This week, Robb Wolf had Dr. Shawn Baker on his podcast, The Paleo Solution.
Baker has been a controversial figure for his embracing a meat-only diet (no plants). Naturally, this has made him a favorite target of vegans, particularly youtubers. What makes him especially interesting is that he’s not just an athlete, but he’s actually setting a number of world records for his age class (over 50!) in athletic benchmarks.
Full disclosure: I now know a number of “carnivore” dieters like Amber O’Hearn who I consider friends. But I likewise have a number of vegan friends as well, many of whom I have worked with to improve their lipid numbers.
Throughout his time on this diet, Baker didn’t take any blood tests until just a couple months ago. This first round of tests were then revealed on the podcast and proved to be quite interesting. While there are a number of them that would be worth commenting on, those I want to focus on were about the energy metabolism (no surprise).
The Glucose and Insulin Labs
- HbA1c: 6.3
- Fasting Glucose: 126 mg/dL
- Fasting Insulin: 2.6 mIU/L
The A1c and fasting glucose are certainly consistent with someone who is prediabetic and likely on their way to full-blown Type 2. Well — that is — until you look at the fasting insulin. In what circumstance would you expect a high fasting glucose with a low fasting insulin?
I see them all the time: low carb athletes.
Ironically, I just got done talking about this on Ketoconnect’s podcast (airing in a couple months). In fact, Lean Mass Hyper-responders (LMHR) are actually the most likely to have a fasting glucose in the 90s or even over 100s while also sporting a fasting insulin below 3. Moreover, this profile typically has lower blood ketones (BHB) when testing compared to their more sedentary cohorts. (I’ll have a blog post on this soon)
I myself tend to be on the borderline of a LMHR or just past the line when fully keto. In that context, I often have fasting glucose in the 90s or lower 100s and an A1c of between 5.5 and 5.7. And that’s bad, right? Creeping back toward risk of Type 2 diabetes? I certainly don’t think so given my average fasting insulin of 3 or less.
But wait — Baker is much, much higher, right? Almost 20% higher in both fasting glucose and A1c. Surely he’ll be piling up the insulin resistance as we don’t see these numbers in any other low carbers, yes?
Energy Demand Leading to Higher Glucose Sparing?
This is where I part ways with so many people in and out of LCHF. What got me into cholesterol in the first place was seeing how it was really just “ridesharing” in a larger energy metabolism. So energy delivery and homeostasis on a greater network-level scale is what I continue to find endlessly fascinating. I’ll let the Benjamin Bikmans and Michael Eades of this world tackle the finer details of the mitochondria, I want to know how the Human OS manages to traffic that energy to our cells so effectively in the first place.
Which brings us back to Baker. This isn’t any ordinary guy. He isn’t just working out for recreation, he’s an athlete’s athlete. He’s training to break these various world records in addition to a variety of other workout regimes. So if you observe (as I do) a degree of adaptive glucose sparing as being more common with low carb athletes, what do you suppose it would be like for this human cyclone?
It’s not enough to just think of where his cells are getting their energy, you have to think of how timely it needs to be at a systemic level. Is Baker more of a slow jog in the morning kinda guy? No. Is he more of an exploding HIIT adventurer that is probably keeping high muscle confusion? Yes. The latter suggests more need for glycogen stores in the muscle with a strong rotation of glucose via the liver.
This is why I asked Baker and many other low carb athletes to please do more testing for us if they (heaven forbid) get injured or for some reason can’t exercise intensively for a period of time. I suspect in such cases if all other things were equal, their fasting glucose would drop. This is what happened to me when comparing my morning glucose in and out of marathon season.
The Cholesterol Labs
Baker had the following lipids:
Total Cholesterol: 192
LDL-C: 141
HDL-C: 40
Triglycerides: 54
For these I had the following notes:
- LDL-C and LDL-P are both on the lower end for a low carber who is as lean and fit as Dr Baker is. I suspect this is due to his emphasis on resistance training, which can reduce LDL scores due to a higher rate of use for muscle repair. [UPDATE: Since writing this article, I’ve since done an experiment that specifically tested this resistance training-induced LDL lowering effect.]
- Small LDL-P is low at 283, and clearly very Pattern A.
- HDL-C — 40 mg/dL is low for a zero carber. However, as he discussed with me, he apparently has low HDL running in the family as well as a prior history of it running closer to 30. At some point, he may what to check into his SNPs and see if there’s some pushdown there.
- HDL-P was highlighted as being low (out of range) at 28. However, I see this frequently with low carbers across the board.
- Triglycerides — 54 is certainly very correlative with a very athletic, insulin sensitive metabolism.
- Lipoprotein (a) — 2 nmol/L is one of the lowest scores I’ve ever seen (maybe THE lowest).
- The score I most care about is Remnant Cholesterol which is calculated by subtracting both HDL-C and LDL-C from Total Cholesterol. His score of just 11 mg/dL is extremely low risk and suggests he has a very efficient fat metabolism. (You can use our reporting tool here if you’d like to calculate your own)
Again, I’m not surprised by the lower LDL-C and LDL-P as I’ve covered this before with my own data. As the theory goes, on one end he’s being powered by fat, necessitating more VLDL secretion. On the other, he’s engulfing LDL-P at a rapid rate for tissue repair, particularly for all that resistance training.
Final Thoughts
Baker, O’Hearn, and the many other “carnivores” are certainly conducting a very interesting, real-time experiment. I’m excited to see how this new data will manifest and what positives and/or negatives will be revealed.
At some point, I plan to do an experiment of my own going meat-only for a month, just as I plan to do likewise with a plant-based diet. I’ll be very curious as to what happens to my blood markers when comparing to my many, many labs before it.
APPRECIATE ALL YOUR AWESOME WORK AND THE TIP ON LEAN HYPER-RESPONDERS. I HAVE BEEN LOW CARB FOR 3 YEARS AND MY TC=294; HDL =102 AND LDL=180 WITH REMNANT VALUE OF 12. I AM 58 AND WEIGH 163 AND HAVE HIGH WORK OUT ENERGY BUT MY A1C HAS BEEN BETWEEN 6-6.2 FOR THE LAST 3 YRS. THANKS, WILL FOLLOW ALONG.
Great to hear, M — cheers!
Thank you Dave for all of your amazing work. I coach low carb/keto/carnivore endurance athletes. We see similar results in regards to triglycerides, insulin and A1C’s.
I enjoy reading our test results. I look forward to seeing your carnivore compared to vegan results.
That’s great, Stephanie. Please consider inviting your members to run their numbers through our report tool ( http://cholesterolcode.com/report/ ) and contribute those results to our “blood pool” data for the benefit of the community! ( http://cholesterolcode.com/blood-pool/ )
This makes me feel better about my fasting glucose. I’m LCHF but not super low carb (4 years or so). I still eat potatoes and get probably around 150g a day. I’m 45 male 5’10 142lbs. I’ve been chasing a high fasting glucose for a couple of years now. It is always in the 90-110 range (I’ve taken probably a 100 readings). I work out at least 3-4 times a week mostly resistance training. However my post prandial numbers seem pretty decent and my fasting insulin is 2.4. I can’t trust my A1C number because I have to donote blood monthly for hereditary hemochromatosis.
As always, I emphasize where I’m being theoretical and where I’m certain. So by no means do I feel this mechanistic explanation is more the latter than the former. That said, I have ample reason to believe lower insulin both fasting and via OGTT testing strongly suggests intentional glucose sparing on the part of the body.
Yes agreed. I also noticed my fasting does seem to come down as the day goes on. I work out at lunch. I even tried full keto (<50g carbs) for 3 weeks and it had no effect on my morning fasting. For the vast majority of people they should take notice when their fasting number starts creeping into the 90s.
I, like you, find human energy metabolism endlessly fascinating. I just listened to his podcast the other day where his blood tests were revealed. I love Dr Bakers attitude in the face of a lot of back lash he receives. Man, could you be on to another paradigm shifting idea??? High glucose no longer means diabetes?? Of course everything has to be taken in context(diet, exercise, overall health):) As always, great blog post and thanks again for sharing your thoughts.
Thanks, Shane. Yes, context is key! As I just mentioned on Twitter: “I think the question with diabetes and hyperinsulinemia is pretty straightforward: does the supply clearly exceed the demand? Who thinks @SBakerMD isn’t using a high volume of glucose and triglycerides at a high frequency?”
Actual picture of boat delivering @SBakerMD ‘s LDL 😉
Nice tight analysis.
A1C likely high due to Extended lifetime of RBC due, in turn, to low sugar damage
As a patreon was hoping you’d hit this and even more so that you try meat only. But I think 4 weeks might be on the borderline: for really locking definitive contrast you might want six…..
You may be right. I was planning to keep both the carnivore and plant-based experiments at equal time allotments. So whichever one I go with I’ll try to match on the other side. Obviously, six weeks would be better than four in both cases.
I have seen studies that show that the standard assumption of 120 days for a RBC in the calculation of A1C can be off as much as +/- 20% in healthy individuals, and even a shorter lifespan for those with diabetic level BG. Doesn’t this kinda cause one pause when worrying about A1C? I am also curious Dave to how you think the “glucose sparing” works. IOW, why does the liver keep BG, and especially FBG, high?
When I’m doing a lot of marathon training, I find my fasting glucose is typically higher in the morning and to me this makes mechanistic sense given I’ve shown that over and over again that’s the very time I’ll be suddenly running several miles. Now to be sure, I also would eat more during these phases of my life, so it could be influenced by that as well.
I’m not saying I know with certainty this is the case with Dr. Baker, but I’d be surprised if it wasn’t at least a strong component given the level of glycolytic activity he engages in.
It seems like no matter how bad the reading, you’re finding a way to justify it because people are low carb.
High blood glucose leads to glycation and increases risk of atherosclerosis. Zero carb has no historical precedence and makes absolutely no sense from any viewpoint other than orthorexia.
What would happen to Shawn if he ate an olive? Would he die? If this guy accidentally had a cup of coffee or some MCT powder (both come from plants) – would he lose strength?
Why are all plants bad?
We’re opportunistic eaters. Carnivore is dumber than vegan because we in the Keto community should know better and aspire to be more than the mirror opposite of vegans.
Here’s another theory – this guy lives on Wendy’s and garbage meats and his gut microbiome isn’t what it should be which is impairing insulin signaling.
He should look into his post prandial glucose responses – anything > 140 and this guy is vastly increasing his risk for heart disease.
