#KetoAF Talk of the Town on Twitter
Around March of this year I began to hear the term “#KetoAF” being used on Twitter. Not just from one person, but from several. The people using the hashtag weren’t using it to mean “very keto” or to exclaim that something was keto in a cool way. Instead, they were using it as a shorthand for “Keto Animal Foods”, or a carnivorous diet where fat was prioritized.
The people discussing KetoAF were also talking about how it helped kickstart weight loss after long stalls, or helped to resolve persisting issues that were lingering even with a more protein heavy carnivorous diet. I was intrigued, especially as I had heard the Paleolithic Ketogenic diet (PKD) discussed at CarnivoryCon earlier that same month.
By April, I was making plans and coordinating with Amber O’Hearn (who coined the term KetoAF) and Josh Blackburn (a fellow KetoAFer) to set up the experiment. This would turn out to be one of the longer experiments in my history, as I wanted to give it enough time to do something – if it did anything at all.
Over the course of the experiment, I ran into a few problems with testing. You can read about the details below, but to summarize:
- I needed to re-test my baseline, I did so by extending my baseline 1 day and re-testing the following morning.
- The baseline microbiome results were lost
- The post-intervention PEG400 data was lost
- The two final tests were confounded by a cold and by a sunburn
The data from the microbiome test I had done at the end of the baseline was lost as well – the company I was testing through (ubiome) discontinued support of the smartgut testing a day or so before I sent in my sample and cancelled my order as a consequence. I did however get a test at the end of the experiment via their explorer kit.
I was able to get a PEG400 at the end of the baseline, and got those results back fine. However the other kit I had for testing at the end of the intervention had apparently leaked in transit, and I wasn’t able to get a replacement fast enough due to an issue with the label on the replacement.
The final two blood tests were confounded due to 1) getting a cold and 2) getting a sunburn by falling asleep outside on accident. This definitely impacted the results, so unfortunately the blood data likely isn’t representative. I was working under some time constraints, and didn’t have time to extend the baseline further, but I did get another test when on unrestricted ketoAF a month or so later, so will provide that at the end, as it wasn’t part of the original experiment.
Prior Diet and Baseline
Prior to the experiment I had been following a predominantly carnivorous diet (barring experiments, etc) as of October 2017 (a little under a year and a half). I had lost an additional 25 pounds from switching to carnivore from omnivorous keto, bringing me down to 140 lbs. For around a year I had been at 143 lbs without additional weight loss. To note, this still left me “overweight” (and overfat, according to a DEXA). Throughout ad libitum carnivore I averaged around 30% protein, 70% fat and negligible carb from seafood and dairy.
The baseline diet was originally intended to be 10 days, starting at May 17th, but was ultimately 7 days, starting at May 20th to May 26th. The first three days of the original baseline had unusually high glucose readings, and I also realized I was eating too fatty for my intended 1:1 target, so these three days were excluded.
During the 7 day baseline I tracked morning glucose, ketones, and weight. I ate ad libitum, and logged all items consumed via pictures.
During this period I consumed:
- Trimmed ribeye
- Vitamin supplements (vitamin D, and methylated B vitamins)
- Electrolytes as needed
After the baseline was completed I tested intestinal permeability with a PEG400 from ICMNI, as well as a slew of bloodwork which was repeated at the end of the intervention.
I ended up having to re-test the bloodwork the next day, as discussed, thus on the 29th I did another set of blood tests which we will consider the official baseline bloodwork, here.
The intervention diet was set up to be ad libitum, eating when hungry until full and avoiding fasting beyond 24 hours if possible (to ensure any weight loss was not due to the fasting/ensuring I didn’t confound any lab results). I wanted to make sure I gave it sufficient time to show positives or negatives so ultimately decided on 26 days. The goal was not protein restriction, but rather fat prioritization so meals generally followed this pattern:
- Eat raw beef trimming until no more was desired (satiety)
- Eat raw beef liver (75g) next – this was included as I had stopped B vitamin supplementation, raw liver was best tolerated compared to other preparation methods.
