Here I come to save the day ....

.... it means that Mighty (Meta)Mouse is on {cue record scratch sound}



A couple of years ago I wrote the following blog post:  Mighty Metabolism Mouse discussing this study:  A high-fat, ketogenic diet induces a unique metabolic state in mice.  









If you take mice and put them on a low protein (5%), very low carb (2%) ketogenic diet, they lose some body weight, despite consuming the same number of calories.  Taubes' theories were already waning in popularity by at the time of that post, and folks were hanging their "metabolic advantage" hats on studies such as this one.  It turns out that they lost weight to the tune of what mice consuming a calorie restricted diet (only 66% of baseline calories, or 1/3rd less) did, and had energy expenditures roughly 11% higher than the regular mice and 15% higher than the calorie restricted ones.  In other words, they don't violate the first law of thermo or the common dietary acronym CICO, but this proved that ketogenic diets increase calories out so that these mice effectively could eat more.

This is why I dubbed the KD fed mouse the Mighty Meta Mouse.  Now, this superpowered metabolism was not without some inconvenient side effects, most disturbingly hepatic steatosis, aka "fatty liver".  But from a weight loss angle, a closer look revealed that this keto diet wasn't all it was cracked up to be in that regard either!  As I've highlighted previously, the low insulin state is associated with fuel partitioning to fat at the expense of lean tissue, not the other way around, as we're told by the insulin is *the* fattening hormone crowd.  The keto mice had more fat and less lean than the chow fed mice despite having one-tenth the basal insulin!!


I followed up that post with some musings on the applicability to humans.  I cannot stress enough how rodents differ from humans, between species of rodents, and even between different strains of the species.  We need to be very careful when extrapolating the results of such studies to humans.  HOWEVER .... Time and again, the rebel-without-a-clue "alternate" nutrition community repeats the same transgression:  
  • Study seems to support your diet, LOOK HERE!!!   Diet not quite yours?  That's OK, close enough.  Pigs are humans right?  Everything your doctor tells you is wrong ... you know the drill.
  • Study seems to refute your miracle diet, DON'T LOOK THERE!  Good thing I'm not a rat (or mouse or pig), that diet is not really like my magic diet, it contains more carbs or the wrong kind of fat, etc.  ... you know that drill too.
You cannot have it both ways.  To me, the moral of this particular experiment was that "unique metabolisms" induced by extreme diets can be created at great expense to the organism.  Would this "expense" be paid by the human?  There's a reason we'll never know for certain.  

But I've been banging one drum about mice for a while vis a vis the whole "insulin is the fattening hormone" thing, and yet another (sigh) book invoking "science" to show how insulin causes us to cannibalize the lean and give to the fat.  Even more simply put, "insulin is the fattening hormone" doesn't hold water in the face of massive amounts of rodent data.  Unless you're going to claim that insulin does different things to the mouse than to you and me (careful, if you do you might as well toss out all that elegans research! ).  The most cognitive dissonance inducing mouse is LIRKO.  That mouse, lacking insulin receptors in the liver, becomes profoundly hyperglycemic and hyperinsulinemic but not obese or diabetic.  Indeed the longer things go for this mouse it becomes hypOglycemic while it's hulk of a  pancreas keeps pumping out insulin ... and still no obesity.  In our Meta Mouse, we have almost no insulin!  And yet, while the standard fed mice averaged 33.5 grams body mass, only 13.5% of that was fat, Meta Mouse only tips the scale at a svelte 29.0 grams!  Yay!!   Errrr ... not so fast, because MM is also 17.8% body fat.  For those into statistical fun and games, that's almost 14% more fat mass in absolute grams, but a whopping increase of 31% of the body fat percentage of a normally fed mouse.  It's just not looking good for the "lower my insulin" gang at the moment.

Oh wait!  These are mice!!  I almost forgot.  Someone remind Fat Head, because if calorie restriction making mice fattier is blogworthy, then surely ketogenic diets doing the same is at least worthy of comment {chirp chirp}.  