But of course I guess that can all be waved away because the scientific community hasn’t taken the time to explore the long term health effects of stupid diets like this.
Right?
Hi Bert — thanks for the comments. 🙂
>>> “High blood glucose leads to glycation and increases risk of atherosclerosis.”
I agree this is generally true. But it might be like BMI, where having that metric alone is good for detecting people in trouble (usually obese), it can likewise fail at the few it’s picking up that are athletic and muscular. This is why HOMA-IR is a better measurement than glucose alone as it has insulin for additional context and thus a greater correlation to all-cause mortality.
>>> But of course I guess that can all be waved away because the scientific community hasn’t taken the time to explore the long-term health effects of stupid diets like this. Right?
I definitely don’t feel that way. That’s why I finished off with excitement in our finding out together. (Note I also mentioned both good and bad outcomes being possible — so I don’t assume it is only good)
I think it’s appropriate to point out to anyone and everyone when a diet is fairly untested (especially in the long term), but for this same reason, we can’t draw conclusions on its outcome. Nothing wrong with that — it’s kind of the basis of many N=1s in the first place. 🙂
Bert – concern of mine, too, until i checked out the underpinnings of the HbAic test. Upshot: if your red blood cells live longer than 120 days on average…your values will be pushed incorrectly higher. If your red blood cells live less (say, due to glycation damage) than 120 on average your HbA1c will be pushed incorrectly lower. Diabetics, therefore, have insufficiently revealing A1c scores. And contrariwise, those with very low/no red blood cell sugar damage will have long-lived RBC and incorrectly high A1c.
That’s why a secondary test like HOMA or fasting Insulin or is needed.
A final note: if Doc Baker regularly donated blood, his ferritin would be lower (this would make PD Mangan happy) and his average RBC lifetime would be shorter — and his HbAic more accurate.
Hope this helps….
Really great comments, Ross!
This sets off bells for me! 6 months ago I switched from LCHF to VLCD >95% of my diet is meat and eggs, bit of cheese. I might grab some cucumber or celery sticks here and there (mimicking random foraging). Only refined glucose is for treating my hypos (I am T1D) but usually less than 10g-15g carbs per day as needed. Workouts are short and intense, Ted Naiman style which has added significant muscle tone and strength to my 47 year old body. Before switching I was putting up AIC’s around 5.0-5.4. Since going almost all meat, I’ve bumped up to 5.7 on my last two blood drawn A1C’s. This last test there appeared a discrepancy between my interstitial CGM A1C ‘estimate’ of 5.0, photo recorded the same time as my last blood draw, and the blood result of 5.7! I accept a normal range of variance but the previous 4 comparisons between my CGM and the blood draw A1C was virtually no error range. This leads me to believe there is truth in the idea that red blood cells are hanging in there just a little bit longer and throwing the blood drawn A1C up while the CGM estimate of real time data is showing something else (blood versus interstitial)! I have to say, this is a totally new rabbit hole I need to dive down. Loving this!
Interesting data, Rob. Yes, this is an area that could use more N=1 controlled experiment and contribution. Keep tracking!
I had the same experience. I tracked my blood glucose 5-10 times a day on finger pricking and there was total discrepancy between A1C vs daily average. Until I used CGM to track, I found out my estimated A1C on CGM was 4.8% vs 6.1% A1c. My fasting insulin was 2.9 and I had the same conclusion- my RBC my live longer than 120 days.
Yes anecdotally/observationally some diabetics have HbA1c which differs significantly from their spot readings – the low carbers tend towards higher A1c, suggesting a longer life for the red cells. Interestingly some of them had fructosamine tested and that came in more in line with the spot BG readings.
A1c was always regarded as too inaccurate to be used for diagnosis until a few years back.
Oops, didn’t see the rest of your thoughtful comment, Bert.
This guy’s post prandial response is steady or negative. In the Robb Wolf interview, i think he said the most it ever rose was 5-10 points.
Where are you getting he eats Wendy’s? He eats ribeyes most of the time, with a little cheese and seafood. You are clearly vegan by your venomous response. Open that closed, pathetic mind of yours. Look up Owsley Stanley, he ate a carnivore diet for over 50 years. Died at age 76, in a car crash. Plenty of people have been doing this diet for 10+ years with amazing results.
Hi Jay — whether Bert is vegan or low carb, I’d want to us to welcome contrarian viewpoints here. Let’s have more of a dialog about the data and not as much about character. 😉
I like your example about Owsley — I think Shawn mentioned him in a podcast but I didn’t have the name to look up before. Thanks!
How can you like the example? Owsley was diagnosed with stage 4 throat cancer prior to the car accident despite the fact he never touched tobacco, not to mention the controversial heart artery blockage surgery he also had to undergo.
Some people just love to discredit nutrition science and rely on insane examples like this LSD hippie that suffered from hallucinations and paranoia.
Wake up
Not to mention entire groups of people. The Comanches, for instance, basically ate 100% buffalo. Would they eat anything else? Sure, if they were starving.
I’ve personally found eating more meat, fewer vegetables better even while on a keto/very low carb diet. I still eat a few vegetables, though. I used to eat vegetables at every meal, now I can go days without eating them.
Dave, I have a low carb doctor whose theory about HDL (HDL-C, though I find this confusing since HDL is not cholesterol) is that it varies based on the amount of good fats you’re eating. (I assume she means animal fats, but I’ll have to ask her next time I see her.) This does seem reasonable. If I fast (no fats), HDL does down. I started testing eating higher protein and lower fat, and HDL went down relative to eating more fat (i.e., higher fat meats). What are your thoughts on this hypothesis, and how could one go about testing this?
I agree. Generally, the more fats you consume (especially saturated fats), the higher your HDL *typically* goes (not always, and not with everyone).
My data has generally shown the more you need to access fat from storage (body fat) relative to fat you’re eating, the lower your HDL. Moreover, the less you consume fat overall, the lower your HDL. Again, these are all general correlations and do vary at an individual level.
Re the post prandial, Shawn mentioned that much of the time his glucose was lower, even 80s, and that meals he stayed the same or had minimal increase. His fasting BG was his highest reading of the day, and he mentioned basically being subject to the dawn phenomenon.
However, I agree may high BG may still be of concern despite the atheltics.
And that’s the key question. As with lipids, my pontificating on it being mechanistically reasonable doesn’t necessarily translate to it being healthier as a result. That can only be shown with more data.
I tend to agree with you –although I’m following a LCHF/Ketogenic/High Protein diet (varies over time) along with intermittent fasting and time-restricted feeding. I have lost 66 pounds with this approach. My A1c was 5.7 last time I check but before entering this eating approach I had all the symptoms of metabolic syndrome and (at least) pre diabetes. Most notably, persistent blurry vision which reverted and resolved completely since going keto (and following the other approaches).
However, although I have a great deal of “confidence” in that my glucose was out of control I cannot tell for sure because I have no relevant recent measures of glucose to refer too (I have very old ones, of many many years ago when I was much younger, leaner and athletic).
This is what I think. Baker has said that he was overweight in spite of rigorous training before adopting his carnivore style. We know that that, coupled with the fact of this long-term training, may be and indication of insulin resistance and elevated blood glucose. I may very well be that his A1c was higher then than it is now. However, we don’t know.
And that’s the point. We dont know. Baker has said that he did not tested. I personally think that that was a very silly approach. There is no baseline to which compare (and even then, it would be only argumentative as no proper control interventions is available).
I could be that his A1c had increase since going carnivore or it could be the other way around. We don´t know.
However, there is one thing that we know: 6.4 is a number you have to take seriously. I would not jump out of the window just because of one measurement, but I would make a point of tracking nutrition, exercise and outcomes (a la Dave) to understand the dynamics behind that number.
The main problem is that Baker made a mistake (considering he is a doctor) –namely, not establishing his baseline and not tracking behaviour and outcomes.
I also agree with you in that and A1c of 6.4 cannot be dismissed simply because your are eating this or that.
I myself observe this number with caution in the sense of acknowledging the possibility that this eating pattern has a negative consequence on blood glucose levels. That being said, I still need more data. If you happen to have references (good references, with well-define controls groups and interventions) showing that very high protein / carnivore diets induce elevated glucose and insulin resistance, please do share it.
Messner
I certainly would have preferred he had baseline measurements for comparison. Likewise, I’d take an A1c of 6.3 very seriously as well.
That said, I’d want to go a lot further with Baker if it were me and get a continuous glucose monitor. Naturally, we can assume he’s a giant glucose sink when he’s doing these high-performance feats. The questions become (1) does this justify the higher mobilized glucose int the first place and (2) regardless of answer 1, will this result in problems of higher glucose exposure typical of a T1 Diabetic?
Dr. Baker did have a 0 on his CAC score after 2+ years carnivore at 50+ years.
Hi Dave,
as always… great post!!
one question on HDL: to my knowledge it primarily serves as an transport molecule for gonads and adrenals and additionally delivers cholesterol to VLDL and LDL. Is this correct?
And is that all it does or do you see different purposes as well?
And btw, if its correct that it supplies to gonads and adrenals, why does not LDL do this? (as it does for the rest of the body)
HDL actually does quite a lot of things. In fact, one possibly important role to me that I’m trying to find out more about is giving a hand to TG distribution direction, which would explain the higher levels tracking tightly with LDL particles in LMHRs. Again, this is fairly new stuff and seemingly theoretical (post-CETP, TG-bloated HDLp using ApoB II binding as the pathway), but extremely exciting if this proves to be the case.
Thank you that makes a lot of sense.
What i forgot to mention before: i was always in the impression that under CHRONIC strain, the body would upregulate LDL in order to deal with it.
Since Dr Baker trains almost daily it would classify as chronic strain. Isnt there a difference between a one-time-hard-workout (that would lower LDL) and a daily-hard-workout (that would lead to upregulated LDL)?
But per my other posts/talks, I believe there’s a higher rate of LDLp (and thus LDLc) removed from the blood from tissues to some degree for reparative roles (via endocytosis).
Dave: great post and I applaud Dr. Baker for sharing this data knowing that it would be the subject for widespread discussion. My limited understanding is that despite his athletic status, the fact of the higher BG levels themselves cause damage to tissue despite the low insulin. Of course all the research I see in this area is in the typical diabetic population and I don’t see research in a carnivore or low carb population happening soon. What are your thoughts on what is causing damage, the BG or the insulin? Both? Is this a case where the body is doing a great job of fuel management but there is a cost to long-term health via the higher BG levels? Is this BG level a red herring with respect to athletics and simply a manifestation of the dawn phenomenon and genetics?
