Thank you again for the articles. Just read them. Dr. Dayspring’s was most helpful. Amazing turnaround with the subject who modified her diet. Fascinating about the cholesterol synthesis markers. Definitely worth looking into this more. I bookmarked it and will return to it soon, I’m sure!
the test was two weeks from quitting coffee and 9 days from quitting tea. I may have said different in the past but I checked to make sure I do not give wrong answer.
Thank you for the time and effort you put into allowing us all to learn. I don’t think I would have the patience or willpower to stay with a carnivore diet. I remember “trying” protein only years ago and gave up after only about 2 days. I felt so lousy and unsatisfied eating only protein that I had to abandon it.
Thanks. I’m not sure anyone really knows how long it takes for changes to take effect. For instance, I did an experiment in 2016 to test the difference between fasting triglycerides and not fasting. One day apart, same time of day. Only difference is that I ate breakfast on the non fasting day two hours before the blood draw. Fasting was a little over 400 mg/dl. Non-fasting was 147 mg/dl!
See, I think THAT is remarkable and noteworthy, because if you visit over at the World Carnivore Tribe FB group, and many like it, you’ll quickly find the opposite testimony from nearly all the members, that they have never felt better in their lives. To me that speaks loudly to how, though we all have the same homo sapiens biology, we are nevertheless vastly different in the subtleties of our individual biological needs. And for us to thrive, we will have to discover how to meet those individual needs. Some thrive on carnivore right out of the gate with zero adaptation period. And some adapt to keto rather quickly (after a mild keto flu). Fascinating.
I recently attended a talk by Jordan Peterson when he was in town and knew he had converted to the carnivore diet primarily due to the positive effects it had on his daughter who had two hip replacements and her body was failing her prior to doing it. It seems what the carnivore diet does is eliminate all foods that your body potentially rejects and allows you to figure out what works for you using meat as the baseline to sustain you while you figure it out.
Yes. If you do just ribeye steaks and water (i.e. Shawn Baker), you can’t get more primal and baseline. On the other hand, I suppose you could start with anything and work your way up. Rice and water (just kidding)!
that is why I said it is premature in my case to conclude that is coffee is the devil. the test is sensitive to the hours since last meal. I am scheduled for another sample in a couple of months to confirm the drop in the TG.
also note that all my samples prior to quitting coffee very much consistent TG wise. I always try to make 10 hours of fasting.
Apob 250. Simply scary. It’s been a week since the last time I’ve drunk MCT or coconut oil. But I can’t take my one spoon of heavy cream in coffee. I hate black coffee. I used to drink coffee and milk, but heavy cream is my only way out now. In Brazil, heavy cream is 50% fat. I drink two spoons a day. It’s the same amount of fat I used to drink with milk.
I don’t eat a lot of eggs. Two per day in average… Im not the greatest fan of meat, not a problem eating less of it. The problem is that keto doesn’t give us much choice. Meat and leafy greens. And eggs. I’m not sure I want to live like that, if I have to count meat and eggs (leafy greens, avocado and olive oil basically!).
I’ll recheck my exams and see how my blood respond. I think the reason is MCT and rapid loss of weight, with a significant drop in calories intake. Or, my body wasn’t made to burn ketones. But I’ll keep on searching before giving up.
Did Siobhan mentioned that decaf creates the same trigs problem? I was so happy drinking decaf. If it doesn’t make a difference, I won’t be able to cut coffee at all.
Are you 100% sure it doesn’t matter if it’s caffeinated or decaf? Im not strong enough to cut carbs, saturated fat, MCT, fruits, starchy vegetables, my beloved yerba mate and now decaf coffee. They’re leaving me with olive oil and water. Next time, I’ll find out water is a problem too o.O Getting nuts here, which is a problem since I got I to keto to treat addictive behavior.
Yeah, tell me about it. Coffee is one of the few items on my menu I thought was safe. I even ordered a bag of chicory and am trying to see if my palate can adapt to the change (another experiment).