- Eat trimmed ribeye (main protein source) until satiated.
The “goal” would be 2:1 fat:protein by macronutrient gram, but if I got full before I reached this, it wouldn’t be forced, and if I ate above the ratio (more fat) this would also be fine. All food was weighed and logged via pictures. Supplements and coffee were discontinued during the intervention period. Weight was taken each day, along with glucose and ketones (BHB).
I had two check-in labs, mostly to verify my folate levels were remaining stable with the removal of supplementation and addition of liver. On June 24th, the end of the experiment I tested the following:
- Microbiome test
- Blood work
Late Game Change to Intervention Diet
Originally, the intervention diet was supposed to include 75g~ of raw beef liver per day. However, after a couple weeks, I began to feel averse to eating it. I continued eating it, as part of the experiment design, however this rapidly turned into nausea after consuming it at meals.
On 6/17 the reaction to eating the liver escalated into becoming physically ill after eating it. In order to make sure I could continue the experiment, I decided to discontinue liver consumption for the duration of the experiment.
I’m not sure why this happened, exactly, as the reaction was disimilar to food poisoning, especially as the reaction increased over time. Some I’ve spoken to have speculated the aversion may have been due to being “topped off” on a certain nutrient (or nutrients) found in liver, but I have no way of verifying this.
During the baseline (5/22-5/28) I remained weight stable, fluctuating between my normal weight of 145-147 lbs. After the KetoAF intervention, I remained weight stable for four days, after which my weight began to decline. My weight continued to decline at a steady rate, with the exception of a period where I had a cold (6/9-6/14) during which I was weight stable. The week after the cold cleared (6/14-6/18) I was also stable at a slightly lower weight, but it is unclear if this is related.
The decline in weight continued until the end of the experiment (6/24). The total weight lost from the lowest weight of the baseline (145 lbs) compared to the lowest weight of the intervention (138 lbs) was 7 pounds. At 5’2″, and considering this is the lowest weight I’ve achieved during my adult life, I would consider this weight loss significant.
Macronutrient and Energy Intake
During the baseline, I averaged 1855 calories per day. During the first two weeks of the intervention, calories dropped to about 1750 calories per day – resulting in about a 100 calorie decrease from baseline. Average fat grams increased from 122g per day to 164g per day, and protein decreased from a daily average of 148g to an average of 51g per day.
On the last day of my cold (6/13) I did not eat as I was not feeling well. This resulted in week 3 having a low average calorie intake. Unfortunately, week 3 is also missing data for one day (6/18). I know I didn’t fast that day, but can’t find picture logs of what I ate. In order to not artificially depress the average, this day has been excluded from all calculations of averages.
Finally, the average calories for week 3.5 was slightly lower than weeks 1 and 2 at an average of 1683 calories per day – on average, 67 calories less per day.
Over all it appears as though eating a carnivorous diet with a high fat content did not result in an increase in energy intake, and indeed seemed to result in a general decrease (100-200 kcal/d). Despite being very energy dense, appetite appeared to be properly regulated. It’s also interesting to note that although week 3 was the lowest calorie week, this did not correlate to more weight loss – in fact, I did not lose weight during this time period.
Ketones and Glucose
Over the course of the experiment, a significant difference in average ketone level was recorded. During the baseline, average ketone level was 1.5~ mmol/L and over the course of the intervention average ketone level was 2.8~ mmol/L.
Glucose levels were not significantly different during the duration of the experiment, with an average of 89.8 mg/dL during baseline and 90.0 mg/dL during the intervention.
At baseline, my Total Cholesterol and LDL Cholesterol were 312 mg/dL and 251 mg/dL respectively. By the end of the experiment these had decreased by 88 mg/dL and 83 mg/dL respectively, to 224 mg/dL and 168 mg/dL.