As with atherosclerosis, I suspect there’s thresholds (tipping points) of control. In the case of Too Much Glucose, we already have several other things commonly in play like hyperinsulinemia and NAFLD. So yes, I’d want to know the proposed pathogenesis of glucose causing damage absent these other confounders.
Is it just a higher rate of glycation to LDLs? Okay — let’s say this is the case and is dose-dependent, hypothetically (so 25% higher atherogenic risk). But in order to *induce* this scenario or higher required On Demand Energy, he’s doing high-performance exercise and is thus enjoying the many benefits of (1) lower insulin, (2) potentially more autophagy, (3) lower waste-to-hip ratio — to name just three. How much do these offset or even improve on that glycation in the trade-off?
I’m a low carber myself and am very sympathetic towards the carnivore diet, but for a second I’d like to put diet aside in the case of Dr Baker.
It seems to me that a lot of the assumptions here are predicated on the idea that this guy is a peak level athlete, so whatever his markers are they must be healthy. I’m not so certain.
While it seems obvious that exercise is good for our health, is it possible that being an ‘athlete’s athlete’ is just another way to put an unnatural amount of stress on our bodies, just like obesity or psychological stress? From a risk perspective, I’d obviously rather be the high level athlete than the diabetic couch potato, but does this mean that pushing yourself to your absolute limits day in and day out is inherently healthy?
It’s tough to set aside the idea ingrained in us by our culture that the athlete is the absolute peak of physical health, but, in a not insignificant number of cases, these guys wind up just flat out dying young.
While I see no flaws in your logic regarding WHY fasting glucose and a1c would be elevated in this example, as far as I’m concerned, it still can’t be said that these markers should be considered by any means desirable until proven otherwise. Particularly not based on the peak athlete/ perfect health assumption I’ve outlined.
I agree with your pondering quite a bit, and there’s certainly a lot of evidence in over-exertion and over-exercising. There’s a low carb marathon speaker who I’m drawing a blank on at the moment, but he often points to how he was “fit, but not healthy” before his current routine/diet, and that always stuck with me.
And yes, the point of your last paragraph is very well taken. But note I didn’t make any assessment of health in this article pro or con. If anything, I regret not further emphasizing my wait-and-see position with good/bad outcome data at the end. 😀
I think you’re talking about Brad Kearns. I recall him saying that several times.
Yeah, that’s him.
Thanks Dave! Love your work!
Thanks, Phillip!
I’m a healthy (no pills) long time low carber, now very low carb higher fat diet; I’m officially an old lady, 70yo, who exercises an average amount, walking 1-2miles 4-5x a week, with once a week weight training; Since I got past 50yo I always have the “Dawn Effect” with my BG up around 100, and it goes higher if I cut calories. Yet, it drops to normal 70-80 as soon as I have any food, and stays there. My very nice (who will never look beyond his training) doctor tries to get me on statins every annual exam, and I tell him I don’t believe in them, but am going to try your protocol to see if I can lower the numbers and flummox him. Will report my results.
Great, Nan — let us know how it goes. If you haven’t already, be sure to read the protocol write up here: http://cholesterolcode.com/extreme-cholesterol-drop-experiment/
I took part in the original carnivore 90 day study and had blood work done at the end of the 90 days. I am a 50 year- old male, 185lbs, 6′ tall, and workout 5-6 times per week. The year prior to the study I ate following the protocol outlined by ketogains.
For what it is worth, my labs were as follows:
HbA1c: 5.5
Fasting Glucose: 93 mg/dL
Fasting Insulin: 2.2 mIU/L
HOMO-IR score: .3
Total Cholesterol: 321
LDL-C: 219
HDL-C: 89
Triglycerides: 39
It’s hilarious, before even finishing your first paragraph I was saying to myself, “this guy is going to be a Lean Mass Hyper-responder”. And of course, you are. 🙂
( I assume you’ve read about LMHR — if not, see here: http://cholesterolcode.com/are-you-a-lean-mass-hyper-responder/ )
I have read about LMHR, and have been following you for quite some time now. Very thankful for your work! Much appreciated, Dave!
Thanks, Jake!
Solve the heart disease question in 1 go with a CAC SCAN. JOB DONE. HE’S RIGHT AGE TO SHOW A HIGH NUMBER. LOW NUMNER LOW RISK..KEEP DOING WHAT UR DOING… u can test all the ldl and hel u want.. CAC SHOWS THE CALCIFICATION
NO HUGH CAC NO INSULIN RESITAMCE NO PRE T2
Hey Dave. Id like to share some blood results. Im a 23 year old grad student who’s very active in the gym. Ive been on keto since june last year. I wen to do a blood test to see where Im at.
Test 1- January
hdl 56
triglycerides 60
ldl 270
total 338
After this, I decided to go on a cut and make most of my fats monounsaturated for around 2 weeks. I went to the gym and HIIT cardio every day. I decided to get a nmr test as well.
Test 2 – february
hdl 48
trig 109
ldl 299
total 369
the particle number was high as well, which makes me suspicious of how much an nmr can calculate cvd risks.
Then I finally went to experiment the feldman protocol by having my calories up to 5400. I got a CRP and a regular blood test done. This time i didn’t do the HIIT cardio these days.
Test 3
hdl 60
trig 60
ldl 199
total 271
My grandmother, who is a nurse, is still skeptical because the cholesterol I consumed in test 3 was around 300mg less that test 1 and 2. Im going to do another test on monday with the protocol again with a higher amount of cholesterol consumed and get back to you on Tuesday. One question I have is that should I be going to the gym and cardio while doing this experiment? I’m thinking it might make my body require more cholesterol and produce more to fulfil.
Love the data, Michael!
– I’m highly skeptical that 300mg of cholesterol ingested had any meaningful impact on your serum cholesterol. Most cholesterol we eat is in the form of cholesterol esters and passes through our digestive system, and the *vast* majority of cholesterol in our bloodstream was made by our body directly (usually 80-85%) — moreover, our body up and downregulates production of this cholesterol against what is being absorbed in the diet. In short, my research is showing the higher cholesterol seen in the blood test is reflective of trafficking far, far more than independent and circumstantial production or absorption rates.
– Actually, your working out is more likely reducing your cholesterol levels overall. But regardless, I’d want you to keep it as a constant whatever your activity level was in the prior tests so you can control that variable and confirm it was the same throughout. better to not increase or decrease it. 🙂
Hey Dave, Just got another blood test result. I agree about that amount of cholesterol difference wouldn’t have a high impact. That’s like around 2 eggs worth of a difference. But anyway, For test 1, I ate roughly around 1,535 mg cholesterol. Test 2 was around 1,417. Test 3 had 1016.
The CRP test I had for test 3 was 1.84 which is considered average.
Now For the test I just took for test 4, I ate 1,670 mg of cholesterol.
Test 4
hdl 69
trig 98
ldl 142
total 231
I made a chart of the results I have so far.
I’m pretty glad that I now have solid proof that eating large amounts of fat and cholesterol will not make my ldl go high.
Great stuff, Michael, thanks for sharing!
Everyone looks at these high glucose numbers here as a progression to type 2 diabetes (hyperglycemia/hyperinsulinemia/insulin resistance), but what if it’s actually an onset of type 1 diabetes (immune attack on beta cells curbing insulin production)?
Contrary to popular belief, destruction of beta cells comes in waves & not all at once. Is it possible that he has lost beta cell function & becoming a type 1 diabetic?
Tests should be run like C-peptide & antibody to make sure his pancreas is ok. We don’t have knowledge of what exactly CAUSES the autoimmune destruction of beta cells. I suspect world class athletes are still human and are susceptible to becoming a type 1 diabetic.
This is actually part of what was suggested by Woo here: http://itsthewooo.blogspot.co.uk/
FWIW, I point out the “sudden wave” with regard to diabetes constantly with my family/friends. They take comfort in slowly creeping upward A1c as though it is controllable and they will “do better” to curb it slightly. But I’m worried about the very effect you outline there.
It will be interesting if Baker gets these further tests and provides them as well.
Hey Dave,
Just did a 6 week run of Carnivore with Pre and post blood work. I’m a pretty lean athlete and would love if you would take the time to give hear your input on my numbers.
Units are mmol/L
Pre (roughly 14 hours fasted)
Cholesterol 4.48
Triglycerides 1.07
HDL Cholesterol 1.50
LDL Cholesterol Calc 2.49
Post (11-12 hours fasted)
Cholesterol 7.31
Triglycerides 1.10
HDL Cholesterol 1.62
LDL Cholesterol Calc 5.19
Pretty cool, Vic! Here’s a comparison of your reports:
Pre: on – ::: 14 hours water fasted…
–==== CholesterolCode.com/Report v0.9.2 ====–
…
Total Cholesterol: 173 mg/dL 4.48 mmol/L
LDL Cholesterol: 96 mg/dL 2.49 mmol/L
HDL Cholesterol: 58 mg/dL 1.5 mmol/L
Triglycerides: 95 mg/dL 1.07 mmol/L
–CHOLESTEROL REMNANTS–
Remnant Cholesterol: 19 mg/dL 0.49 mmol/L >>> Medium-Low Risk Quintile
Remnant Chol to HDL: 0.33 >>> Medium Risk Quintile
Go to https://tinyurl.com/y8hokam2 for more on Cholesterol Remnants
–ATHEROGENIC INDEX OF PLASMA (AIP)–
AIP: -0.147 >>> Lowest Risk Third
Go to https://tinyurl.com/ycccmmnx for more on Atherogenic Index of Plasma
–CONVENTIONAL MARKERS AND RATIOS–
Friedewald LDL-C: 96 | Iranian LDL-C: 105
Total/HDL Ratio: 2.98
TG/HDL Ratio in mg/dL: 1.64 | in mmol/L: 0.71
… And post …
–==== CholesterolCode.com/Report v0.9.2 ====–
…1.5 months on Carnivore/Zero Carb/Meat Only ::: 12 hours water fasted…
Total Cholesterol: 283 mg/dL 7.31 mmol/L
LDL Cholesterol: 201 mg/dL 5.19 mmol/L
HDL Cholesterol: 63 mg/dL 1.62 mmol/L
Triglycerides: 97 mg/dL 1.1 mmol/L
–CHOLESTEROL REMNANTS–
Remnant Cholesterol: 19 mg/dL 0.49 mmol/L >>> Medium-Low Risk Quintile
Remnant Chol to HDL: 0.3 >>> Medium Risk Quintile
Go to https://tinyurl.com/y8hokam2 for more on Cholesterol Remnants
–ATHEROGENIC INDEX OF PLASMA (AIP)–
AIP: -0.168 >>> Lowest Risk Third
Go to https://tinyurl.com/ycccmmnx for more on Atherogenic Index of Plasma
–CONVENTIONAL MARKERS AND RATIOS–
Friedewald LDL-C: 201 | Iranian LDL-C: 194
Total/HDL Ratio: 4.49
TG/HDL Ratio in mg/dL: 1.54 | in mmol/L: 0.68
…..