It seems that the science isn’t crystal clear or conclusive. But there is a lot of chatter:
This article, in Science Daily, claims that “French press coffee, boiled Scandinavian brew and espresso contain the highest levels of the compound, which is removed by paper filters used in most other brewing processes”, and “Removing caffeine does not remove cafestol, however.” It also seems to claim a biological mechanism: “cafestol activates FXR and induces FGF15, which reduces the effects of three liver genes that regulate cholesterol levels.”
This study found a 50% reduced uptake of LDL in cells treated with cafestol.
Dr. Weil chimes in with an article, in which he writes “The compounds in coffee associated with increased cholesterol levels are diterpines, specifically one called cafestol, which is present whether or not the coffee is decaffeinated.”
This study claims that “Cafestol, a diterpene present in unfiltered coffee, potently increases serum cholesterol levels in humans.” Note that they claim it is present in unfiltered coffee (i.e. French Press, etc.). That was my original contention, that I began to see some talk on the internet that filtering would remove the cafestol and therefore render coffee not a concern. They go on to speculate that it is cafestol’s effect of suppressing bile acid synthesis that leads to high cholesterol levels.
This study explores yields of cafestol from different roasting and brewing methods. All yield some level of cafestol, where dark roast Mocha and Turkish preparations had the lowest extraction yields and the French Press the highest.
This study published in the Annual Review of Nutrition, 1997, claims that “Diterpenes are extracted by hot water but are retained by a paper filter. This explains why filtered coffee does not affect cholesterol, whereas Scandinavian “boiled,” cafetiere, and Turkish coffees do.”
And last but not least, the Harvard Medical School, with an article stating this:
“Coffee drinkers concerned about cholesterol weren’t happy about some early study results showing that coffee seems to increase cholesterol levels, and “bad” LDL cholesterol levels in particular. But upon closer inspection, the bad news turned out to be not so bad, because the cholesterol-raising effect seems to be limited to coffee that hasn’t been filtered, which includes Turkish coffee, coffee brewed in a French press, and the boiled coffee consumed in Scandinavia.”
These seven I extracted from a few minutes of Googling. There are many more.
A couple of things come to my mind:
- It doesn’t seem conclusive to me that all coffee in all brewing methods results in high LDL or high apoB.
- Like many things, it looks to me that it comes down to individual testing. I can’t think of any other way to be sure than to test for a period with filtered coffee and see if that makes a difference in blood tests. And then to test again with no coffee for a period, and then more lab work.
As much a hassle and cost all this testing can be, it seems there’s no other way to rule out individual sensitivity to the effects of cafestol.
It’s not pleasant to contemplate removing coffee for me either. Interested to hear input from more of you all on the forum as well!
How can I reset my body? Struggling with bloating
this is amazing
I always felt it has to do with bile. I tried to mention this in previous post but I could not find a prove. because coffee did not bother me until after keto
so why you think it is not conclusive?
only coffee addiction will make you say such statements
Ha ha! Yes, of course. I’m a lifelong addict.
Great question. What I meant by not conclusive is that for me, as far as the science goes, I’d like to see a lot more randomized controlled trials showing that cafestol directly accounts for the kinds of cholesterol levels we’re seeing in our group.
Secondly, I don’t know how individualized this effect is. Is cafestol as potent for all individuals and in all nutritional approaches? I just don’t think we can know this just yet.
Four things come to mind regarding individualization:
- Brenda Zorn’s steak challenge. I love to cite this. Famous on the forums, of course. Her triglycerides soared to 575 (from her normal 120) on a carnivore experiment, while Donna’s stayed at her normally super low “8”.
- Eran Segal’s research showing completely different glucose responses to the same foods / same meals in different individuals, demonstrating a broad range of not only insulin sensitivity, but selectivity.
- We know that genetics lead to individualized nutritional needs and diverse effects to the same foods. Take apoE variants, for example.
- And, changes in the body over time further deepening the lines of individualization. In my case, my triglycerides trended nicely for a decade, averaging well under 100 mg/dl, normally around 60; in 2016 they shot up to over 200 and as high as 400, and have only been within an acceptable range twice in the past 2 years.
