I had one helluva whirlwind trip to London. I don’t have time to discuss it in detail, so here’s the short version… (1) Nick Mailer tweeted about an upcoming event in London I didn’t know about just a week and a half ago. (2) After seeing the people who’d be there, I decided to jump on a plane at the last minute to attend. (3) I got to get in a couple meal chats with two key people I’ve never met in person before, Dr. Aseem Malhotra and Dr. Malcolm Kendrick. Both are well known in the low carb community, but don’t often attend or speak at conferences in “The States”.
On top of that, I got to connect with many of my favs like Ivor Cummins, Dr. Zoe Harcombe, and of course, Gary Taubes. As a final surprise, they invited me to join the panel discussion on the final Sunday.
Social & Comments Growth
Yes, I know I have a big backlog of comments to respond to. Yes, I know I haven’t been as responsive on Twitter as I “normally” am. But please note:
- I just got back from the trip to London (above) and always have a number of post-conference connections I have to work through afterward.
- And more importantly, I’m now getting way, way more comments here and on social media than even a couple months ago — much less a year ago!
Meanwhile, my twitter following had crossed the 10k last week and is already up another 300. Are you kidding me? At the beginning of last year, I didn’t even have 1000.
I don’t say this to brag — quite the contrary — I’m telling you this in order to explain why I haven’t been able to get to everyone’s comments like I once could.
Bill Murray illustrates the feeling I have at times in the movie Lost in Translation…
Even More Shawn Baker
It’s been less than a week since my original post on this and the internet has been on fire over the numbers. Many like The Woo expressed grave concern in her very wry prose while others like Peter of Hyperlipid were breaking down the deeper biochem pathways involved (something he’s exceptionally good at).
I got some criticism lobbed my way as though my prior post was an endorsement of ignoring higher glucose and A1c. To be honest, I found that kind of amusing. But perhaps it will be helpful to really hammer home what my current position is on both the general and specific.
- If you have a Fasting Glucose of 126 mg/dL, an A1c of 6.3, and an unknown insulin — you likely have a high fasting insulin and are at risk for diabetic complications.
- If you have a Fasting Glucose of 126 mg/dL, an A1c of 6.3, and a high insulin level — you likely are at risk for diabetic complications.
- If you have a Fasting Glucose of 126 mg/dL, an A1c of 6.3, and a low insulin level — …I have no idea what you are at risk for.
I spent about two hours looking for any studies with a focus on heightened glucose with low insulin that includes no genetic abnormalities – and (…prepare to be shocked…) I came up empty. Yes, this is an extremely unusual circumstance around an unusual individual. Would you believe Shawn Baker at 50+ setting athletic records while only eating meat would be a corner case?
So to get this on the record with extra emphasis: I have no worldly idea of what the long-term health ramifications are for Shawn Baker. But I haven’t heard a compelling case in either direction to sway me yet. It’s just a lot of unknowns… and that’s okay!
Maybe I’m the odd one out here, but I expect lots of uncertainty and appreciate the opportunity to tackle it.
I wonder if there is any data on the Inuit (eating a traditional diet only) on blood glucose levels? I cannot think of any other traditional populations eating a meat only or very low carb high animal product diet.
One question I had on Shawn’s numbers is whether the FBG was measured or calculated? I had a similar A1c (6.1) and low insulin (under 3) and high calculated FBG, but when I measured the BG it is never that high. I don’t think we know a lot about “optimal” states on a low carb or Keto individual.
Good points, Colleen. I may do some more looking into calculated FBG myself…
It may be wrong. My last HbA1c level was 5.0 (not totally meat diet…but nearly so), which calculates to an average blood sugar level of 97. However, my continuous glucose monitor showed that level only in the morning,and estimated my HbA1c in the low 4s.
Inuit had a genetic mutation that altered their metabolism to avoid ketosis, which was interesting. They may not be comparable to blood labs in a non-mutated person for that reason.
Hi Dave. Thanks for all this – glad things are going so well.
I feel that the waters are further muddied with Shawn, not in spite of but because of his levels of physical performance. On the one hand it’s hugely encouraging that he’s so physically capable, but on the other, it’s a bit of a confounding factor. His body is subjected to an unusual level of….use. If it were to, er, wear out early, it might be difficult to say whether that was because of an unusual diet, or because he demanded a lot from it. I’m not saying he shouldn’t do what he’s doing – I’m doimg it myself, but as you say, it’s hard to draw any conclusions, and I’m not sure whether time will in fact tell in this case.
Your point is definitely well taken! But corner cases are also good for inspiring new ideas on how the metabolism works even when it’s failing. We can see what it’s trying to do at one of the spectrum, successfully or not.
Some people will want to apply Shawn’s unique circumstances to themselves, but I don’t find that a compelling enough reason not to examine it openly and with interest.
I would have thought wear and tear on the body would show up on his HS -CRP. CRP flies when the body is under stress, his was 0.6 That is the confounder to me. His fructosamine test will be more revealing.
