Which Fats Get You Into Ketosis Faster?

science
(Kelly Silverman) #9

I saw that upload but didn’t watch it…but I wanna say this…

I don’t think any of those will get anyone into ketosis faster if they’re NOT restricting carbs and having ZERO sugar.

I recently watched a video with Ben Bikman and Mike Mutzel and they said how sad it was that alot of the population are guzzling exogenous keytones and MCT oil, ONLY to show positive on their blood strip…those things aren’t going to metabolically put anyone into a state of Ketosis.

And it is actually kinda sad when I think about it, because many are mislead :frowning:

(Kelly Silverman) #10

In my opinion, doing an upper/lower body split at the gym and depleting all your glycogen stores from your liver is the quickest way to go.

(Bob M) #11

I would say you are correct. It takes me days to get that high in ketones anymore. Last time, I only hit 1.9 after 4.5 days fasting on my Precision Xtra (which, oddly, seemed to read exactly 1/2 of my Keto Mojo in the many tests I did; did not have KM strips at that time though).

Not sure why one needs to be in higher ketosis, but if I did, higher PUFAs would be the last way I’d do it. The last. Dead last. I even less chicken because of PUFAs.

(L. Amber O'Hearn) #12

I understand, but I personally think the omega 6 PUFA fears are overblown. Arachidonic acid is awesome. Did you know that ketosis raises circulating PUFAs, and tissue arachidonic acid?

Even saturated fat will up your ketosis, though. Last time I experimented with KetoAF (no plants, 80% fat) I was eating primarily raw pork fat from a local farmer, which was probably about 10% PUFA. If I remember correctly, within a day my ketones went from normally around 1 or less to over 2. Within a couple days they were consistently over 4. All this while eating.

(bulkbiker) #14

Yep my highest ever ketone levels are usually on the third day of a fast.
Have done a few extended fasts and that has always been the case for me…

#15

Is this because incoming fatty acids are stimulating the release of PUFA stored in the adipocyte?

(Erin Macfarland ) #16

@atomicspacebunny, @carolT, and @amber thank you for once again sharing some wonderfully detailed and fascinating information that questions the assumptions regarding the relative benefits of different types of FA’s and why having higher blood ketone levels doesn’t necessarily promote or indicate a healthy metabolic state. Amazing women, all of you!!

#17

I’m not going to start chugging corn oil or anything. :stuck_out_tongue_winking_eye: Animal source PUFA doesnt scare me much, even if the grain/grass fed ratio is a bit different. :woman_shrugging: Whale blubber though… :thinking:

(Bunny) #18

I did post about the Arctic Variant by Chris Masterjohn and it seems to be really rare?

Three factors seem to be involved, thermal conditions (extremely cold climate), fasting (availability of food perhaps?) and and amount (gluconeogensis) of raw, cooked, fermented protein and fats consumed? (i.e. eating too much or not enough?) In order to have a mutation you have to have a cause[5]? So is it a high fat/protein diet or extremely cold environment that switches off CPT-1 {outer mitochondrial membrane} CPT2 {inner mitochondrial membrane})? I would go with extremely cold climate and not enough adequate carbohydrate consumption to avoid it i.e. level or degree of cold thermal adaption?

Apparently CPT-1a can be passed on to children.

I would not jump to the conclusion that is ketosis that causes this arctic variant mutation or genetic dietary adaption in humans or animals, nor is it constantly high ketones, but the constant activation of BAT[5] by extremely cold arctic conditions in the absents of carbohydrates because BAT acts like muscle tissue in an extremely muscular human or animal?

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Footnotes:

[1] “…The families, two Inuit, one First Nation, live in areas of Canada geographically very distant from each other. The CPT1 and CPT2 genes were fully sequenced in 5 of the patients. All were homozygous for the same P479L mutation in a highly conserved region of the CPT1 gene. …” …More

[2] “…P479L mutation because it is very common in Inuit and because symptoms suggesting CPT1A deficiency … The protein consists of a single 773 -amino-acid polypeptide chain containing both a…” …More

[3] “…P479L) in the carnitine palmitoyltransferase 1A (CPT1A) … for only a small minority of disease-causing mutations. … One of the public health efforts undertaken in Alaska that…”…More

[4] Increased Missense Mutation Burden of Fatty Acid Metabolism Related Genes in Nunavik Inuit Population “… The increased number and frequency of deleterious variants in these fatty acid metabolism genes in Nunavik Inuit may be the result of genetic adaptation to their diet and/or the extremely cold climate. In addition, the identification of these variants may help to understand some of the specific health risks of Nunavik Inuit. …”.

