrient for 99.99% of the human population for at least the past 10 millenia and more can actually be "safe".  Sorry, but I call things as I see them, baaayybee!   

It's another long piece, and I just can't stomach reading much of Jimmy's self-delusions anymore.  But I am interested in this whole notion that somehow we're all somewhere on a diabetic spectrum and our carb-induced post-prandial glucose spikes are lining our rat poison sprinkled paths to an early grave.  The post includes a long response by Dr. Ron Rosedale, pastor at the Church of the Not-Too-Late-in-the-Day Spiked Leptinade Drinkers.  

I'm going to address a few of the cited studies and Rosedale's basic claims.  (I'll be breaking this up in parts).  
The crux of the ‘safe starches’ argument is that no harm will come of this and it is, in fact, healthy. It is acknowledged that blood glucose will elevate after eating ‘safe starches’, but will generally stay below 140 mg/dl that Jaminet says is perfectly safe. Is it?? The science writing (below) is on the wall and the answer is…clearly no.
It is important to realize that this answer is no; there is no safe intake of sugar, nor a threshold level of blood sugar below which no harm will come, and I will shortly devote a fair amount of time to show this.

Now it would have been nice for Rosedale to include links to his science ... you know, just to make it a bit easier for the curious to go check out the studies in their entirety.  But by not doing so only those pesky blogger types like moi will likely bother. 


First up we have: Is There a Glycemic Threshold for Mortality Risk? Balkau et.al. This study looked "the 23-year mortality data from the Paris Prospective Study of the 7,018 men, aged 44–55 years, who were not known as diabetic at the baseline examination". Rosedale quotes (emphasis his):

“…the lowest observed death rates were in the intervals centered on 5.5 mmol/l [99mg/dl] for fasting glucose and 5.0 mmol/l [90 mg/dl] for 2-h glucose.
CONCLUSIONS: In the Paris Prospective Study, there were no clear thresholds for fasting or 2-h glucose concentrations above which mortality sharply increased; in the upper levels of the glucose distributions, the risk of death progressively increased with increasing fasting and 2-h glucose concentrations.
The first thing that jumps out at me, before even tracking down and looking at the study was that first quote:

 Lowest observed death rates 
centered on FBG of 99mg/dL

Note this is ALL causes of death.  Umm ... maybe there's something to the "we're all diabetic" meme after all, because last time I checked, that FBG level was just a measly 1 mg/dL shy of prediabetic!!  Or for the teaspoon crowd we might as well just forget the teaspoons, this is but a grain of sugar if that!  The conclusions are interesting, but the absence of a clear threshold where a fit curve "takes off" does not mean that there is no safe level of glucose ever.  Sheesh!  I also think this paper is the source of the the "shallow U" I've been referring to seeing somewhere (I still think it was Ned's Health Correlator blog).  Here's some worth-more-than-1000-words plots for you, for all deaths (top) and cardiac deaths (bottom):

From the conclusions: 
It is noteworthy that the relationship between glucose concentration and mortality followed a  J-shaped curve, except for fasting glucose concentration and death from CHD, which had a positive and linear relationship. The observed and the modeled relative risks were higher at very low glucose levels ... The modeled relationship between fasting glucose concentration and CHD mortality was linear, although a higher death rate was observed in the lowest fasting glucose class; the number of CHD deaths may have been too low to show a significant curvilinear relationship.
... When the 308 men with newly diagnosed diabetes were excluded from the analyses, there were still positive and curvilinear relationships between glucose concentrations and both all-cause and CHD mortality, except for fasting glucose concentration and CHD mortality, for which there was no statistically significant relationship.
Those J-shapes are tricky, especially when the leading side of the J appears more pronounced in the observed data vs. the model, and the bottom of the J appears awfully flat.  If we're talking health and life, CHD is only part of the equation.  One might even say that mild hyperglycemia is protective from the results of this study, that perhaps there's no clear threshold below which mortality risk doesn't also increase.  *I* didn't pick this study to make a point, Rosedale did.
Death rates were higher for the men with the lowest glucose concentrations ... [the discussion lists suspected cirrhosis and lower smoking rates as possible confounders] ... The curvilinear relationship between 2-h glucose concentrations and both all cause and CHD mortality remained when the men with these low 2-h glucose concentrations were removed from the analysis, whereas there was no longer a statistically significant relationship between fasting glucose concentration and CHD.
... There is no doubt that the increasing all-cause and CHD mortality associated with increasing concentrations of both fasting and 2-h glucose is in part due to the worsening risk factor profile with increasing glucose concentrations. The hazards ratios decreased after adjustment was made for other risk factors, but the fasting glucose levels still carried a statistically significant for all causes of death, as did the 2-h glucose concentration for both all cause and CHD mortality. 
In the Paris Prospective Study, there was no clear concentration of either fasting or 2-h plasma glucose above which the risk of death or death by CHD sharply increased. 
OK ... perhaps one of you dear readers can help me out here, but a diagnosis of diabetes here in the US begins with an FBG of 126 mg/dL or higher = 6.93 mmol/L.  So when they talk about excluding diabetics is that just looking in the center there?  Clearly above around the 7 mmol mark the curves seem to "take off".  Are the slight differences significant in the normal range?  Is lower better?  Or does being on the high end of normal mean that many of those men progressed to full-on diabetes in the two-decades following?