I would’ve thought likewise. This will be in my upcoming article, btw. When I’ve done very long distance runs (half and full marathons) — my CRP shot through the roof! My guess is Shawn’s body is far more adapted to these stresses given the exercise load he regularly takes on.
RE: Dr B’s results: Well, I found something interesting re HbA1c and get bacteria:https://www.medscape.com/viewarticle/893776?src=soc_tw_180314_mscpedt_news_mdscp_micobiome&faf=1 So is it lack of fiber causing (via Microbiome ) A1c to rise? Wild Wild West down in the gut!
Cool find, Shaza! It certainly would be very interesting if this actually came back to the gut biome.
I’m a gut bacteria questioner. Amber O’Hearn (http://www.empiri.ca/) has looked into this. Not only does she also eat only meat, but she also has arguments that “fiber” is not necessary. I tend to agree, especially considering entire segments of the human race get along fine without much if any fiber (see Comanches in the US, which ate basically buffalo). I think your body and your bacteria adapt to whatever you eat. If it didn’t, we’d be dead as a human race thousands of years ago.
I eat very few vegetables (no grains, no fruit…90%-100% meat, depending on day) and my HbA1c was 5.0 last time I checked it. I only workout 2 times per week, though.
Good point. I had a discussion the other day, about gut bacteria adopting to whatever food we feed it and gave as an example, the British who had his biom mapped, before spending time with the Hadza and eating whatever food they ate. Upon his return, he got retested and discovered that his gut was now populated with new spices of bacteria. Alas it didn’t last, once he went back to eating what he was used to.
Currently, I’m on meat only diet after transitioning from Keto. During this time, I saw my HBA1c drop from 4.6 to 4.3.
Correction: GUT bacteria
“If you have a Fasting Glucose of 126 mg/dL, an A1c of 6.3, and a low insulin level — …I have no idea what you are at risk for.”
People with untreated Type I Diabetes have high FBG and very low insulin. They die an early death. Insulin is a good thing.
My husband is a type 1 diabetic, they get sick very fast and do not linger at the gym before diagnosis! Shawn does not have type 1 ! I did carnivore trial and remained so, I had same thing in Australia, daily glucose averaging about 4.6 with range 4.3 to 4.9 yet my A1c was 5.3! I am going to have fructosamine test that zeros in on 2-3 weeks via albumin. I can not repeat A1c as it is only offered once a year in Aus to non diabetics. ( for free that is!)
I didn’t say that Shawn has Type 1 Diabetes. I was responding to Dave’s insulin-centric analysis, which seems to suggest that low insulin is the Holy Grail. One counterexample is enough to show that low insulin and bad health can coexist. I doubt that much can be made of one FBG of 126, regardless of insulin, other than it’s a little weird. Then again, eating only meat by choice is a little weird.
I’m not sure where you gathered I was suggesting “low insulin is the Holy Grail.” I was actually highlighting uncertainty above.
My work is very much centered on energy homeostasis and T1D have physiological challenges in this capability. This is why they can have a terrible rollercoaster ride of high and low glucose even when managed. Simply having low or no insulin isn’t the only component of this analysis — it’s whether it is due to dysregulation. T1D isn’t just the *circumstance* of having low insulin.
Hi Sharperhawk, if you had T1D insulin levels you would lose body mass quickly. Obviously Shawn has enough insulin to bulk up. It’s just the case that his insulin response isn’t so interested in endogenous glucose as it is in digested protein.
His picture is similar to this.
@ Dave feldman, Here is another pattern emerging with the carnivores, super super low HS CRP! Here is a contrast: My husband a type 1 diabetic on LCHF runs CRP 3.7.
Type 2 diabetics are notorious for higher CRP values.
On LCHF I was 1.4, after Carnivore trial CRP plummeted to 0.6. Shawn’s CRP super low too, 0.6 as well.
How can type 1 or 2 have super lower CRP? ( they don’t on normal diet) . For me that is the deal breaker re these higher A1c reading with low CRP and low DAILY glucose readings. Shawn’s last daily glucose he posted after 300g steak was 4.9 or 88. Shawns daily glucoses are low too. That is where is mystery is!
Lots of papers on high CRP pre type 2 diagnosis. I don’t think Shawn is pre-diabetic.
Interesting points, Shaza. Speaking of which, I hope to have an article out on CRP myself soon…
Fantastic, It is an area I think will hold a lot of clues, if not answers. (Sorry late thanks, I am in Australia vis a vis big time difference) What if all meat diet is a way to lower CRP and all the knock on effects. Before LCHF my CRP was 1.6, on LCHF it was 1.4 before Carnivore. After carnivore trial it came in at 0.6 Now I am adding small carbs back to diet to what happens on next HS CRP …. about 20 – 40 g a day. Will take blood test in 6 months.
Perhaps through glucagon mechanisms??
Yeah, I’m hoping Shawn will get a fasting glucagon test soon. I’d be interested in its index with insulin.