HDL remained within my normal range throughout the experiment at 45 mg/dL, while my triglycerides decreased by 26 mg/dL from 82 mg/dL to 56 mg/dL.
It’s possible that these results were confounded by the cold and sunburn at points 6/13 and 6/24, however a follow-up lab on 8/2 showed Total Cholesterol of 231 and LDL-C of 155 mg/dL, as well as triglycerides of 45 mg/dL so I find it likely these are representative. HDL at follow-up was 67 mg/dL but it is unclear if this is a one-off or a new normal. Further testing on all of these points will be beneficial.
Vitamin B12 and folate both increased during supplement cessation and liver inclusion and dropped somewhat post liver exclusion. A longer time trial without liver would be needed to see where they settled longer term.
Throughout the experiment Vitamin C levels remained steady with a small decrease in Vitamin A and a decrease in Iodine. It’s unclear if the decrease in Vitamin A was impacted by cessation of liver consumption.
Glucagon increased from baseline and insulin generally decreased (excluding one datapoint on 6/13 from when I was sick; not shown). They appeared to mirror each other over the course of the experiment.
Free T3, and IGF-1 both decreased over the experiment. Longer term tracking of Free T3 would be needed to gauge relevance versus fluctuation. Low T3 is not entirely surprising due to a very high fat, low carb diet as mentioned in this post. No hypothyroid symptoms were noted during the course of the experiment, and energy levels remained stable.
Uric acid, interestingly, increased over the course of the experiment. Further testing would be required to gauge whether the increase in Uric Acid was temporary due to a deeper level of ketosis (as evidenced by higher ketones) as noted by Westman Et Al that this can cause a temporary increase in Uric Acid during keto adaption. The follow-up test from 8/02 showed uric acid was back to 6.2 (data not shown), so this is suspected in this case. Further testing over a longer time period is warranted.
Finally, although possibly confounded by the circumstances of the last two data points, lipoprotein(a) levels generally decreased during the experiment, just as LDL-C did. This is consistent with Lp(a) following LDL levels over the course of various experiments, with its role as an acute phase reactant in mind given the cold and sunburn of the last two tests (possibly elevating it above what it might have been otherwise). Longer term tracking would be interesting to see if this is sustained over a longer time period.
Ultimately I greatly enjoyed ketoAF as a way of eating over the course of the experiment, minus the liver incident. Since the experiment, I’ve been using ketoAF as my baseline diet including at conferences (e.g. at Low Carb Houston I ordered moist brisket with a side of butter). I find it easy to do even when away from home, and my food enjoyment has increased.
I’ve found it to be a helpful tool post-High Carb Experiment (post on this one coming soon), to help come back from the weight gain and adverse side effects that lasted long after the experiment. I find I will likely continue it longterm as long as I continue to enjoy it. Longterm data will certainly be interesting, especially if it allows me to come down to a normal/lean weight/bodytype given enough time.
This is great! Can you clarify the raw beef and liver trimmings part. I love raw meat but dont eat it often due to sanitary concerns. Dont think I would enjoy raw fat. Did you actually eat all that raw as described? Thanks
Hi – I was getting all of this from a local butcher and local farm and the liver was frozen for several weeks prior to eating it, hence why I was comfortable eating it raw. I did eat both the fat and the liver raw, the ribeye was cooked. All of that is just preference, on my part, and of course if you ever do eat raw do so with caution, there’s always a risk, etc.
Wow! This is truly remarkable. Glad I didn’t bet money on the outcomes! Strong work.
What was your diet heading into this test (i.e. what was responsible for the TC and LDL of 312 mg/dL and 251 mg/dL)?
And what do the PEG400 results mean? Is lower recovery % good or bad?
Diet heading into the experiment is explained under baseline diet. It was a higher protein carnivorous diet.
PEG400 tests intestinal permeability – sorry if I didn’t explain! Essentially it’s checking for “leaky gut”, which has been correlated to various health issues. How it works and what they’re measuring is explained in-depth here. Between the solid lines is considered “normal”, typically those with increased intestinal permeability have a higher recovery %.