I believe Rosedale and I are in agreement that the hyperglycemia of diabetes is not the disease but the symptom.  He blames leptin resistance due to leptin spikes caused by carbohydrate consumption.  And yet he seems to be making the seminal error of equating the symptom with the cause.  Let's apply a uniform standard here, shall we?  It is pretty indisputable that LDL concentration correlates with CVD risk -- this is seen in an overwhelming number of studies --  but is not seemingly "causing" it by "clogging arteries" as they say -- rather it's a symptom of metabolic dysregulation.  Well, so, too it likely is with blood glucose levels.   The FBG and 2-hr post glucose-challenge levels are more markers for insulin resistance -- the underlying pathology of fasting hypeglycemia (liver IR) and impaired glucose tolerance (skeletal IR).  It is not dietary carbs per se that cause this no matter how many times the Taubesians try to repeat the mantra.  The dietary instigators of IR are, if anything, fat and fructose, not glucose which promotes insulin sensitivity.

So what we're looking at in this Paris Study is men starting in middle age (44-55) and their IR markers at that age.  And oddly enough, the fewest deaths from all causes occurred within 23 years in the group that had FBG's on the threshold of "prediabetes" diagnosis.  Is it possible that mild hepatic IR is protective after about age 50 for men?  I'm not saying this, just throwing out hypotheticals.

Bottom line:  This is "science writing" number one that fails to support Rosedale's contention that there is no safe level of BG "spike".

To be continued ...

In the meantime, enjoy a hump-day Happy Hour cocktail on me!  Cheers!!

23 comments:

Chris said...

It is all to weird. I have no idea now what Jimmy is talking about with "some non-nutrition-related concerns" that stop him testing safe starches or how "some medical doctors I was advised it probably wouldn’t be a good idea for me right now considering some issues with fat metabolism/insulin resistance that I’m working through"

All too strange

Sanjeev said...

If Moore has been very low carb for a very long time I'm wondering what has been up regulated and what has been down regulated in his body.

All the way from digestion (intake) to sweat/hair/urine/anus/lungs (elimination).

Even if he gave "safe starches" a fair try I would guess he would feel terrible for a while.

Stabby said...

It does kind of seem odd that the lowest blood sugars wouldn't fare the best. Could there be such a thing as the pathological inability to induce insulin resistance, which is a manifestation of a bigger problem? Or how about an excessive insulin secretion problem? Too much insulin all of the time could cause low blood sugar but be indicative of a problem. It's certainly a problem when diabetics overuse insulin.

I know that's thinking way outside of the Science Krispies box, but I just have a hard time believing that lower sugars wouldn't be optimal in the case of true optimality. This is what I see in the paleo world, and this is what we see with the Kitavans.

What I have the biggest problem believing is Rosedale's hypotheses. They seem to be purely mechanistic and they conflate a pathological condition with normal functioning that looks like the pathological condition for all of an hour.

Diana said...

Evelyn,

Would MacDonald's oatmeal cookies be in the unsafe starches category? Something tells me yes. I've eaten 6 of them in the last week. I'm down to 135 pounds. What is wrong with me? Will I die soon?

Thomas T said...

Hi CS! Apologies for posting something not relevant to this posts topic but I noticed the boards aren't being frequented as much...

I have a question that may seem obvious to some, but I have learned that logic doesn't always help in the area of bodily processes & nutrition!

Would someone with IR lose (approximately) the same amount of weight/fat given 2 identical people, but one with and one without IR? i.e. is IR in any way a disadvantage when losing weight besides things like havingto measure/track blood glucose? Perhaps a study on the effect of IR with a non-IR control group, both groups on identical diets, in a ward/chamber study with DEXA/hydro measurements at the end?

Thanks!

Sanjeev said...

Since insulin is a satiety signal (one of many) one could make the case the insulin resistant person will lose more fat because the higher insulin could make them spontaneously eat less.

Also insulin resistant fat cells don't trap fat as well as the insulin sensitive fat cells of an insulin sensitive person.

insulin and fat loss

also check out James Krieger's series on
insulin myths (this link is to one of several articles)

Sanjeev said...

> could make the case the insulin resistant person will lose more fat
___
if one wanted to do as much cherry picking as some gurus

Thomas T said...