Note your Remnant Cholesterol came out EXACTLY THE SAME!!! Very impressive data!
Technically, your AIP improved by a little as well.
I read the study about remnant cholesterol, it was a bit difficult to understand but did it not say it had to be non fasted though?
Ah yes — this is why I’ll ultimately be linking to a different study soon. FWIW, fasting and postprandial RCs are closely correlated in all the studies I’ve found that compare the two. There’s a mechanistic reason for this explained well by this paragraph from http://www.jlr.org/content/41/9/1428.full.pdf
“These results are consistent with the concept that one
of the principal determinants of postprandial triglyceridemia
in HTG patients (irrespective of the molecular basis
of their HTG) is the fasting triglyceride and/or TRL-TG
level. This is because chylomicrons of intestinal origin and
VLDL of hepatic origin are catabolized via the same metabolic pathway (18–20). Chylomicrons secreted into the
blood circulation after the ingestion of a fat-rich meal are
catabolized by lipoprotein lipase, with apoC-II as cofactor,
the same molecules that are responsible for the hydrolysis
of VLDL in the fasted state. The more the lipolytic pathway
is saturated in the fasted state, the greater the magnitude
of postprandial triglyceridemia. Postprandial triglyceride
concentrations are thus significantly correlated with
fasting triglyceride levels, and as we have found in the
present study, postprandial RLP concentrations are significantly
correlated with fasting RLP levels.”
I plan to be doing a bigger “deep dive” post into Remnant Cholesterol soon.
Thank you, Dave, for this very informative post! I follow Shawn Baker even though I am not a carnivore myself. I’m not sure if I’m a LMHR – my remnant cholesterol is 10; fasting glucose 84; triglycerides 48; LDL 143. Maybe I’m just a low carber 🙂
Yeah, your LDL is too low to be a LMHR. But I suspect that will be true for a lot of carnivores.
Hi Dave, as always great thoughts.
When thinking about your work i came to realize that im unable to explain something from your earlier research .. may you help me back on track: –> inverse pattern and LDL-P… why is there this 2 day gap?
I cover my theory about 1/2ish of the way through in this podcast: https://t.co/HEcJzYvWoq
Dave, I read previously that adipocytes can only release free fatty acids back into the bloodstream at a rate of approximately 31 calories per pound of fat on the body.
I assume that as Volek etc found an up-regulation of fat burning for athletes following substantial carb restriction (Faster study) that the number quoted may be able to move north considerably. That being said, at some point of fat loss, energy demand will outweigh what the adipocytes are willing to give up.
If this is true, then for lean people like yourself and Dr Baker, this would mean that less fat, and therefore calories, are available from adipocytes even if available.
This would make organ/muscle stores of fat extremely important for normal activity. Could it also lead to excessive levels of glucagon leading to excess glucose in the blood and eventually hyperglucagonemia?
I’m not so sure if I follow on that last part. Yes, I believe lower adipose mass (per V & P) necessitates higher offsetting bioavailability of energy — this is why I point to it with regard to LMHRs. It’s also why I point out that higher fasting glucose is expected for those LCers who are lean and athletic, particularly when they do more explosive workouts that would likely require glucose/glycogen supply speed relative to fatty acids.
I just don’t know that I’d call it “excess” — as that implies too much. This isn’t a claim that it *isn’t* in excess, only that I haven’t been convinced either way as of yet. I’m inclined to trust the body’s regulatory outcome as designed until I see evidence to the contrary.
Thanks for the reply Dave.
I’ll try to better explain my thought experiment. And by the way, I’m the first to suggest I’m likely way off with my limited understanding.
Ben Bikman suggests that when protein is eaten during low carb and especially when fasted, glucagon goes up substantially whilst insulin is affected minimally.
In a diet such as Dr Bakers, protein is very high. This would appear to drive Glucagon up very high whilst having little effect on insulin. This will drive glucose production via gluconiogenesis. Possibly moreso when bodyfat is low due to a lower rate of fat store release.
My thought experiment raises the following questions
1. Could higher blood glucose be due to the insulin/glucagon ration not allowing storage or at least limiting the rate of storage?
2. If ‘overfilling the tank’ can lead to insulin issues, could a long term ‘low fat store’ coupled with a high protein diet cause issues due to high glucagon? I think this unlikely, but possible.
1 — I doubt it. If so, I’d expect we’d see sustained higher levels of glucose overall — closer to that of a T1D.
2 — Interesting idea, but I couldn’t say with any certainty. I’d expect this to be something you’d have to see and study in a non-athlete.
but is it optimal to have high blood glucose while fasted ?
performance wise and autophagy wise
It’s a good couple of questions. I think for the first it could be physiologically preferred (per the article above), but I have no idea on the second. Certainly, it is possible that what is working for your needs in the short term can be trading off with something in the longer term (short-term gain, long-term loss). But I’m not convinced there’s strong enough data to show us until we’re testing it specifically for this context.
Hmmm…I wore a continuous glucose monitor and tested higher protein (a lot higher, 120 grams at a meal) and did not find any increase in blood sugar. However, I’d need two of me to do a real test. During that time, my HbA1c was 5.0. Unfortunately, I can’t test glucagon or insulin. I’m also not lean.
Thanks for the added data, Bob. See if your doctor will approve future tests with Fasting Insulin when you get your blood draw. Couldn’t hurt to ask. 🙂
i would also suggest going 1 feed/meal every 2-3 days
as that is probably the closest to maximum efficiency
ps hope you have a demanding sport to play
Hi Dave, I just listened to your podcast with Keto Connect and I’m very interested in your research. I just started moving toward a keto diet about 17 days ago. I’m 48 yrs. old and last year, I was diagnosed with familial hypercholesterolemia. My total cholesterol at that time was 275, and it only dropped minimally when I tried simple diet changes in order to avoid going on statins. My doctor felt that because my father’s side of the family (my father and his only brother) also have/had high cholesterol, in addition to the fact that I’m not overweight and I am active daily, a more disciplined dietary change wouldn’t be likely to bring my numbers down enough either. My cardiologist prescribed Atorvastatin, and later added Zetia. By February, my total cholesterol was down to 153, with a remnant cholesterol of 27. I am very interested to know where this number falls in the severity range. Regardless, after just starting the ketogenic diet and I’m fairly certain, after listening to your podcast, that my numbers are probably sky-high now. I’m writing to inquire about whether you know the effect of statins and Zetia when a person switches to a ketogenic diet? From my understanding, Zetia absorbs fat in the stomach, so what happens when an individual is trying to eat higher amounts of fat for energy? I’m certain my cardiologist is going to tell me I’m so mistaken for doing what I’m doing, and I do have doubts that I’m doing what’s best for someone in my situation. Like you, however, I feel so much better eating a keto diet that it’s hard to imagine it could bad for me. Thanks so much for any input you have.
By the way, I’m in great overall health, no heart conditions, no calcium build-up so far. My father lived into his mid-80’s, despite having high cholesterol and his brother is still alive, healthy and active in his 80’s. My dad used statins, but his brother used diet and exercise (I.e., lifelong marathon runner) and is comfortable with a 240 total cholesterol level. I initially started keto to loose an extra few pounds I had gained, but I’d like to continue because I feel better. I’m 5’7” and 134 lbs.
This is an extremely common story. I have a number of followers who regularly tell me about their family having “sky high” cholesterol and regularly living into their 80s and 90s. Anecdotal, yes, but still very relevant nonetheless.
Hi Dave, It has now been two months since I messaged you… and since I started keto… and I have been anxious to get new labs done and get back to you. I have not been taking my statins regularly because I feel so good on keto that I don’t even think about medications. I’m also not nearly as worried about cholesterol since hearing about your research. Today I had my labs redone and here are the results:
==== CholesterolCode.com/Report v0.9.2 ====–
…2 months on Keto (less than 20g carbs) ::: 13 hours water fasted…
Total Cholesterol:
264 mg/dL
6.83 mmol/L
LDL Cholesterol:
178 mg/dL
4.6 mmol/L
HDL Cholesterol:
69 mg/dL
1.78 mmol/L
Triglycerides:
86 mg/dL
0.97 mmol/L
–CHOLESTEROL REMNANTS–
Remnant Cholesterol:
17 mg/dL
0.44 mmol/L >>> Medium-Low Risk Quintile
Remnant Chol to HDL:
0.25 >>> Medium-Low Risk Quintile
Go to https://tinyurl.com/y8hokam2 for more on Cholesterol Remnants
–ATHEROGENIC INDEX OF PLASMA (AIP)–
AIP: -0.264 >>> Lowest Risk Third
Go to https://tinyurl.com/ycccmmnx for more on Atherogenic Index of Plasma
–CONVENTIONAL MARKERS AND RATIOS–
Friedewald LDL-C: 178 | Iranian LDL-C: 166
Total/HDL Ratio: 3.83
TG/HDL Ratio in mg/dL: 1.25 | in mmol/L: 0.54
In comparison to the results in my previous message, after two months on keto, my triglycerides have improved. My LDL has gone up, and I’m guessing that I’m what you call a hyper-responder. My remnant cholesterol is much better at 17 mg/dL. You said before that you were on the fence about my informal diagnosis of familial hypercholesterolemia. What are your thoughts now? Do you feel that my numbers are within normal range now? My doctor recommended going back on statins, but I don’t think it’s necessary, knowing what I do now about why my LDL went up on a ketogenic diet.
I’m loving the ketogenic diet so much that for the first time ever, I’m leaving behind my husband and 3 kids and flying to Austin for KetoCon! Can’t wait to hear your presentations!