Why raw liver and raw beef?
And, maybe I missed the point, but what was the objective of the experiment?
Just preference on my part. I don’t like liver in general, and especially dislike it cooked, and I dislike the texture of cooked fat unless it’s in very small amounts.
The objective outlined in my hypothesis/set up post (posted to CC members prior to starting) was just exploratory. Essentially, just to try it and see what happened to weight, blood markers, etc. I wasn’t sure what to expect so I didn’t really have any guesses.
Maybe I should upper my fat intake rather than CHO to normalize my LDL 🙂
Heh, well I’m not sure if it will sustain that way long term, especially if I come down to a normal weight/lean out. I suppose we’ll see though! If anything interesting comes up, I’ll do an update post down the road.
Excellent work. Very interesting!
Liver has a lot of vitamin A. Too much can be toxic. Your body was probably telling you you’re getting too much vitamin A..
Vitamin a toxicity is fairly unlikely for most people: https://youtu.be/C_ufMDJ0OxI?t=239
Your reactions after eating liver are consistent with vitamin A toxicity.
Hi, I’m also interested in what you meant by “trimmed ribeye”. Does this mean you trimmed the meat off to leave more fat or the other way around? I’m trying to get my fat content up to 2:1 protein but finding it difficult with regular ribeye and other steaks. Trying also to cook eggs in tallow but doesn’t taste that good. Also, just wondering if you tried cooking the liver would it have made it more palatable?
Thanks for your work on this.
Hi, trimmed ribeye means I was trimming off the fat and cooking the lean and eating it (after consuming the raw fat). This is just because I dislike the texture of cooked fat, generally, so was just taking it off prior and eating it raw along with additional fat. If you’re trying to find ways to get more fat you may want to check out this post on the keto animal foods blog. Instead of tallow you might want to try lard/pork fat – I find I prefer the taste it imparts compared to using tallow.
I’ve also had cooked liver a ton of times. Raw was actually the most palatable, hence why I chose it. But, that’s still a low bar as I still dislike it no matter how many different times or ways I try it lol. Perhaps it’s just not for me!
Hi Siobhan, your experiment has been illuminating, especially about the liver. I commented earlier in the experiment that I have been eating liver almost daily since I realized it gives me some kind of energy boost and mental clarity. My intake was sometimes lower than yours, usually ranging between 40-80 grams, and always raw. I have also noticed if I go more than 3 days without the raw liver, the benefits go away and my mood is lower. I have been trying to figure out what nutrient(s) I must be deficient in, so if anyone in your community has a guess, would lover to hear. I eat lots of eggs, other organs (here in Spain we get nose to tail easily), and no supplementation other than D/K2 irregularly. I rarely eat plants, sometimes an avocado or olive oil. I eat rare or raw in the warm months and more cooked meat in the cold months. Been eating carnivore for nearly 3 years now but the liver just the last year.
When I saw that you were supplementing with methylated Bs, it made me wonder if you were getting too much of one or more B vitamins during your experiment. Were you taking them concurrently with the liver? What was your reason for including them? My apologies if you have explained this and I missed it. Thanks for all you do – it’s been a fascinating experiment to follow.
Hi – no, I think I mention it in the post but I was taking b vitamins during baseline, then stopped during the intervention as liver was introduced. My reason for including the liver is I wanted to stop all supplementation as there’s been some speculation they can sometimes do more harm than good in some cases.
The reason I supplement is my folate runs low – not sure if that’s a forever thing or something else, but if I don’t supplement for too long I’ll start getting symptoms again.
So, in short, I wasn’t both supplementing and taking the liver. It was one or the other, not both.
In theory you’re also supposed to excrete excess B vitamins as they’re water soluble anyway, but I don’t know really.