Now the other day on Facebook, Jimmy Moore posted this in response to a new study on a ketogenic diet in mice:


Here's the PubMed Link.  The responses in comments were typical, a bit amusing, and at the same time quite annoying.  To paraphrase the worst:  
How can the mice become diabetic if they eat no carbs.  This makes no sense!
You're right.  That makes no sense if you have a simplistic view of diabetes as fed to you by the irresponsible advocates of low carb "science".  To be fair, this idea that carbs cause diabetes has been somewhat adopted in the mainstream,  but this does not excuse the so-called geeks and buffs who claim to regularly research this stuff.     First of all, while there is SOME evidence that ketogenic diets are a treatment for diabetes, there is no evidence, that I'm aware of, that ketogenic diets are preventative for metabolic syndrome or diabetes.  As a treatment for T2, keto almost never seems to improve -- either anecdotally or experimetally -- insulin action in response to a glucose load.  Let's be clear here as well.  We're talking ketogenic diets, not low carb, most of which are not ketogenic after several weeks.   How many "my glucose goes over 200 when I eat a small potato" accounts do we need from formerly non-diabetic low carbers before they wake up?  

There is very limited human data on this.  The rodent data does NOT look promising.  For all of the "get off the meds" claims made about low carb diets, the longest study in diabetics didn't really deliver quite what it was hyped to.  It seems that "resting" your pancreas isn't doing it much good after all.    

Before I delve into this new study, it seems that Richard Feinman had a "me too" moment about keto mice that don't lose weight.  Heck, he even managed to make them obese!!  Paging Fred "you can't get obese on LC" Hahn!!!  Feinman tweeted out a link to this study on Pinterest:  Response of C57Bl/6 mice to a carbohydrate-free diet.   The chart of the weights of these mice shows a different story vs. Kennedy (the Meta Mouse).   The difference? Perhaps because Feinman's mice consumed a higher protein (20%) chow than did Kennedy's (5%).  So ... maybe protein really is like chocolate cake after all, because while initially they consumed about 10% more calories, this leveled out after 4 weeks and they ate comparable amounts.

WHAT?  You read that right, in this study, as compared to the Kennedy study, the keto mice ate roughly the same amount of calories but just got bigger and bigger and appeared to be getting bigger still!  Feinman and co-author's conclusion?  
The results suggest that rodent models of obesity may be most valuable in the understanding of how metabolic mechanisms can work in ways different from the effect in humans.
Ya got that??  Get a result different than expected, or different than other researchers got (that bolstered your views) and now rodents become useful in elucidating our differences.   Because you see in mice:
Consistent with the obese phenotype, experimental mice had fatty livers and hearts as well as large fat deposits in the abdomino-pelvic cavity, and showed impaired glucose clearance after intraperitoneal injection.
Worry not though, because ...
The high fat-fed mouse is a widely investigated model of obesity, insulin-resistance and susceptibility to diabetes. The C57Bl/6 strain, in particular, when subjected to high dietary fat, shows increased consumption, increased efficiency of fat storage (weight gained/calorie) and becomes insulin resistant [1-4]. As a model of human obesity and insulin resistance, however, it suffers from the severe, if under-emphasized, limitation that high-fat diets do not generally cause these conditions in humans unless the diets are also high in carbohydrate.[No Citation Here]

That last paragraph is from the Introduction, so as we can see, there's no scientific bias going in here.  Regarding the C57Bl/6, the impression is given that these were bred to be particularly susceptive to obesity, something I found no evidence for in the literature last time I looked.   They will fatten in response to a "fattening" diet, however.  Here's the JAX low down on our ketoschizo mouse.  Here's the concluding paragraph from reference 4:
Our findings suggested that when mice were fed an HFC diet, they could develop initial compensatory response to resist the increased energy balance; however, a prolonged consumption of an HFC diet appeared to disrupt this adaptation.
It is interesting to see Feinman -- in peer review print -- try to rationalize away the very same thing he would use to justify his insistence that a calorie is not a calorie.  Remember that debacle of a paper?   Feinman (and his cohort in thermodynamics-mangling crime, Fine) relied heavily on two things for their metabolic advantage:
  1. The metabolic cost of gluconeogenesis, and
  2. Thermogenic differences between macros as ascertained by Eric Jequier.  
Regarding #1, is Feinman now saying that gluconeogenesis is not energetically costly?  I know mice require less glucose for their tiny brains but they still must make it if they are on an essentially zero carb diet.    But surely someone as familiar with his work as Feinman has seen Jequier's Pathways to Obesity paper.  I blogged on that here.   The image at right from the blog post and F&F's paper shows their progression of effective calories for 2000 calories -- beginning with 55% carb, 15% protein and 30% fat, then substituting 1:1 protein and fat for carb.  Leaving aside their math error, they say that at 21% carb (47% fat, 32% protein) you have a 100 calorie deficit in net calories after TEF.   