"Since insulin is a satiety signal (one of many) one could make the case the insulin resistant person will lose more fat because the higher insulin could make them spontaneously eat less.

Also insulin resistant fat cells don't trap fat as well as the insulin sensitive fat cells of an insulin sensitive person."

What about if they were both on identical diets (i.e. disregarding hunger/satiety for the sake of argument)

john said...

Stabby,

What kind of Paleo diet gives very low blood glucose? Low fat, low protein usually does. Low carb will usually be higher but of course nobody on this blog would suggests that that's better...

Sanjeev,

That doesn't make sense...if you're insulin resistant with higher fasting insulin, then you're implying you need that more to do the same thing. Insulin doesn't just hang around and "work." Lucas of Ketogenic Nutrition did a good post on hypothalamic insulin and leptin signaling.

Lerner said...

This one was interesting enough to me so that I read the study. I'd say that Table 2 is where the heart of things lies.

The hazard ratios for CHD death adjusted for age and also for systolic blood pressure, cholesterol concentration, iliac circumference, and current smoking are:

Fasting BGs
7.8 vs. 6.0 = 1.04 (0.81–1.33) [that's 140 mg/dL vs 108]
7.0 vs. 6.0 = 1.02 (0.88–1.18) [126 mg/dL vs 108]

2-h glucose
11.1 vs. 7.7 = 1.31 (1.11–1.53) [that's 200 mg/dL vs 140]

Doing the same for all cause mortality:
1.31 (1.02–1.36)
1.08 (1.01–1.15)
and
1.38 (1.29–1.47)

It seems to me to be not a worry in the absence of the other risk factors unless BG levels are very high.

Tonus said...

"Even if he gave "safe starches" a fair try I would guess he would feel terrible for a while."

Which would be a sign that they are harmful. As opposed to how some people feel when they start low-carbing, which is just the body going through a sorely-needed adjustment period before they can fully experience the Goodly Goodness of Goodity that is low-carb!

Sanjeev said...

> implying you need that more to do the same thing

in response to resistance there is more but it's not doing the same thing.

obviously it's not ... blood lipids, blood pressure ...

Which effects of insulin are reduced at high chronic levels? I don't know.

What reactions are encouraged at high insulin (which don't happen or happen at low to zero rates with normal insulin)? I don't know.

> What about if they were both on identical diets (i.e. disregarding hunger/satiety for the sake of argument)

if they were twins and you magically gave one IR, then kept both on identical diets I would think their body compositions would be roughly the same.

> experience the Goodly Goodness of Goodity that is low-carb

giggidy giggidy giggidy. Is it a coincidence that the skinny one gets most of the action?

experience the Goodly Goodness of Goodity that is Goofy Gary's grasping at straws Glucose free diet for the gullibly gormless.

Evelyn aka CarbSane said...

@Chris: The problems HAVE to be "non-nutrition related" because otherwise his supposedly botched-up metabolism can only be blamed on his LLVLC these days. I believe you've followed Jimmy for a while and are probably aware that several years ago he was remarkably insulin sensitive ... this seems to have deteriorated a bit (as Sanjeev surmised due to up/downregulation). He's got to have something new going on for 2012!!

@Thomas T: I answered your Discussion question. (I presume that's you). I finally fixed my notifications so that I don't have to check in each day so I'll try and be more active and see if we can't get some action going back up again.

I think all things being equal, IR would have little or nothing to do with weight loss. The only thing that might differ is that the IR person might lose slightly less if insulin does stimulate oxidative phosphorylation RATE in mitochondria thus increase metabolic rate to some measurable degree.

Evelyn aka CarbSane said...

Ahhh Tonus, thanks for the laugh! Goodly Goodness of Goodity. Triple-G!!

Welcome to the Asylum Stabby! I'm not sure that between-population comparisons are applicable here ... too many confounders. The better health of PopA with lower fasting insulin and glucose (better insulin sensitivity) vs. PopB on average tells us nothing really about the variation within PopA or B. In the Paris Study, there can be detrimental factors associated with low BG. It could be a minor glycogen dysfunction leading to lower RQ. Perhaps fat burning isn't as conducive to longevity?
http://carbsanity.blogspot.com/2011/10/do-carb-burners-live-longer.html

Good point Lerner. Rosedale is also trying to use fasting or 2 hr numbers to try to convince folks that postprandial levels above these are somehow harmful.

Thomas T said...

Thanks CS, much appreciated! ;)

Stabby said...

John: I kind of just eat everything instead of restricting macronutrients, I think that low fat, low protein and low carb are all unhealthy in specific ways. I do limit to omega-6 to about 3% of calories and emphasize nutrition.

Stabby said...