As for your enjoying liver, I think that’s what I tend to go with. If you enjoy it and feel better eating it – that’s good! Maybe keep doing it. If you’re like me and you dislike it and it makes me feel worse – I think I’ll skip it. Or, like my mom, eat it when you crave it (which for her is once every few months, and a tiny amount).
I find the reaction to it, going from anecdotes, seems to vary by person so perhaps it depends on the individual and their circumstances. Not sure, really. For now I’ve decided to forego it for the foreseeable future.
What symptoms do you get when you don’t take folate?
They’re somewhat nonspecific in that it could be caused by many things, but include longlasting tingling and numbness in my extremities at one point to the point of reaching halfway up my arm, erratic heartbeat, and breathlessness. Most notably this is paired with low folate on a blood test, which is why I say it is related to low folate (as I supplement, blood measure goes up, and symptoms go away and return if I stop supplementation for long enough).
As always, although I’m not a doctor, if trying to determine a vitamin deficiency I make sure to verify it if I suspect it via a blood test instead of just going off of symptoms.
I much prefer lamb’s liver, tried that? I fry it lightly in EVOO with a giant mushroom,, seasonal greens lightly boiled, and BACON! I have a couple of slices every couple of weeks, so far only with benefits – cheap and nutritious and a much better flavour and texture than beef liver.
I’ve had fresh chicken liver, beef liver, and I believe lamb liver from my mom’s lambs – but I’m not sure on the last one. Since liver makes me nauseous now (not as a property of taste) I’m just avoiding it entirely for the time being. If I ever want to reintroduce it, I’ll try lamb liver!
Hi, thank you for your great website, I also watched your video and it made me less worried about my recent Cholesterol test. I started keto in January 2019, here are my numbers before keto and while being on keto:
CHOLESTEROL, TOTAL: 189
HDL CHOLESTEROL: 60
CHOLESTEROL, TOTAL: 259
HDL CHOLESTEROL: 63
CHOL/HDLC RATIO: 4.1
NON HDL CHOLESTEROL: 196
I would love to try your method before my next test but was wondering if the “no coffee” and “no MCT oil” would be only for those three days prior to the test or all the time? Thanks again
Hi – if your LDL has gone up from a low carb diet, you would be what is called a hyper-responder. Although we can’t say whether you should worry or not, we can provide resources that may help you come to your own conclusions about what you’re comfortable with. For example, Dave did a presentation on risk from a cautiously optimistic point of view, and we also have a post from Dr. Nadolsky from a cautiously pessimistic point of view. We also have the CholesterolCode facebook group where a lot of great discussion is had, as well as the latest studies relevant to cholesterol, risk, etc.
As for the coffee and MCT question, the coffee is for the fasting period (12-14 hours water only prior to the blood draw), and the MCT/coconut oil is for the total time of the experiment. Hope that helps!
I don’t want to be too harsh, but this sentence had me in stitches : ” if your LDL has gone up from a low carb diet, you would be what is called a hyper-responder”. And if one bleeds from a gun shot, he’s just genetically hyper-sensitive to high-velocity lead thrown his way.
Are we going to claim the trove of data accumulated over half a century was all faked? Give me an egg, my LDL is going to jump up. There’s no magic there, you add dietary cholesterol to your diet, it goes into your blood following a rather accurate formula.
Even Loren Cordain (pre-Paleo nonsense; bring in the easy money), in a 2004 study he co-authored, recognized the protective range for LDL to be within 50-70 based upon every available data.
Next up : Obesity is protective against infections!
No worries about being perceived as harsh, questions and critique are appreciated. By a hyper-responder, I don’t mean someone who is genetically predisposed to higher cholesterol on a low carb high fat diet, quite the contrary this is a pattern that pops up for people who’ve become leaner (sometimes their LDL initially goes down if they were obese to start with). This is unlikely to be genetic, as it has appeared across a wide array of people, of many different ethnicities and backgrounds (not to mention ages and genders).