This is disingenuous because the only way reducing carbs is TEFtacularly metabolically advantageous is to use protein in the substitution.  Because if you just replaced the 34% of carb in the above experiment with fat, you would end up with about 30 more calories of net energy.   For the mouse, that usually gets about 80% calories from carb and replace that with fat.  For every 100 calories of carb replaced with fat, you get 4.5 more net calories from the fat.  But their KD chow was higher in protein.  But ... but ... Oh yeah ... that doesn't count in mice though ..... (Long time readers are probably aware that my view is that TEF is likely irrelevant for a warm blooded animal, as that is just that much less energy that must be used elsewhere to generate heat).

Must be something ELSE going on.

OK ... Finally, let's get to that new paper:



They used a keto diet (PDF download) from Research Labs.  Now, some are hanging their hats on this having corn oil in it (works out to just under 12% total energy).  The rest is Primex(?) which I cannot find any info on.  Perhaps someone in this community that works for this establishment might know ;-)   Here's how the macros are reported in the paper.


In any case, they took 10 week old mice (so they'd been eating the standard low fat -- usually 10-15% fat -- for about 6 weeks at the start) and put them on KD or standard chow.  The dark circles are KD, and they initially dropped weight, but recovered and matched their controls by about the 10 week mark.   So were there other differences?  Yes:
Our data show that long-term KD causes dyslipidemia, a pro-inflammatory state, signs of hepatic steatosis, glucose intolerance and a reduction in beta and alpha cell mass, but no weight loss.
Boy am I glad I'm not a mouse eating corn oil and Primex!!!   Nothing to see here.  Not so fast!  I looked into this aspect of things a while ago as well.  Here:  Ketogenic Diets & Fatty Liver.  Be forewarned, that I get a bit snarky at Peter Dobromylskyj aka Hyperlipid in that post.  In my opinion his advocacy of high fat diets crossed a line when he began openly admitting to manipulating data to fit his biases. The acronym CIAB is pretty well known in these circles because of him, standing for Crap In A Bag.    Peter will write off any inconvenient results when the diet contains PUFA or transfats, and yet when other studies use those same fats and get positive results for his view, that's ignored, as are studies that yield negative results using lard or butter.   As stated in the post, when one casts the net a bit wider we find that butter is actually quite "toxic" and fatty-liver promoting ... and INFLAMMATORY.    Peter has also "speculated" about how a fatty liver might even be beneficial, and is likely responsible for people around the IHC referring to "physiological insulin resistance" as something beneficial.  Heck, some have followed his lead so far as to imply it is life saving (but only if Robert Lustig is chasing you with a syringe full of insulin and you are not diabetic).

What made this study unique is that they investigated what happened to the pancreas ... and not just the beta (β) cells (that produce insulin) but also the alpha (α) cells (that produce glucagon).  In most diabetics, it is the β-cells that are compromised (in T1's completely) while the α-cells remain intact.  Glucagon's major role is to prevent hypoglycemia by stimulating endogenous glucose production, EGP, in the liver, a combination of glycogenolysis (glycogen breakdown) and gluconeogenesis (synthesizing glucose from glycerol, certain SCFA or certain amino acids).  Contrary to low carb lore, if protein "spikes" your blood sugar, it is because of an inadequate insulin response to glucose to suppress glucagon.  (The Cause of Hyperglycemia in Type 2 Diabetes).  