A, Evelyn responded to me, I didn't see that. It looks like we're on the same page, I suppose the Kitavans aren't a great example for that reason. I suppose my question is "what would fasting glucose levels be in the case of no significant dysfunction of any type?" but that's probably beyond knowledge at this time. I think that it is lower, but overall I agree with the premise that lower doesn't always mean better.

That's a great post, by the way. I'm slowing working through all of them. Thanks

Evelyn aka CarbSane said...

Yeah, Stabby, I'm not sure we can really ever know the answer to the question of what FBG would be in the optimally functioning human metabolism.

Lerner said...

from NEJM online today:

http://www.nejm.org/doi/full/10.1056/NEJMoa1105816

Long-Term Persistence of Hormonal Adaptations to Weight Loss

"One year after the initial weight loss, there were still significant differences from baseline in the mean levels of leptin (P<0.001), peptide YY (P<0.001), cholecystokinin (P=0.04), insulin (P=0.01), ghrelin (P<0.001), gastric inhibitory polypeptide (P<0.001), and pancreatic polypeptide (P=0.002), as well as hunger (P<0.001)."

-----

I just checked on Amazon and so far there is still no book titled, "Gastric inhibitory polypeptide and cholecystokinin made you do it". Could be a best seller, it has a ring to it.

Evelyn aka CarbSane said...

Hey Lerner, When I first read the excerpt I thought "damaged metabolism", *sigh*. Then it hits you that the reductions in leptin and insulin, for example, SHOULD remain lower. I think my book will be titled the Magical Mitochondrial Tour (de Farce).

Diana said...

@Evelyn, "I'm not sure we can really ever know the answer to the question of what FBG would be in the optimally functioning human metabolism. "

Yeah - I'm getting suspicious of the whole prediabetic thing myself. I never paid much attention to the whole thing until I bought a blood glucose monitor and voila, I'm pre-diabetic. So I began to pay attention, and I began to wonder -

Is "prediabetes" like osteopenia? In other words, a condition of no real medical significance created by the fact that we are now testing large #s of people for the 1st time in history?

Genes. Evelyn, I know that you don't like genetic excuses ("my genes made me eat 12 donuts for breakfast") but in this case, the shoe fits.

(I don't discount gene expression, of course. If you eat the 12 donuts for breakfast, and you have a certain genome, you'll end up with a different FBG than another guy.)

Different ethnic groups, sexes, ages, etc. have different "normal" FBG, I suspect.

Sure, if you have an FBG of 250, you are diabetic. But 100 is pre-diabetic? I don't know. 70 may be normal for some and too low for another.

In any case, I think this is yet another manufactured anxiety of the Paleohack crowd. It's almost as if in their dismissal of cholesterol anxiety, they have to substitute another equally bogus concern.

Chris, yes, it is strange. If Jimmy feels like eating a fried pecan log and fried apples, it's all good. If I feel like eating a non-fried apple as a course of my normal diet, I'm indulging in a metabolism-wrecking habit that will put me into a pre-diabetic coma and shorten my life-span by 20 years. I will end up in an assisted living facility with my limbs amputated. OK I exaggerate, but not by much.

Quarrel said...

I've thought for a while that the biggest problem with the online n=1 LC, Taubsian debate is that essentially the ONLY thing your mug punter at home can measure is their blood glucose.

When all you've got is a hammer, everything is a nail.

Beyond weight, most people are limited to just testing their BG- so like Jimmy, they start seeing EVERYTHING through this prism. Anyone that has read much here, at PHD, or from Stephan or elsewhere in the Sane-O-sphere knows that this is a seriously multi-dimensional problem.

Unfortunately they get fodder from the Rosedale's of the world, feeding them such nuggets as ALL glucose spikes (above their already high LC levels???) are DEADLY. Of course Rosedale also tells me in his latest offering at Jimmy's that I should be suspicious of Oxygen and probably not breath, so it's getting easier to ignore him.



--Q

Evelyn aka CarbSane said...

Hi Diana, I linked to my discussion with Rosedale and I think you'll see that a goodly contingent at PH is not on board with this. I've actually been quite surprised by how many folks there are relatively high carb. So let's not paint them as glucophobes!

What is interesting is that when I did IF back in 09, I saw my FBG's slowly rise. Nothing horrible, but a few times I hit 110. But most of the day I'd be in the 70's and 80's. One of my highest ever BG's was after a vigorous 30 min bike ride (feeling great!) at around 3pm w/last food around 8pm the night before. I was in the low 70's before and as memory serves was somewhere like 126 after. Yikes!! Now that's a glucose "spike" LOL.

I have a study somewhere in young nurses from back in the 30's (or 50's -- it was an odd decade leading number) and that was the first evidence I had that we're blowing this way out of proportion in many cases.

Post a Comment

Moderation is currently on. Thanks in advance for your patience.