Recently I read this from Dr. Thomas Dayspring, maybe providing some fresh insight:
“Another key point regarding absorption synthesis markers is that these change in response to nutrition, drugs, aging, other morbidities and they are not ever too be used as a onetime assessment. In at risk persons, like lipid and lipoprotein and other biomarkers, they need to be repeated with each and every blood draw.”
His comment that there are some biomarkers that are never to be used as a one time assessment, and that many variables affect outcomes. To me this is reminiscent of what Dr. Jason Fung has brought up often, is that our biology is dynamic. Yes, it may mean that we can be more of a “moving target” so to speak, but to me, thinking that way frees me of the trap of thinking that one test is an “end-all, be-all”.
I just think in science, it’s more useful to lean toward the idea that we know very little, and should always be ready to welcome discovery. I used to think my blood lipids would remain pristine for the rest of my life. Not so sure of myself anymore. I’m just trying to discover causes, and help others as well if I can. But I think we will have to stay vigilant and be ready to change course if our body’s needs or demands change.
Sorry for the long winded reply. I’m becoming pretty passionate about this.
One month in and I'm suddenly bloating
True. I think it is individual thing.
I have the habit if something works for me I love to see other people do the same.
My Experience w/ LCHF, Primarily Carnivore
2018- Post 14m LCHF/Carnivore
Dramatic change for the better
That looks really fantastic on TG! Was there anything in particular that so dramatically moved the needle on the TGs in 2018, or do you think it was just a function of more time?
I think it was a function of correcting insulin resistance. At the time of the recent test, I was down 112? lbs. I eat at a min 2lbs of fatty meat a day (probably more like 2.5-3lbs). Cutting sugar was a good start but really eliminating grains, seed oils, veggies was profound. I make an effort to get either sardines or salmon multiple times a week. Quite frankly since Ive discovered the Season Brand Boneless Skinless sardines, its 6x a week. Also supplementing ~10,000iu D3 daily and making an effort to be outside to walk once a day. Vit D level was at 74 when I was tested earlier this month. Takes a lot.
High insulin correlates to high Triglycerides.
Also worth noting, I did not attempt any kind of “Feldman Protocol” to manipulate the results. With how much false fear there is about carnivore/fatty meat, I really wanted to see what my normal routine was doing. Temporarily hacking a test doesn’t help anyone
Interesting. Just curious Chris, are you a big guy? The reason I ask is because I’m not, and interested in body composition. I’m a smaller guy at 5’8" and 135 lbs. I love me some ribeyes, and can easily woof down 2 lbs. of meat a day. But I’m trying to leave no stone unturned when it comes to the TGs.
Interesting about the insulin. Mine has been low ever since I’ve tested (normally in the 1.5 to 3 range fasting when on keto, 4.8ish when carnivore, and when I did my Ghetto OGTT it peaked at 11 2 hrs post-prandial). But it definitely went up on carnivore, along with fasting insulin and HBA1C. I believe now, in hindsight, and with a little more reading on what happens to glucose supply and demand on carnivore, that in time that would “normalilze” (or maybe not - look at Shawn Baker’s 6.0 HGA1C but rather spotless coronary arteries…who knows?).
My gut is that, given time, the carnivore way of life would correct a lot of things. I’m beginning to believe that when I’m ready to start again and ditch the coffee for good, time will have a lot to tell. Charles Washington seems to believe so.
Thanks for your input.
Just to add one thing.
Something else is on my mind I’d like to search out but don’t know much about it now. And that’s this: what dose does it take to “make the poison” in all this?
What I mean is that, for instance, we know that carbs raise blood glucose. But how much does it take to move the needle? It seems that we know more about sugar and glucose than any food or substrate. It’s been studied the most. And we know quite a lot about how much carbohydrate it takes to elevate blood glucose in research and also many, many people in their own home testing.
But how much cafestol does it take to raise cholesterol to “x” amount? What is the mg dose needed to raise LDL by x mg? I don’t know that anyone has these kinds of answers.
I guess my point is that, would it hurt to drink coffee occasionally? Or alternate between tea, coffee, and so on.
I think this would help a lot of people feel like they don’t have to altogether ditch something they truly enjoy, especially if there’s no evidence that enjoying it occasionally will lead to a chronic disease state.