So:
  • Triglyceride content of the liver was more than 2X controls
  • Circulating lipids, hormones, etc.:
  • I would note that in this case (vs. Kennedy) circulating triglycerides were also elevated in KD.
  • The progression of glucose tolerance.  Early on, there was reactionary insulin hypersecretion to maintain normoglycemia.  By 5 weeks there is a worsening of glucose tolerance that is described as "profound" by the 12th week.  Note how the early peak of insulin (though not pronounced in controls seems to be muted in the KD).   It's important to note not only insulin levels but changes and the impact on glucose levels.  At 20 weeks, the mice appear to be hyperinsulinemic in the fasted state.

  • "After 22 weeks beta cell mass in KD-fed mice ... was decreased. The density of islets was unchanged, but the median beta cell cluster size was significantly decreased. This was due to a relatively increased number of islets with a size smaller than 2500 μm2 in KD-fed mice."
  • "The alpha cell mass was reduced by 50% in KD-fed mice after 22 weeks"
  • Taken together the ratio of alpha to beta cells decreased
"This indicates that long-term high-fat, low-carbohydrate ketogenic diets lead to features that are also associated with the metabolic syndrome and an increased risk for type 2 diabetes in humans."
Interestingly, these researchers did address the fatty acid content of the diet:
Dyslipidemia and the pro-inflammatory state induced by KD may be the consequence of the high content of saturated fatty acids. It was shown that a short-term polyunsaturated fat enriched KD did not adversely alter lipid metabolism in adults (15). Also supplementation of a high-fat diet with omega-3 polyunsaturated fatty acids has been shown to prevent high-fat diet-induced insulin resistance by reducing inflammasome-dependent inflammation in rodents (41). However, in our study the higher content of omega-3 fatty acids in the KD could not prevent pro-inflammatory effects on the long-term. Whether further modification of the fatty acid content of KDs can attenuate dyslipidemia and the pro-inflammatory effects on the long term needs further study.
What about choline?  Addressed:
However, the similar methionine and higher choline content of KD in our study did not prevent signs of steatohepatitis on the long term. 
There were two other major points in the discussion (without repeating the obvious).  First, that their study was longer and in somewhat older mice than previous studies.  Short term results were not predictive of the long term effect of a diet.  Keep this in mind when human studies on keto and LC diets last in the 3 to 6 month range.  It is quite possible that some of the trajectory of weight rebound is metabolic adaptation as seen in the mice.  But this is a stark reminder that short term improvements cannot be translated to the long term.   Here is where I always get myself in trouble, but I can't help but point this out.  The ONLY long term human data we have is anecdotes from LC advocates, yet another one of whom passed away at age 71 "unexpectedly" of undisclosed causes last month.   We're told all the time -- and I agree to a large degree -- that we can't always tell a person's state of health by looking at them.  All of these healthy looking low fatties are really just one Oreo away from dying ... don't let appearances fool you!!   It's the low carbers who look generally less robustly healthy than their peers ....   (sigh)

The second discussion point is in regards to the alpha cell demise.  They write:
In relative terms this decreased alpha cell mass was even more pronounced than the reduction in beta cell mass resulting in a major decrease of the alpha-to-beta cell ratio. Decreased glucagon levels lead to less gluconeogenesis from the liver, which may prevent hyperglycemia in KD-fed mice.  Whether this change in alpha cell mass is a direct consequence of KD or a response to counteract glucose intolerance remains to be elucidated.
These mice did not have elevated fasting glucose and it would appear to be due to reduced glucagon levels.    I wonder what some of these long term low carbers have for glucagon levels?

EDIT:  I'm going to add this one more study (ht Charles Grashow) so they are all in one place.  A high-fat, ketogenic diet causes hepatic insulin resistance in mice, despite increasing energy expenditure and preventing weight gain.  Similar story:  Increased hepatic lipid accumulation, hepatic IR and diminished whole body glucose disposal.  /EDIT

In Summary:

  • Ketogenic diets often result in short term weight loss but over longer terms they can even result in obesity.
  • KD have a propensity to produce hepatic steatosis
  • KD often result in most/all features of metabolic syndrome
  • KD appear to reduce pancreatic function
... in mice.  I'll leave you with two more old studies/blog posts of mine:  How Fatty Diets Cause Diabetes, and Revisiting the Fatty Diets & Diabetes Study ~ How to Make Mickey Fat or Fattier.

What do ketogenic diets do in humans over the long term?  Do YOU want to be a guinea pig??