Hey Dave. I’ve been enjoying your website and videos on cholesterol. I am metabolically dysfunctional with high trigs. My first goal through keto/lchf is to impress the socks off of my cardiologist in June. It is my understanding that I need to reduce my trigs first. I also understand that my overall cholesterol panel will somewhat normalize as I lose weight. Is it correct to believe that the key to lower trigs is to stop sugar? If so, I’m on the right track. I also understand that prior to my blood test I need to stop using body fat as energy, lock that fat up into cells so it’s not free in the blood, by means ingesting high amounts of good fat. You mentioned you ate bread for a couple of days prior to your blood test. Did that raise your glucose? I want both to be stellar. Also, I have a question. How does the fat (trigs, even cholesterol) leave the body? Through poop? Burned up as energy? I see a lot how it is recycled through the liver and redistributed. But I want it gone. Does that only come with decreased adipose tissue, or will I be fighting my doc over statins forever?
Can I have you plug your numbers into our report tool before moving forward? It helps to see the nature of your lipid panel and especially how long you’ve fasted before the test (this can explain the higher triglycerides too).
Just go here: http://cholesterolcode.com/report/ — and copy/paste your report text back here. 🙂
CholesterolCode.com/Report v0.9.2 ====–
…1.5 months on Keto (less than 20g carbs) ::: 12 hours water fasted…
Total Cholesterol: 242 mg/dL 6.26 mmol/L
LDL Cholesterol: 164 mg/dL 4.24 mmol/L
HDL Cholesterol: 39 mg/dL 1.01 mmol/L
Triglycerides: 239 mg/dL 2.7 mmol/L
Remnant Cholesterol: 39 mg/dL 1.01 mmol/L >>> Medium-High Risk Quintile
Remnant Chol to HDL: 1 >>> High Risk Quintile
Go to https://tinyurl.com/y8hokam2 for more on Cholesterol Remnants
–ATHEROGENIC INDEX OF PLASMA (AIP)–
AIP: 0.427 >>> Highest Risk Third
Go to https://tinyurl.com/ycccmmnx for more on Atherogenic Index of Plasma
–CONVENTIONAL MARKERS AND RATIOS–
Friedewald LDL-C: 155 | Iranian LDL-C: 256
Total/HDL Ratio: 6.21
TG/HDL Ratio in mg/dL: 6.13 | in mmol/L: 2.67
First, as always, I emphasize I’m not a medical professional and this doesn’t constitute medical advice. I’m just an engineer obsessed with lipids. 🙂
– Yes, certainly I’d recommend tackling your triglycerides (TG) right away. If you drop your carbs down substantially, this will typically reduce your TGs, but this can take a while depending on how far along you are with insulin resistance and metabolic dysfunction. Sometimes this can take quite a while to heal.
– I *don’t* recommend doing the protocol for two reasons, (1) you’re very early into the diet and (2) you should be seeking a “baseline” first so you have a good idea of what your normal numbers are.
– I *definitely don’t* recommend adding carbs. While I share my findings with regard to my Phase II experiments, I emphasize they are preliminary and much harder to control. Carbs can hit an overage point where you get the worst of both worlds, higher glucose AND higher TGs/Cholesterol. I’m a special case now given how much I’ve been “mapping” my metabolism to know the threshold points.
More than anything, I think the triglycerides by themselves are the most important thing to focus on. High TGs are far more associated with both CVD and all-cause mortality overall than LDL cholesterol by far.
Here’s a study of a population with HbA1c 6.9% and low insulin.
Looks pretty good, if you avoid glucose spikes, as Shawn does.
So I just did the 3 day protocol and this is so cool. I have a spreadsheet of all my food data and test results (I tested at home with the cardiochek almost everyday) I also have several years of test results, and the results of the three day protocol support supports what you are saying, it is really cool!! Are you interested in any of this data from people? and if so is there a place to send the excel sheets to? Thank you so much for your work. Next I am testing if I can get the same results with a little less calorie intake, it was not a fun 3 days LOL. Have you considered seeing if there is a percentage of calorie increase that will work per individual based on their normal calorie intake?
Hi Dawn! Any data we can add to our blood pool is appreciated, you could submit in the comments as text or if you’d prefer to send the file in to the team you can email it to me at email@example.com or to the general cholesterol code email at firstname.lastname@example.org
As for calorie intake, I’m not too sure, perhaps it is something Dave has thought about, so I’ll ask him when he’s back from his hiatus. 🙂
Agreed on the difficulty though! I’ve done the feldman protocol as well, and despite how it sounds eating a lot is just not fun!
While doing the Feldman protocol, he mentions avoiding coffee. Is this because of caffeine? If not, why?
Caffeine, and possibly coffee in general, increases fat trafficking in the body and can increase triglycerides and LDL. This isn’t 100% confirmed yet but has shown to be a source of problems for people who have done the protocol, and there is research to back up the mechanism so it’s recommended to avoid it as it may skew results.