Rather than cholesterol being the driver of this change, however, the pattern we’ve spotted (called the inversion pattern) instead seems to suggest that fat based energy is the driver, not the actual cholesterol content of the food. This is explained in the following presentation, and data on this pattern – in which very high fat intake leads to decreases in serum cholesterol – can be read up on here, here, here, here, and here.
Note that because animal based fats were used in much of the original data as well as the replications that serum cholesterol was decreasing as dietary cholesterol increased. Likewise in some of those you can see that fasting increased serum cholesterol – which reflects the energy model – even though no cholesterol was ingested. This is reflected in other published research, not just our own data.
Ironically, in the post you’re commenting on you can also see the self experiment I did (eating a very high fat animal-based diet) resulted in a decrease in LDL over the course of nearly a month – not an increase.
So no, no one here is claiming that the current ideas are fake – merely there is now additional information which may support other conclusions. The energy model (linked prior) formed from this new information would likewise explain why obese people who go on low carb high fat diets tend to see LDL decrease initially, only to go back up if they become lean, mentioned in this presentation.
We also make no statements as to whether this is harmful or benign – as although there is some research indicating that if HDL is high, and triglycerides low, that this does not increase risk for CVD/all cause mortality even if LDL is high – this is not definitive. In fact we currently have the Low Carb Cholesterol Challenge that’s currently ongoing to find any studies that indicate the opposite in this specific context (the ‘low carb triad’). Feel free to post any studies you have that fit the criteria – there’s even a monetary award that’s currently unclaimed.
The ‘hyper-responder’ comment is more so to explain why the increase likely occurred, and that it’s a not uncommon pattern. Not to dismiss that it happened. From there the person can take that information back to their doctor to discuss and decide on whatever they would like to do – further testing, steps to move away from the profile, etc. We also tend to link this ‘cautiously pessimistic’ view of high LDL in a LCHF context that they can also read so they can see both sides of the current discussion and decide for themselves along with the help of their health team.
We do not offer medical advice here, and in many of the comments where it’s not already clear we state that as well as the fact that we’re not doctors. It also says this at the bottom of the website. It is also recommended to take any information from the website back to your doctor to discuss it and decide on follow up steps from there. We merely provide information, both from self experimentation, replication from others in the community, and published research, so people can better decide for themselves.
And if someone is uncomfortable with their higher LDL based on the research they’ve read, or conversations they’ve had with their doctor, we’ll generally inform them of the (generally dietary, but not always) strategies that other people in the community have taken to lower their cholesterol so the person in question can see what methods tend to work best (to date the most reliable and effective is swapping some dietary fat for carbohydrates usually to the tune of 75-100g of carbohydrates per day, which goes along with the energy model) so they can work their doctor to follow this strategy to see if it works for them, based on their health goals and concerns.
We do not encourage them to go in any particular direction and encourage all who come here to read both sides (hence why we have the post from the board certified lipidologist Dr Nadolsky that is commonly linked) so they can work with their doctor to make their own choices, including getting further testing to measure disease or disease progression if desired. In fact, there have been many times that we’ve stated the benefits of working with your doctor on these types of issues, and encourage discussion with their health team above all else, as well as emphasizing that this question of the profile (high HDL, low triglycerides, high LDL) is not fully answered so everyone must proceed with caution and make decisions that they are comfortable with longterm – whatever that is.
Thanks again for your comment, and I hope this helps clarify a few points.
This sort of pseudo-scientific advice is putting his life in danger. Don’t you have any sense of honor? Send him to his GP presto instead of rambling on unproven mumbo-jumbo pushed by egg-board funded quacks.
Don’t be so rude Sam P. Please take yourself elsewhere. The rest of us are here in a genuine attempt to consider ALL the evidence. Any of us who are worried, can go get medial advice at any time. Thanks Siobhan and Dave for your work toward improving understanding of this complex question.