Comments

charles grashow said…
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2980360/

A high-fat, ketogenic diet causes
hepatic insulin resistance in mice, despite increasing energy
expenditure and preventing weight gain

"In conclusion, the present study shows that a high-fat KD causes hepatic insulin resistance in mice, which can be attributed to an increase in hepatic DAG content, leading to PKCε activation and subsequent impaired insulin signaling. Moreover, this study found that a KD increases energy expenditure, which results in weight loss. Given the widespread use of
KD in the treatment of obesity and the role of NAFLD and hepatic insulin resistance in promoting type 2 diabetes, these results may have important clinical implications, as obese patients on such diets could lose weight but develop NAFLD and hepatic insulin resistance."
charles grashow said…
Jimmy Moore
6 hours agoWe visited the world-famous Dain's Place (http://dainsplace.chopshack.com/)
in Durham, North Carolina for lunch on Sunday with Dr. Eric Westman
before our book signing in Raleigh. When I looked at the menu, I
couldn't help but notice a very
peculiarly named menu item--"The Defibrillator!" Of course, they're
poking fun at the people who think consuming a high-fat meal will give
you heart disease and it reminded me of the same tactic used by the
Heart Attack Grill franchise (http://www.heartattackgrill.com/) out west.


Of course, you know me, I wanted to provide a little pizzazz and
bravado when I ordered this thing sans the bun and chips. I said, "Can I
have a side of butter instead?" The startled waitress asked, "Butter?
What's that for?" I explained that I consume a bite of butter with every
bite of food being on a low-carb, high-fat diet. So she brought me a
couple of pats and I asked if I could have more than that. "How much
butter are you going to need?" I said, thinking conservatively, that 6
pats of real butter should do the job. The look on her face was
priceless!

I could have easily consumed a whole stick of butter
with the Defibrillator meal, but I think I freaked the server out. She
called her owner and he was so intrigued that he asked her to take a
picture of me eating big chunks of butter with my food. This is normal
to me, so I didn't have a problem with it. They were so enamored by it
that they posted the picture on their Facebook page: https://www.facebook.com/photo.php?fbid=474812415964000&set=pb.376035655841677.-2207520000.1390233265.&type=3&theater


I guess you could say I doubled-down on what they thought was already a
pretty high-fat meal. They ain't seen nothin' yet! Something tells me
that server will be telling this story to any customer who orders this
from now on. Next time I come back, I said I wanted a full stick of
butter with it! LOL!
Tolovana said…
It appears to be a commercial product for Deep Fat frying:
http://www.stratasfoods.com/Products/Food-Ingredients/Brands/Primex.aspx

Their pamphlet states that it's Palm based.
David Pete said…
One day that poor man is going to stay out in the sun too long, and end up a big puddle of grease.
carbsane said…
Thanks! Could be some transfats. Palm is generally considered LC/paleo friendly.
carbsane said…
FYI FOLKS


Disqus Dashboard has been hanging up for me for a day or so now. I try to approve the newer comments in moderation using email (mostly those with links, others should go through unless it's your first time), but just wanted to give a heads up in case you feel I'm snubbing anyone.
Lighthouse Keeper said…
Wonder if it was Kerrygold though ?
charles grashow said…
the Defibrillator meal includes a hot dog - processed meat - very bad to eat
charles grashow said…
Are hot dogs noe paleo/primal?
Karin said…
It looks like the guy behind JM is ready to vomit into his napkin. I share the sentiment.
Derek Hurst said…
Do all of his militant followers actually find this appetizing? At least following the bacon brigade, the pictures of bacon doesn't absolutely turn your stomach.
ExEffectsGuy said…
I doubt the owner and waitress were "enamored" with JM.He needs to check the dictionary. Incredulous is probably more appropriate.
Bob Joey said…
Actually Plant Positive is back to save the day, crushing Taubes and the NuSI into smithereens:

http://www.youtube.com/watch?v=Gap7v2fNpas&list=UUHZOzR0lYzbECKm8dhiDSMA

Enjoy.
David Pete said…
So I was looking at JM's facebook page after seeing that picture and found this little gem
"Is Fat or Sugar Making Us Fat?: http://www.eatchicchicago.com/blog/is-fat-or-sugar-making-us-fat ~ A Chicago-based RD named Amari Thomsen from "Eat Chic Chicago" absolutely nails it on calories, cholesterol, sugar and the hormonal impact of it all. I'm so encouraged to see young dietitians like Amari speaking truth of nutrition rather than simply parroting the party line that the national dietetics organizations would have them to say. She quotes from and references the work of people like Tom Naughton and Dr. Robert Lustig while echoing many of the messages you have heard from the leading voices in the low-carb community over the years. ENJOY!"
The Work of Tom Naughton?!?!? LMFAO
Tolovana said…
A bit of research turns up that Primex Z is "zero trans fats per serving" but I couldn't find out what the serving size was, or find a nutrition label.


Regular Primex is hydrogenated.


The American Heart Association shows that regular Primex is Palm and hydrogenated Soy oil : http://www.heart.org/HEARTORG/GettingHealthy/FatsAndOils/Fats101/Saturated-Fats_UCM_304609_Article.jsp


This company sells it as a lab diet component: http://www.dyets.com/ingred.html (I found this source cited in this study: http://ajpgi.physiology.org/content/302/8/G840 )
Lighthouse Keeper said…
A nice little delve into how pseudoscience hijacks science, well spotted David.
charles grashow said…
Jimmy Moore
7 hours ago


My low-carb, high-fat, ketogenic meal today: 4 pastured eggs cooked in Kerrygold grassfed butter with Colby Jack cheese, pimiento cheese, salsa and sour cream. Yep, that's a ton of dietary fat, but it's what helps me get into nutritional ketosis in conjunction with my personal carbohydrate tolerance and protein threshold levels. This one meal could hold me for upwards of 18-24 hours at a time! Looks freaky to people who fear fat, but this is the
ketogenic life for me. My fasting blood sugar this morning was 73 and I feel fantastic.
carbsane said…
I very much appreciate your taking the time to find this. I just don't have the time at the moment to chase things that don't come up right away.

So we've got some transfats involved in this study, but not- to my knowledge-- the others. Must revisit. Thanks again!
ExEffectsGuy said…
That Kerrygold is MAGICAL!
ExEffectsGuy said…
Tom is a nice guy and lives on a farm. I believe he might even have killed a chicken PERSONALLY! What more credentials does one need? He actually seems like a nice guy but a bit dogmatic and I doubt he himself would try to pass himself off as an expert.
Now if he hadn't begun the whole video with minutes upon minutes of picking away at Attia's career or statements, I think it would've been an overall good argument.
carbsane said…
Is this McDougall? I feel like I'm left out on one of those open secrets not being part of this side of the nutritional sphere.
No, PlantPositive is a videoblogger/blogger. He's actually commended your efforts in one of his videos vis-a-vis Taubes and the CIH.
carbsane said…
NOTE TO SELF: If ever suffering from insomnia, listen to PP videos. ;-)
carbsane said…
Not knocking him (except I was cold and wired last evening and after putting that on dozed off nicely ;-) ) , just I've seen McD refer a lot to PP videos, so wondered if that was an "open secret".


I kinda wish this person wouldn't alter his voice with software.


Thanks for the clarification.
Heh. The deal over his voice is funny. Because initially, a lot of people thought it was Don Matesz while Colpo and others were just making jokes that he's too soft voiced from eating all that vegan food.

A lot of folks in the vegan and plant-centred sphere refer to this videos, so McDougall wouldn't be the only one. He's quite content making his own videos from what I've seen.
carbsane said…
Funny you should mention Matesz. I always thought it was him early on and if someone asked me to guess, I don't think there's even a close second. I just thought McD's mention of some of these vids in his interview with Jimmy might have been a tell. Still, there's something about PP that whispers former insider :)
Bob Joey said…
Unsubscribe.


Joshua Kline
Legal and Financial Translation
DE-EN, FR-EN, ES-EN

joshuaklinetranslations@gmail.com
josh.kline@yahoo.de
Granada: (+34) 680.110.503



Disqus schrieb am 16:45 Freitag, 24.Januar 2014:

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A new comment was posted on The Carb-Sane Asylum
Yeah, I could see why people thought that but just couldn't accept Matesz. Something about the tone, focus and style of language employed by PP just doesn't align with the kind of material produced by either Matesz or McDougall. Matesz tends to repeat too often and McDougall's much more to the point. I guess he's just referenced because he bothers to go on for as long as he does in his videos. Taking the video above as an example, I think the first five minutes were largely pointless, but that's my opinion.