Hi Dana–
Firstly, I find that probably 90%+ of the time one is diagnosed with Familial Hypercholesterolemia (FH), it is from simply having higher levels of cholesterol alone. I vehemently disagree with this practice. The “F” in FH means it is indeed genetically determined. This is why as people say “I have FH” or “I was diagnosed with FH” my immediate follow-up question is, “do you have GENETICALLY CONFIRMED Familial Hypercholesterolemia?” As you can guess, this is usually not the case.
There’s a very big relevance to whether you have genetic FH as it can mean different things based on its type — and technically there are five types. But the most commonly diagnosed and presumed version involves a mutation in the LDL receptor (LDLr) that reduces clearance in the blood. You can find this out for yourself through a genetic profile like 23andMe.
So with all that said, we can know a lot more about your previous lipid profile and your current one if you run your numbers through our report tool here: http://cholesterolcode.com/report/
If you can — do that first and copy/paste your report back here in a comment and I’ll follow up (if before Monday — I go on a hiatus for 2 weeks after that).
Dave, Thank you so much for your replies. I really appreciate and value your thoughts on this. Below are my numbers, as generated from the report. I started a ketogenic diet just 2 weeks ago, so I haven’t had my new levels checked yet. I apologize is that is the information you were requesting. Please let me know if that’s the case.
Initial Cholesterol Test (2/9/2017):
..47 years on Standard American ::: 12 hours water fasted…
Total Cholesterol:
275 mg/dL
7.11 mmol/L
LDL Cholesterol:
172 mg/dL
4.45 mmol/L
HDL Cholesterol:
64 mg/dL
1.66 mmol/L
Triglycerides:
197 mg/dL
2.22 mmol/L
–CHOLESTEROL REMNANTS–
Remnant Cholesterol:
39 mg/dL
1.01 mmol/L >>> Medium-High Risk Quintile
Remnant Chol to HDL:
0.61 >>> Medium-High Risk Quintile
Go to https://tinyurl.com/y8hokam2 for more on Cholesterol Remnants
–ATHEROGENIC INDEX OF PLASMA (AIP)–
AIP: 0.126 >>> Highest Risk Third
Go to https://tinyurl.com/ycccmmnx for more on Atherogenic Index of Plasma
–CONVENTIONAL MARKERS AND RATIOS–
Friedewald LDL-C: 172 | Iranian LDL-C: 239
Total/HDL Ratio: 4.3
TG/HDL Ratio in mg/dL: 3.08 | in mmol/L: 1.34
After 25 days on statins (10/30/17):
–==== CholesterolCode.com/Report v0.9.2 ====–
…47 years on Standard American ::: 12 hours water fasted…
Total Cholesterol:
209 mg/dL
5.4 mmol/L
LDL Cholesterol:
134 mg/dL
3.47 mmol/L
HDL Cholesterol:
62 mg/dL
1.6 mmol/L
Triglycerides:
63 mg/dL
0.71 mmol/L
–CHOLESTEROL REMNANTS–
Remnant Cholesterol:
13 mg/dL
0.34 mmol/L >>> Lowest Risk Quintile
Remnant Chol to HDL:
0.21 >>> Medium-Low Risk Quintile
Go to https://tinyurl.com/y8hokam2 for more on Cholesterol Remnants
–ATHEROGENIC INDEX OF PLASMA (AIP)–
AIP: -0.353 >>> Lowest Risk Third
Go to https://tinyurl.com/ycccmmnx for more on Atherogenic Index of Plasma
–CONVENTIONAL MARKERS AND RATIOS–
Friedewald LDL-C: 134 | Iranian LDL-C: 114
Total/HDL Ratio: 3.37
TG/HDL Ratio in mg/dL: 1.02 | in mmol/L: 0.44
After 3 months of Zetia (Ezetimibe) added to statins (2/8/2018):
–==== CholesterolCode.com/Report v0.9.2 ====–
…48 years on Standard American ::: 13.5 hours water fasted…
Total Cholesterol:
153 mg/dL
3.96 mmol/L
LDL Cholesterol:
62 mg/dL
1.6 mmol/L
HDL Cholesterol:
64 mg/dL
1.66 mmol/L
Triglycerides:
137 mg/dL
1.55 mmol/L
–CHOLESTEROL REMNANTS–
Remnant Cholesterol:
27 mg/dL
0.7 mmol/L >>> Medium-High Risk Quintile
Remnant Chol to HDL:
0.42 >>> Medium Risk Quintile
Go to https://tinyurl.com/y8hokam2 for more on Cholesterol Remnants
–ATHEROGENIC INDEX OF PLASMA (AIP)–
AIP: -0.03 >>> Lowest Risk Third
Go to https://tinyurl.com/ycccmmnx for more on Atherogenic Index of Plasma
–CONVENTIONAL MARKERS AND RATIOS–
Friedewald LDL-C: 62 | Iranian LDL-C: 104
Total/HDL Ratio: 2.39
TG/HDL Ratio in mg/dL: 2.14 | in mmol/L: 0.93
Hi Dana–
Given your first lipid report, I’m on the fence as to whether I think you have FH. While those are “high” cholesterol numbers, they appear to be downstream of an energy surplus (as indicated by the higher triglycerides). The high TG is certainly something I’d want to tackle in your shoes
The good news is that your HDL is nice and high at 64 and this is certainly correlated with reduced risk of heart disease.
I’ll be interested in your keto lipid numbers, but you may want to give it a few months before testing as your lipid profile can be very volatile at first.
Thank you so much for your feedback on these, Dave. What would lowering triglycerides look like on a ketogenic diet? I’m generally eating 20-50 grams of saturated fat (e.g., MCT oil, coconut oil) per day. Should I put a halt to saturated fats as much as possible, or will the reduction in carbs and sugar that are part of a keto diet potentially lower triglycerides enough? I read that you feel a triglyceride level of 60 or lower is optimal; however, the charts used by my doctor list <150 as normal. Should I ignore this? On a side note, I have two children, ages 10 and 12, and my 10 year old daughter seems to have the same tendency as I do toward high cholesterol. Her numbers are: total=240, triglycerides=117, LDL=157, HDL= "normal". This has been a big concern to me, and from what you said, I should really focus on getting her triglycerides down as well.
I’ll do an article on high triglycerides eventually, but here’s the two tweets I had from earlier:
—–
1. Look for “leaks” where you’re getting more carbs than you thought
2. Lower liquid forms of fat
3. Consider intermitted fasting
4. Consider overall drop in total calories
— I usually advise in this order of succession trial-and-error with friends/family
and
FWIW, 80%-ish turn out to be (1). And almost 100% of them don’t think it’s that until I “get forensic” with their diet and help to find where the leaks are. People get very comfortable with high fat when on #LCHF and don’t realize if they relax their carbs a little, it’s a biggie
—
Trigs below 100 are optimal (below 60 usually takes being athletic). 100-150 usually means a sedentary low carber, and while I’d prefer it were a little lower, I don’t consider this a red flag.
So, for those like myself who aren’t nerdy on this stuff… Does that mean he’s healthy? Does his blood work show he could maintain this long term and be “healthy”?
Short, layperson version: I don’t know.
I just know there’s a mechanistically sound reason from where I’m standing as to why this might be appropriate for energy supply to meet his current demands. Long-term health implications? No idea.
Thanks for your response and honesty.
I wish the answers could be simpler, dammit!
You know, FWIW, we’re making some pretty impressive strides with just Citizen Science alone. I think we’ll keep ramping up the good data and have a better sense of it sooner rather than later.
Hey Dave just wondering when you are going to try the diet and experiment?
Oh definitely. It’s just a matter of scheduling. I have the Gaining Weight experiment first (just announced), resistance training after, then probably this experiment shortly after that (my guess is in the Fall).
Makes sense. I did a test of myself (now ketogenic but former T2D) against a triathlete friend who is also ketogenic. His fasting Blood Sugar was relatively high compared to mine at start. We both ate a 50g Whey protein bolus at the same time and measured our blood sugars. His went down and mine went up. Mine took longer to normalize. Put link to results in the website link.
Hi Dave,
I am hoping if you can help me by giving your opinion about my cholesterol test result.
I just did my first blood test after two months on Keto diet, I did a lot of reading and researched in these two months on the subject cause getting into kept adapted is not as easy as I imagined.
I did a blood test 6 months ago as a general checkup, everything is under the guideline, and I didn’t know I was gonna change my diet to LCHF in four months.
The reason I got into LCHF is because I am an seasonal athlete doing ocean outrigger paddling, long two to three hours paddling across channel between island…etc.
I felt like my recovery time and endurance is getting worse and worse every year after four years of paddling, I just turned 45, and I hate carb loading, but there is no other options till I came across LCHF diet.
The past two months has been GREAT, I feel great, not hungry. full of energy….you know what I am talking about.
SO,I did my FIRST LAB TEST AFYTER TWO MONTHS on LCHF diet, I was expecting the Cholesterol number to changed and it did.
My Cholesterol went from 186 to 254
HDL stayed the same as 66
LDL went from 104 to 149
CHOL/HDL Ration went from 2.82 to 3.85
THE MOST SHOCKING TO ME is my Triglyceride went from 80 tp 197 !!! I am concerned since I don’t know why/how it happened.
My doctor want me to quit the diet (cut back dietary fat and take more grains) or take medication.
Thanks to your research and experiment I now have a better understanding of the lipid system/mechanism but I have no clue why the triglyceride number will jump to 197.
As I said the first blood test was just a regular check up without any purpose of it, at that time, I was pretty healthy, not overweight, no major health problems, I did consume a lot of carb (carb load for paddling), and a lot of it is actually beer !!! and stupidly I didn’t think it’s carb !! overall I just started to feel the inflammation level in my body is getting higher and higher, as you can imagine.
So because I did the second lab test after two months in LCHF diet, I asked my doctor to do the A1C and EAG test also the CRP-HS test, A1C came back 5.2 and EAG is 103, CRP-HS is 1.18
I didn’t do those 6 months ago so there is no comparison to it but I personally feel there is an improvement on my inflammation level even it’s still borderline 1.18 on the CRP-HS number, my recovery from exercise is way better and I have way more energy during training. And I am not hungry !!
My first month of LCHF diet was not easy, luckily I was very willing to try and change, I listened to how I feel and really pay attention to what I eat and be strict about the macro. The second month went a lot better, I checked my blood glucose/ketone several times a day and I can also predict the number now since it’s pretty stable this month, my glucose number is usually up or down around 80 through out the day, my ketone number are mostly over 3, sometimes over 4 through the day. I don’t know why my ketone number are on the high side? Maybe I ate too much FAT? I kind of mainly focus on limiting the carb and protein intake for my diet and not limit the Fat to get to ketone adapted, can this be the cause of the Triglyceride number up high or my ketone number always above 3?