How did you decide to use the phrase “unproven mumbo-jumbo”? When she provides multiple high-quality research articles and evidence that succinctly disproves your comment:” Are we going to claim the trove of data accumulated over half a century was all faked? Give me an egg, my LDL is going to jump up. There’s no magic there, you add dietary cholesterol to your diet, it goes into your blood following a rather accurate formula.” You are clearly unwilling to consider new data that refutes your point-of-view and instead fall on the old standby of dismissing science as unproven and pseudo science. If this hyper-responder was sent to a GP they would put them on a statin for sure of which it is well accepted in current medical science that the use of statins is based on some of the most absolute horseshit scientific research ever produced.
[…] #KetoAF Experiment Results – Trialing High Fat Carnivore […]
So,if your glucagon went up and your insulin went down, this would imply your blood sugar went up. Did it?
It states in my post that my glucose stayed about the same, but ketones went up.
Sorry, I’m an idiot. I must have been looking on my phone and did not see the graph. When I looked again on my computer, I saw it.
I know you and Amber O’Hearn have different ideas, but I think you just proved Peter D.s’ Protons theory hypothesis from Hyperlipid. As another data point, check out this other N=1, where he goes from carnivore to a high stearic acid (but with wheat and other carbs) diet and loses weight:
No worries – happens to the best of us. 🙂
I’m not sure about “proved” as there are definitely multiple factors involved in the experiment, but perhaps potentially supports… maybe. Brad’s experiment is definitely on my radar, and I do find it quite fascinating. I may go about doing something similar in a carnivorous context to see what it does.
Just heard your great interview on Low Carb MD podcast, and would like to take you up on your offer to leave comment here.
65+ male doing LCHF / KetoAF for 2 years, IF 16:8 for 1 year, high intensity resistance training to MMF for 5+ years.
17% BF (per Bodpod), BMI = 21, waist to height = 0.48
Total Cholesterol (fasted) = 347, LDL = 240, HDL = 94, TG = 66, (TG/HDL = 0.7)
Fasting Glucose = 108 mg/dL
Hemoglobin A1C/Total Hemoglobin = 5.5%
Fasting Insulin = 11.1 uIU/mL
HOMA IR = 3.0
Given my diet and life style I expected high LDL but not the high Insulin.
Would appreciate your comments
Glad you enjoyed the podcast! It was quite fun to record. 🙂
That is quite interesting, especially with the context of the rest of your blood results. Although we’re not doctors, and can’t give medical advice, I’d likely want to follow-up to see if I can see what was causing it, assuming it wasn’t a lab error (which is always a possibility with any testing). Was there any possibility of odd circumstances prior to the blood draw? Were you 12-14 hours *water only* fasted at the time of the blood draw (e.g. no coffee, no tea, etc), any recent illness/high stress situations, normal diet in the week leading up?
It actually looks like you have the profile of a Lean Mass Hyper-responder, who typically have insulin on the lower side, which makes it all the more interesting.
If it were me and I’d ruled out the possibilities listed above, I’d likely also want to re-test under normal circumstances (normal diet, normal stress level, 12-14 hours water only fasted) to verify it wasn’t just a lab error.
Thanks for your feedback.
It was a 13 hour fast (not even water). Other possible factors were:
– tested at 7:30 am (since posting I have read about “dawn effect”)
– sleep is not great
– take allopurinol long-term (doc doesn’t want me to stop although I don’t know if gout is an artifact of my pre-LCHF self and would no longer be an issue)
I have also come to the conclusion I have to re-test before I wear myself out chasing edge scenarios
Thanks for your efforts (and Dave’s) on educating the citizenry
I am curious as to since I started carnivore my liver enzymes have increased alot. My ALT went from 16 -55 since starting carnivore. The test was 6 months into carnivore. My AST also rose from 23 -40. They did an ultrasound and hepatic bloodwork and everything was normal. I would love some input.