From his earlier videos, there are some confessions about being allured by Paleo but then not going down that path. One can speculate further on that premise, but I can't draw any conclusions. Maybe he is a former insider--I wouldn't be surprised if he were--but I think he's probably one of the younger more focussed types in how he tends to tackle topics and address the gurus of the scene.

Also, to be honest, I am not sure if he's using a voice filter or if that's his real voice.
carbsane said…
I can't relisten to tell you where, but there's a point in this video where his voice changes and then fades back to soft. I always suspected a filter, but he messed up there ;-)


For the most part I can't find fault with what he does. If/when he misrepresents something I'd call him on it, but eh ... he should contact me behind the scenes to exchange notes because he seems to find some stuff I haven't and vice versa (and perhaps gets some of his stuff from me and runs with it).


Either this person is UBER polished, or they spend a ton of time on these videos. I've made a few. They are quite time consuming no matter what. A smart dude, knowledgeable of the literature. It's the agenda I will always be skeptical of. (As others are of my supposed one, which is fair until it devolves into personal attacks).
LWC said…
I never considered he might be using a filter. I just thought his voice sounded odd.



Can't argue with his documentation though, as you note. I think he's up front with his agenda. At least it seems so to me.
carbsane said…
Yep ... no problems with the agenda ... it could lead to bias, but for the most part his references back up his assertions. I wish I could remember where in this video the voice changes. But it does!
That's quite a spot, Evelyn. I have made somewhat of an effort to watch his videos.

Agreed on the other points. I mean, when I first got wind of this guy, I was put off by his agenda, but going through his videos, I found that his agenda was actually beside the point and where it does take centre stage, he actually manages to support it just find without having to resort to painful mental acrobatic. There is little fault or objection to his take on the science when compared to the contrary folk on the web who sometimes spread absolute false information in the name of their biases or allegiances.

At the end of the day, everyone has a bias and an agenda, which is fair in my books. It's the manner in which people defend their biases and agendas, and the effectiveness with which they pull off such defence, that determines the legitimacy of their form and even the agenda itself.
Lighthouse Keeper said…
One would say his academic background is rooted in philosophy and especially logic. He does have close links to Don Matesz and Healthy Longevity . His immediate agenda seems to be the debunking of the low carb and paleo ideologs which he does rather well. With their cherry picking reaching near agricultural levels it's a case of the more debunkers the merrier.
LWC said…
Okay. So.... it's too cold to go out tonight which is my excuse for listening to the presentation posted above to try to hear the change in his voice. #yesIknowIhaveissuesleavemealone I expected that the "glitch" would be in the first 36 minutes (in the link that Bob Joey posted)... and so my guess is roughly the 25:51 mark. But then the presentation went on, so maybe you meant sometime later...


I need an adult beverage.
carbsane said…
Have one on me. You found it :D
I'd take his debunking over the massive echo chamber that's forming on the internet with regards to the fickle state of Pop Paleo.
ZM said…
"One would say his academic background is rooted in philosophy and especially logic."

He surely does not apply it. I've mentioned before that I think that the majority of his stuff is rubbish and he's no better than the low carb or paleo gurus he criticizes. In fact, he may be worse given the amount of misinformation he spreads about cholesterol and saturated fat for example.
ZM said…
"They represent their ad hoc conjectures as facts while ignoring or contradicting well-established science."

Wow, this is exactly what PP does. For example, I was watching his newest videos on saturated fat and all he does is create a bunch of ad hoc explanations for the failure of every saturated fat study while at the same time demonstrating his ignorance of statistics! He seems confused by statistical adjustments. Yes, if you're PP, every single saturated fat study is flawed. Even every clinical trial on saturated fat is flawed judging by his older articles. Of course, he never actually shows that saturated fat is harmful, he just complains about the lack of evidence.
Glenn Dixon said…
Cave men had dogs. And fire. So sure! :)