I felt what you said when I saw you telling the story of JILL, I am so lucky to see your lecture online and feel ease on my Cholesterol number being high on LCHF diet.
I need your opinion about my Triglyceride number been high cause I don’t know what to do to change it, my doctor want me to quit the diet or take medication.
From what I understand the high Triglyceride number comes from carb but in these two months, at least the past month I was very strict on my macro, my carb daily is 25gm and protein 50gm, I am 145lbs now, I only lost about 9 lbs in the two month of LCHF diet, I am 5’7” age 45 asian live in Hawaii.
My other thought is maybe this is still temporary as I am only two months on LCHF diet and maybe if I keep doing it and run another lab test next month or wait for another 4 months to do another test?
Hi Jeremy,
I’m helping Dave with comments while he catches up on a few things…
First off, there is some variability in triglycerides (it appears to be one of the more variable markers), but I wouldn’t expect to see triglycerides go that high on low carb in general. There are some things you can take a look at to help figure out what’s going on here. It is definitely worth trying to pinpoint where the issue is.
1) Do you track what you eat? Sometimes there can be some unexpected carb creep, in things like sauces or condiments or even heavy whipping cream that says 0 or <1g of carb per tbsp which could actually mean 0.5 or .8g of carb. That can add up pretty quickly, and can be quickly caught out by logging everything and taking a look.
2) How long were you fasting during the second test? Fasting under 12 hours or over 14 hours can skew results, including triglycerides
3) Are you a heavy coffee drinker, or did you have coffee on the morning of the test? There's some possibility (both in viewing other people's data, and some studies that have been done) that show coffee may influence triglyceride numbers
4) Any MCT or coconut oil on the morning of the test? Another possible confounder
I would say start tracking everything for now, and see if you can spot any possible leaks, make sure you fast the proper amount, and be on the lookout for anything that may influence. Once you do that, it may be beneficial to go ahead and get a follow up in a month and see where it's at. Granted your small amount of time on low carb may influence as well, but making sure it's not anything else is important too.
Hi Siobhan,
Thanks so much for the information.
I do track what I eat but it is possible that I missed something.I was VERY strict of what I ate, I made my meal 90% of the time, mostly fatty meat and cooked green leafy vegetables with animal fat, I don’t usually use any kind of salad dressing. But I only keep tracking the protein and carb though, fat and oil I kind of just go with it cause I was trying to get adapted. I already cut back on fat since my ketone/glucose reading are pretty stable now.
What I don’t understand is, 6 months ago when I did the lab test, I was still drinking bear, most all IPA, at least one a day and sometimes two or three, my triglyceride number was 80. After going into Keto for two months and the number went to 197. It’s totally possible that I missed some carb but my carb intake is definitely way less then before. Just make me wondering if there is anything else I should look into?
I didn’t eat anything the night before test starting 9PM and I did the lab around noon time the next day, I don’t recall drinking coffee, just water with some lemon in it, can that be the problem?
I am not a heavy coffee drinker, one cup a day usually in the morning, I would drink coffee (sometimes with oil sometime without) and usually have my first meal of the day around 1-2PM.
again thanks for the info
Just did another lab after two months from last one, probably not the right place to post this but did it just so can see the comparison since I posted the questions back then. Definitely caused by early stage of changing diet also not stricly tracking what I eat everyday.
Starting tracking everything after the first lab and two months later, numbers looks pretty good?
–==== CholesterolCode.com/Report v0.9.2 ====–
…2 months on Keto (less than 20g carbs) ::: 15 hours water fasted…
Total Cholesterol: 254 mg/dL 6.57 mmol/L
LDL Cholesterol: 149 mg/dL 3.85 mmol/L
HDL Cholesterol: 66 mg/dL 1.71 mmol/L
Triglycerides: 197 mg/dL 2.22 mmol/L
–CHOLESTEROL REMNANTS–
Remnant Cholesterol: 39 mg/dL 1.01 mmol/L >>> Medium-High Risk Quintile
Remnant Chol to HDL: 0.59 >>> Medium-High Risk Quintile
Go to https://tinyurl.com/y8hokam2 for more on Cholesterol Remnants
–ATHEROGENIC INDEX OF PLASMA (AIP)–
AIP: 0.113 >>> Highest Risk Third
Go to https://tinyurl.com/ycccmmnx for more on Atherogenic Index of Plasma
–CONVENTIONAL MARKERS AND RATIOS–
Friedewald LDL-C: 149 | Iranian LDL-C: 219
Total/HDL Ratio: 3.85
TG/HDL Ratio in mg/dL: 2.98 | in mmol/L: 1.3
–==== CholesterolCode.com/Report v0.9.2 ====–
…4 months on Keto (less than 20g carbs) ::: 13 hours water fasted…
Total Cholesterol: 267 mg/dL 6.9 mmol/L
LDL Cholesterol: 172 mg/dL 4.45 mmol/L
HDL Cholesterol: 79 mg/dL 2.04 mmol/L
Triglycerides: 78 mg/dL 0.88 mmol/L
–CHOLESTEROL REMNANTS–
Remnant Cholesterol: 16 mg/dL 0.41 mmol/L >>> Medium-Low Risk Quintile
Remnant Chol to HDL: 0.2 >>> Medium-Low Risk Quintile
Go to https://tinyurl.com/y8hokam2 for more on Cholesterol Remnants
–ATHEROGENIC INDEX OF PLASMA (AIP)–
AIP: -0.365 >>> Lowest Risk Third
Go to https://tinyurl.com/ycccmmnx for more on Atherogenic Index of Plasma
–CONVENTIONAL MARKERS AND RATIOS–
Friedewald LDL-C: 172 | Iranian LDL-C: 156
Total/HDL Ratio: 3.38
TG/HDL Ratio in mg/dL: 0.99 | in mmol/L: 0.43
Yes, Jeremy — I quite agree! IMO, this new lab looks substantially better, particularly for the drop in triglycerides and RC!
LDL cholesterol levels should be less than 100 mg/dL. Levels of 100 to 129 mg/dL are acceptable for people with no health issues but may be of more concern for those with heart disease or heart disease risk factors. A reading of 130 to 159 mg/dL is borderline high and 160 to 189 mg/dL is high. A reading of 190 mg/dL or higher is considered very high.
HDL levels should be kept higher. A reading of less than 40 mg/dL is considered a major risk factor for heart disease. A reading from 41 mg/dL to 59 mg/dL is considered borderline low. The optimal reading for HDL levels is of 60 mg/dL or higher.
Baker’s numbers aren’t good no matter how you spin it.
Hi Colin–
You might be new to my research and general theory. Through a series of experiments, I’m providing evidence that appears to substantiate an energy model for cholesterol influence. If one is primarily powered by fat, there is a physiologically sound reason they would be trafficking more VLDLs and thus more resulting LDLs.
I’m a 58 years old female. On a strict carnivore diet since mid-February of 2018. Feeling great. Lost more than 42 lbs. (from 189 lbs to currently 146. Eating once a day, when I get hungry. Eating mostly fatty steaks, some butter and a little bit of heavy cream in my morning coffee.
Exercising almost every day mostly with moderate weight kettlebells. My energy level is getting better and I feel better than before starting this way of eating.
I feel more alert and able to focus. I’m an ICU nurse and I feel that I can perform better my work. My chronic joint pain has almost disappeared. I used to have migraines secondary to allergies and I was taking acetaminophen and/or ibuprofen on a daily basis to function. I suffered from anxiety and I have a tendency to get depressed. All the above issues have been gone since I started on the carnivore diet.
My blood pressure is 119/85 and the moderate swelling I experienced during the first weeks of eating just meat has resolved. My allergies are gone and I haven’t needed to use any bronchodilators nor antihistamine drugs. My GI tract is still adapting to this way of eating. Sometimes I get liquid stools but I ‘correct’ this issue having a piece of aged cheddar cheese.
I went to my family doctor and shared with her my decision to change my dietary habits and she recommended some blood tests. To the list she had, I requested to have my fasting insulin and C-peptide levels, which surprised her because in Canada these biomarkers are not investigated regularly.
All my labs are normal except for my cholesterol levels. I’m attaching my results here for your review.
My doctor phoned me to book another appointment to discuss my high cholesterol levels. I want to be prepared to answer to her questions and explain to her why cholesterol is not a meaningful biomarker by itself. I appreciate her concern for my health and I understand she is doing the best she can with the information she has. I feel the professional duty to share with her the evidence-based data available about cholesterol and health within the zero carbs diet as the rationale for my decision to embrace a carnivore diet high in saturated fats from animal sources.
Would you please help me with a short summary recontextualizing cholesterol levels on a low carb high fat diet? Can you guide me to find studies to support this recontextualization?
I thank you beforehand for your help and for all you do to educate the public and by leading with the example.
Sincerely,
Maria Schneider, RN, BScN, ACCN
250 571 9471
canadanahuatl@gmail.com
Suite 140
230-1210 Summit Dr.
Kamloops BC V2C6M1
*Please find attached my lab results on the next page
I’m trying to send you my lab results after following your protocol. I have them on PDF or JPG. Thank you fro your help,
Maria
I appreciate this post. I have a remnant score of 10 based on TC 249 LDL-C 180, HDL-C 59, TG 51. However my LDL-P was a whopping 2005!! Been Carnivore/LC for over a year now. Any thoughts on the excessively high LDL-P, and any reason for concern there?
With concordant LDL (e.g. LDL that is not of the “small dense” type) typically LDL-P is roughly LDL-C times ten.
So 2005 LDL-P within range for an LDL-C of 180.
So, keep in mind that if you are utilizing fat for energy (as you would eating fatty meats) your need for transportation vehicles (LDL-P) goes up, and the emergency life vests stored in these vehicles (LDL-C) also goes up merely as a result of more vehicles being around due to the need to transport fat at a higher rate.
Dave’s presentations from Breckenridge 2017 and 2018 may be some help in imagining how this system is working exactly.
If you’re altogether concerned you could combine your lipid panel with your other markers – signs of insulin resistance, fasting insulin, hs-CRP, etc and see what sort of story that is telling you. Is the context this higher LDL-P in telling you it is a healthy system (low CRP, low insulin, low HOMA-IR, higher HDL, etc), or a sick system?