Interesting – I’m not a doctor, and can’t give medical advice, but out of curiosity has your physical activity changed at all? If not in type, or intensity, in timing. I came across someone a while ago who saw an increase in liver enzymes and it turned out it because they were doing a lot of high intensity exercise + exercised in the days leading up to the test (and I think on the morning of, but I don’t recall exactly).
I also sometimes see this in people who do a lot of heavy lifting, etc.
This is awesome! I was in Keto about 1 year and been on Carnivore for 5 months now. My A1C is 6.1, glucose is 123, Triglyceride is 109, HDL 59, LDL 377. I ate most ground beef 80/20. Could you give me your thought please?
Hi, I’m not a doctor and thus obviously can’t give medical advice, but I can provide some questions and info to see if it may help clarify.
First, a couple questions:
1) Are you particularly physically active? Especially something like HIIT, weight lifting, karate, etc?
2) Were you 12-14 hours water only fasted for the test? E.g. no coffee, no tea, etc
3) Did you happen to get insulin tested?
I’ve seen higher glucose/hba1c in carnivores who are active, and this may be because their glucose is increasing during exercise to meet energy demands. Shawn Baker for example, is an extreme of this as he exercises I think pretty much every day with a lot of high intensity stuff. As you can see in this post his hba1c and fasting glucose is higher, but his insulin is quite low. From people who have continuous glucose monitors, we can also see their glucose rising during their workouts, then going back down after they’re done – perhaps providing a hint as to what’s going on.
But, in this case insulin is almost always on the lower side, so if it were me I’d want to take a look at that and confirm the context. This also helps rule out something else causing the higher glucose (or provide a case for further follow-up/troubleshooting). Not properly fasting can also skew results in some cases, even if it’s just coffee so that’s why I asked about that.
Hopefully these questions provide a couple hints for follow-up initially to get a bigger picture view.
I really enjoyed your experiment above. You really kept detailed track of all the variables. I’m curious for your theory of why Keto AF would be better than Keto plain.
I’ve found that when I do Keto Af for a while, I tend to get muscle cramps, sometimes in the legs and sometimes in my whole body. I’ve supplemented with salt, potassium and epsom salt baths. I’m curious if you have any other ideas.
There are a couple theories as to why. I’ve been carnivorous for a while now, and switching to high fat seems to generally be benficial – Amber O’Hearn has looked into the science of it a lot more than I have, I think she discusses it here, specifically. As for keto vs carnivorous keto/ketoAF there are a couple possibilities (higher quality nutrients, less irritants, etc) but it’d mostly be speculation on my part to even guess.
Regarding the cramps, I can’t give any medical advice as I’m not a doctor – and I’m not really sure if electrolytes aren’t working. I know for some people they seem to need way more salt than they might otherwise suspect, especially during transition into lower carb/higher fat. Dave, for example, eats a ton of salt – just by salting to taste/sipping on slightly salty water throughout the day. It may be worth a try to up salt intake until eating it to taste and see if it helps. Otherwise I’m not sure, and if it were me, would likely seek out a keto/carnivore friendly coach who may be able to help me troubleshooting.
Could you tell us how many meals per day did you had during this experimentation? and also at what time did you have them? (cf circadian rythms)
Hi – it was an ad libitum diet so my first and last meal timing depended on hunger. I went back through my picture logs, and they were pretty consistent though. They were always at the beginning and end of the day between 6-10am (the majority between 6-7am) for the first meal, and 6-7pm for the second meal. High protein baseline was the same wrt frequency and timing. I wasn’t hungry enough to warrant any third meals.
In case you’re curious, I am doing ketoAF now (sans liver, and with slightly different food but similar fat:protein ratios), and have been doing it on and off since the experiment (sometimes with dairy, sometimes without – currently feel better without) mostly on. I am currently still doing 2 meals a day, one around 5-8am, and the second around 8-10pm. The only difference is I have a biphasic sleep schedule so the second meal is “late in the day” but is actually a bit after I get up from my second sleep phase. Daily average still at 1750ish cals per day.
Hope that makes sense and answers your question.