As mentioned in the Top Ten Studies post, even in those with genetic reasons for high LDL-C (and thus LDL-P) the main difference between those who fared poorly and those who didn’t were signs of insulin resistance.
Hey Dave, great work. A couple questions.
I’ve been LCHF for over a year. But my cholesterol or triglycerides kept going up.
So now have been Carnivore 3 months. Weight has stabilised. Been pretty strict, meat and water. Occasionally grab a handful of blue berries. Not very often. I do drink coffee, working midnight shift over 30 years. So I redo my blood liped. Total cholesterol stayed about the same. 368. Always has been high. But I was expecting my tri’s to go down on this WOE. But they have shoot up from 406 in March to 696
As of yesterday. That’s alarming. I am 54 , 6’3″ 215. Started at 250 on LCHF. Lost a few more pounds on Carnivore. But has stopped losing. Workouts have been infrequent. Any help would be appreciated.
Hi Rock–
This phenomenon is of particular interest to me. We’ve seen a small subset of those who go carnivore that observe their triglycerides going up substantially.
As it happens — and this may be a legitimate coincidence — there does appear to be a common denominator with coffee.
Would you be willing to give up coffee for 10 days, then retest with no other changes to your diet?
Absolutely, I will start today and retest in 10 days. Going to be close, as we leave for vacation on the 15th. I use walk in labs, and they are usually pretty quick. Thanks, I’ll post up ASAP. THANKS
Dave, the last test was just the standard cheap blood liped test. The one before was the NMR any chance that’s makes a difference?
Which test should I run?
Well Dave here you go. Tri’s
Cut almost in half from 10 days no coffee. From 696 down to 292. And HDL rose 10 points to 45 . But total and LDL both went up . Is there a way to post pics of the tests on here ?
Wow, my math sucks too. Over 400 point drop. Thank you. So I assume I should quit drinking coffee , permanently?
Hi Dave,
Below is my report from a test that I got yesterday. I have been on the carnivore like diet for the past 2 months and take Lipitor 20 mg (have been taking for 10+ years). My results seem to have freaked my doctor out and he has told me to go see a specialist. I have also posted the report further below from my last year numbers (when I was on SAD). Remnant cholesterol seems to be okay. What do you think about the results?
–==== CholesterolCode.com/Report v0.9.2 ====–
…2 months on Carnivore/Zero Carb/Meat Only ::: 17 hours water fasted…
Total Cholesterol: 506 mg/dL 13.09 mmol/L
LDL Cholesterol: 422 mg/dL 10.91 mmol/L
HDL Cholesterol: 65 mg/dL 1.68 mmol/L
Triglycerides: 95 mg/dL 1.07 mmol/L
(VLDL value is 19 mg/dL)
–CHOLESTEROL REMNANTS–
Remnant Cholesterol: 19 mg/dL 0.49 mmol/L >>> Medium-Low Risk Quintile
Remnant Chol to HDL: 0.29 >>> Medium-Low Risk Quintile
Go to https://tinyurl.com/y8hokam2 for more on Cholesterol Remnants
–ATHEROGENIC INDEX OF PLASMA (AIP)–
AIP: -0.196 >>> Lowest Risk Third
Go to https://tinyurl.com/ycccmmnx for more on Atherogenic Index of Plasma
–CONVENTIONAL MARKERS AND RATIOS–
Friedewald LDL-C: 422 | Iranian LDL-C: 378
Total/HDL Ratio: 7.78
TG/HDL Ratio in mg/dL: 1.46 | in mmol/L: 0.64
Test from last year (07/28/17):
–==== CholesterolCode.com/Report v0.9.2 ====–
…3 years on Standard American ::: 12 hours water fasted…
Total Cholesterol: 230 mg/dL 5.95 mmol/L
LDL Cholesterol: 143 mg/dL 3.7 mmol/L
HDL Cholesterol: 64 mg/dL 1.66 mmol/L
Triglycerides: 117 mg/dL 1.32 mmol/L
–CHOLESTEROL REMNANTS–
Remnant Cholesterol: 23 mg/dL 0.59 mmol/L >>> Medium-Low Risk Quintile
Remnant Chol to HDL: 0.36 >>> Medium Risk Quintile
Go to https://tinyurl.com/y8hokam2 for more on Cholesterol Remnants
–ATHEROGENIC INDEX OF PLASMA (AIP)–
AIP: -0.1 >>> Lowest Risk Third
Go to https://tinyurl.com/ycccmmnx for more on Atherogenic Index of Plasma
–CONVENTIONAL MARKERS AND RATIOS–
Friedewald LDL-C: 143 | Iranian LDL-C: 159
Total/HDL Ratio: 3.59
TG/HDL Ratio in mg/dL: 1.83 | in mmol/L: 0.8
Hi Aman,
apologies for the very late reply on this, we had an issue with some accidentally deleted comments and are in the process of addressing these…
As for your results the difference between the two results looks to me like shifting from someone on a lower fat, higher carb diet to a higher fat, lower carb diet. If I, personally, had the most recent result I likely wouldn’t be particularly concerned as – from what I’m aware of – it’s just reflecting someone who is fueled by fat.
However, I do tend to want to take a look at other markers too, to make sure I’m taking the results in context, such as fasting insulin and CRP.
But I’ve yet to come across a study (although I have been looking) in which high HDL and low triglycerides presented a higher risk, regardless of LDL level – for what it’s worth.
I would love to know what fat metabolism polymorphisms Dr. Baker has.
Me too. Perhaps one day he’ll post his genetic profile.
Dave, I was following your experiments for quite a while, thank you very much for the awesome work you are doing!
Don’t you think that Shawn could have early stages of hepatic insulin resistance? His muscles are insulin sensitive, but liver might be not, so it does not stop secreting glucose if insulin levels are low, therefore high fasting blood glucose.
I became interested in low carb diet myself when my fasting glucose and A1C started slowly climbing up about a year ago. I used to eat very low fat, and fairly low protein, mostly fruits, vegetables, grains, fish, some eggs, some meats, etc. I was always moderately active, always around 185lbs, 6.3 tall. My lipids were for many years very good according to conventional standards, fasting glucose OK, roughly about:
Total cholesterol ~175
HDL-C ~50
LDL-C ~115
Trigs ~65
Fasting glucose ~90
Last year in July my results were:
Total cholesterol 209
HDL-C 49
LDL-C 144
Trigs 82
Fasting glucose 104
A1C 5.4
After that, I started eating mostly in 8-10 hour window twice a day low carb for a month and then keto for a month, results after 2 months (that was the first time I did NMR lipoprofile):
Total cholesterol 242
HDL-C 47
LDL-C 177
Small LDL-P 431
LDL-P 2039
Trigs 90
Fasting glucose 77
Fasting insulin 2.7
I was reading Peter Attia’s blog at the time and he was writing that some of his patients who were on keto and had high LDL-P lowered it by cutting saturated fat. So I decided to try to live for a month basically on a green salad with avocados, olives, a lot of olive and avocado oil and sardines or salmon with very little eggs, chicken and dairy. Results after that month were unexpected:
Total cholesterol 248
HDL-C 43
LDL-C 181
Small LDL-P 1267
LDL-P 2260
Trigs 119
Fasting glucose 99
I decided to continue with low carb diet with intermittent fasting without trying to stay in ketosis for a year or so and see what my bloodwork would be after a longer period of time. So last year I ate mostly all kinds of meats with salads, eggs, cheese, butter and olive and avocado oil. I had a cheat day with a burrito or pizza every few weeks or so. Surprisingly during all that year I never had ketones, even after 2 day water fasting. I did bloodwork a month ago:
Total cholesterol 258
HDL-C 53
LDL-C 192
Small LDL-P 507
LDL-P 2158
Trigs 63
Fasting glucose 104
A1C 5.9(!)
I was surprised my A1C was higher than when I was on a high carb diet. A1C 5.9 translates to 123mg/dl average glucose level, so if my fasting glucose was 104, to get 123 average I should have had 150+ postprandial glucose. So I started preparing for glucose and insulin stress test by eating about 200g of carbs every day for 5 days and did the test:
Glucose:
Fasting 105
1 hour after 75g of glucose, 76
2 hours after 95
3 hours after 83
4 hours after 79
Insulin:
Fasting 3.6
1 hour after 27.5
2 hours after 13.6
3 hours after 2.9
4 hours after 1.7
After a year of experimentation, I have worse total and LDL cholesterol, worse blood glucose, worse A1C and more questions then when I started. I decided to try to go back to low fat high carb diet for 3-4 months and see what’s gonna happen. Maybe my fasting glucose and A1C comes down if I eat carbs and will have higher levels of insulin, and my cholesterol becomes “normal” again? Is A1C test not useful? I obviously cannot have an average glucose of 123 unless I have >>150 glucose when I sleep (I hope http://www.gluco-wise.com/ or someone else will release their noninvasive glucose meter soon). Do I have hepatic insulin resistance and the early stage of a metabolic syndrome? If I do have an early stage of metabolic syndrome, is HFLC diet the best diet if I want to maximize long term health even if I get high total cholesterol, high LDL-C and LDL-P? Peter Attia and some other smart guys think that high LDL-P shouldn’t be ignored, but what are the alternatives to HFLC for hyper responders with metabolic syndrome?
I know that’s a lot of questions and no one knows 100 percent right answers, but any insight will help.
So firstly, I want to know your body fat and fitness level. As with SB from this article, I’m curious if your body has a reason to upregulate fasting glucose, particularly if any of your workouts land in the daytime.
Aside from that, I’d be willing to bet you my avatar graphic for a week that if you wore a continuous glucose monitor while LCHF, you wouldn’t see your average glucose at 123 mg/dL (or higher) — it would likely be much lower. Did you do more testing of your glucose throughout the day before meals and before bed?
And sorry to pile on more of my generally positive opinion of your numbers, but that Kraft challenge test looks pretty impressive. Compare your outcomes to this: https://idmprogram.com/understanding-joseph-kraft-diabetes-in-situ-t2d-24/
Thanks for replying, I really appreciate your input! I don’t know exactly what my body fat is, but I always was skinny and tried to do at least 1-2 hours of at least some physical activity every day – martial arts, basketball, running, cycling or hiking. The rest of the day I usually spent not moving way more than I’d like. Never lifted any weights, hated them, but 2 years ago started having problems with the knees, wasn’t able to run or do any sports that involve a lot of jumping, so started lifting, just basic stuff – squats, deadlifts, Olympic lifts. Now I alternate lifting days with hiking, light cycling, HIIT or yoga mostly. I workout usually in the morning, before the first meal which I’m having around noon. I’m a few months shy of 40yo by the way.
Regarding glucose – I see that my muscle insulin sensitivity is great. I just wonder if it’s possible that my liver’s insulin sensitivity is impaired and it doesn’t shut down glucose secretion even if it’s high enough. Also, the fact that I didn’t have any ketones, even if I ate low carb for a year, makes me question if my gluconeogenesis isn’t pathological. Or maybe fasting glucose at 105 is normal and increased after I started lifting weights? Actually, that happened about the same time.
Another thing I’m pondering on is lipids. If I was insulin resistant, I would choose HFLC diet anytime – having glucose and insulin stable and low for sure wins over potentially increased risk of CVD from higher LDL-P, of course, if, and big if, the increased risk of CVD is the real thing. But if glucose is stable and low with HCLF diet, but with HFLC diet LDL-P goes through the roof, is it a net gain or a net loss from HFLC diet? When you will be on Attia’s podcast you can ask him this question too 🙂
BTW, I liked very much not being hungry all the time on HFLC diet, having steady energy levels throughout the day, but when I started eating carbs again a few weeks ago I realized how much more explosive energy I have now! With HFLC I could lift or do some light cycling for a few hours without problems, but barely could go through HIIT workout, or let’s say do 10 box jumps without losing my breath completely. While with carbs after HIIT I can go lifting no problem, it’s really night and day for me. Maybe I should try to stay in ketosis for a half a year or so and see what my energy levels would be, but eating low carb without being in ketosis feels like giving away doping or something. I’m not competing, so it’s not a big deal, just an observation.
Is there a problem with the comment I posted a couple of days ago as a reply to this comment of yours? I still don’t see it. I see Siobhan is talking below about accidentally deleted comments, maybe mine was deleted by accident too? Thanks!
It looks like one of my comments is gone somewhere, I’m reposting it again below. Please delete it if original one reappears, thanks.
Thanks for replying, I really appreciate your input! I don’t know exactly what my body fat is, but I always was skinny and tried to do at least 1-2 hours of at least some physical activity every day – martial arts, basketball, running, cycling or hiking. The rest of the day I usually spent not moving way more than I’d like. Never lifted any weights, hated them, but 2 years ago started having problems with the knees, wasn’t able to run or do any sports that involve a lot of jumping, so started lifting, just basic stuff – squats, deadlifts, Olympic lifts. Now I alternate lifting days with hiking, light cycling, HIIT or yoga mostly. I workout usually in the morning, before the first meal which I’m having around noon. I’m a few months shy of 40yo by the way.
Regarding glucose – I see that my muscle insulin sensitivity is great. I just wonder if it’s possible that my liver’s insulin sensitivity is impaired and it doesn’t shut down glucose secretion even if it’s high enough. Also, the fact that I didn’t have any ketones, even if I ate low carb for a year, makes me question if my gluconeogenesis isn’t pathological. Or maybe fasting glucose at 105 is normal and increased after I started lifting weights? Actually, that happened about the same time.
Another thing I’m pondering on is lipids. If I was insulin resistant, I would choose HFLC diet anytime – having glucose and insulin stable and low for sure wins over potentially increased risk of CVD from higher LDL-P, of course, if, and big if, the increased risk of CVD is the real thing. But if glucose is stable and low with HCLF diet, but with HFLC diet LDL-P goes through the roof, is it a net gain or a net loss from HFLC diet? When you will be on Attia’s podcast you can ask him this question too
BTW, I liked very much not being hungry all the time on HFLC diet, having steady energy levels throughout the day, but when I started eating carbs again a few weeks ago I realized how much more explosive energy I have now! With HFLC I could lift or do some light cycling for a few hours without problems, but barely could go through HIIT workout, or let’s say do 10 box jumps without losing my breath completely. While with carbs after HIIT I can go lifting no problem, it’s really night and day for me. Maybe I should try to stay in ketosis for a half a year or so and see what my energy levels would be, but eating low carb without being in ketosis feels like giving away doping or something. I’m not competing, so it’s not a big deal, just an observation.
No issues with the post – you would be correct, it got delayed because of the issue you mentioned – we’re working on fixing the issue, but I restored it manually for now. Thanks for the heads up!
Thank you!
Very Interesting about Dr. Bakers Glucose reading. I have been on the carnivore diet since beginning of December, and my recent blood test I had a blood glucose of 120. My doctor wants me to eat more fruit and vegs, and even be vegan one day a week, even though I have lost 10 pounds and feel great. I will have to do some more testing, but I am thinking I need a new doctor…
Long term fasting high glucose will eventually lead to higher insulin levels in most people. However, I always go by fasting insulin with A1c, but mostly I look at fasting insulin and fasting glucose. If insulin is normal and glucose is high it’s because the body is keeping readily available sugar in the bloodstream to be used by muscles since in low carb or carnivore diet there is low or no muscle glycogen available for immediate use. The body is extremely adaptable and this is it’s way of adapting. Is it a good thing? I have yet to see studies proving it good or bad, but common sense might tell me that high blood glucose can cause organ damage IF blood glucose is too high for long periods of time. The other reason would be clogged receptor sites at the muscles, but I highly doubt it. I see this in people who eat a bunch of junk carbs and sugars! I’ve been in the health industry for nearly 3 decades!
I don’t know about most people – it’s possible that context matters. An intriguing parallel is those with glukokinase mutations who have similarly elevated glucose levels, but no co-occurring hyperinsulinemia necessarily, and they don’t present with higher levels of macrovascular/microvascular complications (noted as “rare”) compared to diabetics. They have these levels from birth. To note they have a steady, higher baseline – not glucose that fluctuates up and down from meals (quite different from diabetics/people eating unhealthy diets). Certainly not exactly the same, but does give one something to think about.
In order to really know if those poses a problem for lean, athletic folk on low carb diets you’d have to study them specifically though. There is a facebook group with plenty of them, and no one has reported back issues so far, but complications would of course take time to develop.
No mention of his pathetic testosterone levels? I mean, come on.
Yeah, he sure looks testosterone deficient. You need to look at the big picture.
Excellent reading and thanks Dave for all the useful research you do. When are you going to publish your book? 😉 I have just finished Why We Get Sick for a further insight into the world of the amazing hormone Insulin. I found Shaun’s BG levels compared to insulin quite puzzling, would that be the effect of the other major hormone Glucagon?
Thanks.
The book is in the works – we have a few other items we need to get out the door first, which is the main reason it’s not out yet. 🙂 Stay tuned.
RE: Shawn I’m not sure of exact mechanisms, as there are probably multiple parts, but I would guess glucagon would be a part of it as it stimulated glucose production. I’d guess other factors too – likely the same ones that result in increased glucose during high impact exercise.
Have you seen Shawn Baker recently? He lost all his muscle and looks gaunt and frail. Not exactly a good poster child for the low carb movement.
Thank you Dave Feldman. You are a saint. And some idiot doctors will now criticize the carnivore diet based on Baker’s fasting glucose and hemoglobin a1c.
Enjoyed this analysis. A1c is still a concern for overall aging even if one can possibly make the case that his other parameters make his CVD risk low per your analysis. I wonder if he is addressing this by including more animal fats as opposed to protein which is most certainly causing this. I certainly would not be happy with that A1c and would be concerned for long term effects.
I believe a little while ago he changed his exercise and eating schedule which resulted in lower glucose throughout the day, and presumably lower A1c as well. He’s on twitter, so you could ask him or search for his tweets on it.
I am a 58-year-old female I do jujitsu eight hours a week. I’ve been carnivore since January my A-1 C is creeping up. It was 5.7 on keto I cured my pre-diabetes with keto but since going carnivore it has gone up to now 5.9. I am a LMHR. Tc-341,T 46, hdl 99ldl 238 Vldl 4. Does an elevated H1C mean damage in my body? I feel tremendous, high energy clear thinking!
Hi Annette – we’re not doctors and can’t give medical advice so we can only comment with our thoughts in case they may be of interest.
We can’t say whether a higher or lower marker than normal is of concern or causing damage (see above point about not being doctors) but as Dave discusses here about others we’ve seen with similar situations (including Baker at the time of this post) I would be curious to see what the insulin level is and what the glucose levels are throughout the day if it were me. These can help provide a bit more context, so that you (and your healthcare team) can decide what to do from here in terms of making changes to diet, if you wanted to do so, since it sounds like carnivore was what caused (or correlated with) the change initially. Since, as far as I know, this subset of the population (in the case of higher hba1c and normal insulin levels) hasn’t been well studied in terms of outcomes etc it would be up to the individual to decide how they feel about it and what they feel is the best choice for them in terms of responding to it (making changes, keeping an eye on things, etc).
How would you diagnose between Adaptive Glucose Sparing in a Lean Mass Hyper-Responder (LMHR) and early onset of Latent autoimmune diabetes in adults (LADA) aka Type 1.5 Diabetes?
I’m 43, skinny, athletic and exercise a lot. My blood sugar went up from 5.3 to 5.8 after I started a low carb diet last year. I also do intermittent fasting, sometimes one meal a day. I did a C-Peptide test and my result is 0.8 (just barely within the normal range of 0.8 – 3.9 ng/mL), and a fasted insulin test, where I got a 3 (again, just barely within, the standard range, 3 – 28 mUnits/L).
While I’m relieved I don’t have T2D, now I’m worried about T1D and will go have some antibody tests done to check.
Is it normal for LMHR types to have low fasted insulin? Could this be the reason the fasting blood sugar stays somewhat high? (it actually goes down when I eat, so I’m never above 130).
Dr. Baker’s HOMA-IR score, a favorite of Ted Naiman, M.D., is 0.81 indicating insulin sensitivity (opposite of insulin resistance).
When I first started keto 3.5 yr ago my A1C went to 4.9. (Before that I was a poster boy for high carbs. ) Since then in the past couple years it has gone up to now 5.6 despite testing blood sugar often and that average is about 95 so a big disconnect. Also now a 3.5 fasting insulin. I have seen where red blood cells may have a much longer life than the usual 3 months assumed for the A1C calc. I have a BMI of 19.2, and exercise – p-ups and chin-ups . Am 71. High Chol and LDL but good HDL and trig’s. Am glad I found this article!