[5] Carnitine Palmitoyltransferase 1 Increases Lipolysis, UCP1 Protein Expression and Mitochondrial Activity in Brown Adipocytes

#19

It’s my understanding that the CPT1 alteration is a limiting factor in hepatic tissues and limits beta oxidation, therefore both ketone and glucose production. CPT2 is associated with utilizing fat at the muscle, so a defect in one area of the genome may or may not affect both/either? I’m a bit fuzzy on the genetics here. :thinking:

As to which is the dominant force for the mutation… since CMJ and @amber disagree on the finer points of Inuit metabolism, I am more a spectator in the discussion at this point. They are both about 100x smarter and well-informed than I am. :smiley:

(Bunny) #20

Here is the thing about this; when you practice cold thermal adaption you can burn up glycogen storage real fast and any carbohydrate you eat like sugar gets burned up directly (UCP-1) or immediately rather than stored as fat and at the same time the BAT starts beiging (inserting iron rich mitochondria into WAT) or browning WAT and burning it up (simultaneously) for fuel or something to that effect.

The difference may not be ketones (or higher ketones) or being in ketosis although that is somewhat a factor but it is more about UCP-1 (including levels of polyunsaturated fatty acids/DHA/EPA in the diet) being activated and the extent and degree it is activated in BAT?

I wanted to expand on what we are discussing here a little more, when we are talking about the ketogenic diet we are discussing what is taking place in the liver with the mitochondria and dietary fat adaption as well as the heart, skeletal muscle, brain, kidneys, thyroid, spleen, pancreas etc.

When we are talking about adipose tissue and cold thermal adaption we are discussing what is taking place inside the fat cells with the amount of mitochondria within a fat cell and exposure of the human body to colder conditions etc.

When your in ketosis, you can likely burn body fat but with cold thermal adaption any carbohydrate you eat gets immediately and directly burned for fuel without exercising.

(L. Amber O'Hearn) #21

Some researchers think it’s because they are getting used less for inflammation and anti-inflammation purposes.

(L. Amber O'Hearn) #22

But have you ever tried eating, say 80% fat by calorie for comparison?

(Bob M) #23

I started out eating “low carb”, then went to eating very high fat after reading Jimmy Moore’s Keto Clarity. So, I added butter to my steak, ate fat bombs, even tried buttered coffee for a while. Ate all high fat meats if I needed something to eat beyond dinner. I don’t calorie count, though, so I don’t the level of fat.

I then decided to buy a CGM so I could prove Ted Naiman’s higher protein theory was wrong. I fully believed I would see skyrocketing blood sugar. After eating many high protein meals (for these, I actually did count calories), and not finding any blood sugar rise whatsoever, I decided I liked higher protein in general than higher fat.

So, in general, I now eat low fat hams and the like and keep these on hand for if I’m hungry past dinner. I do eat higher fat meals, but most times I concentrate on higher protein, especially for the meals right after I exercise.

How does this affect ketones? To be honest, I have thousands of samples over the course of almost 4 years, and I’ve given up trying to guess what my ketones (or blood sugar) will be. One of the reasons is shown below, where I tested using three calibrated ketone meters and in the morning:

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After comparing Keto Mojo and Precision Xtra for a month or so, and determining that KM is twice PX in general, and KM has many anomalous readings, I gave up. The tools suck.

As an engineer, I want the tools to tell me what’s going on, and these tools don’t do that.

(bulkbiker) #24

Depending on what I eat beef or chicken and fish say my macros vary between 50 and 80% fat anyway. Do you think higher fat helps?

#25

A metabolically healthy person shouldn’t see an increase (or decrease) in glucose after a meal. An unhealthy one might. It’s more likely that you’d see a higher sustained glucose level with lower ketones, as opposed to a lower GKI. [because ketones offset the brain’s demand for glucose] But as you know, tracking low level signals is difficult to near impossible with random sampling and multiple factors affecting them.

It also depends on whether you have room available in muscle glycogen for the combination of insulin and glucagon to provide a sync for the glucose. Or the glucose could be going into fat cells instead given the right context. Either way, looking at blood glucose doesn’t tell us where the glucose goes.

(L. Amber O'Hearn) #26

Yes, that’s what I’m trying to say. For me personally, and according to some other anecdotes I’ve heard, going very high fat can elevate ketones as high or higher than fasting.

(bulkbiker) #27

But why would I want elevated ketones unless I’m fighting cancer…
I’m happily in ketosis all the time anyway on my mainly carnivore eating…

(Bacon is a many-splendoured thing) #28

Or, as I read it, your manly carnivore eating, lol! :rofl:

(L. Amber O'Hearn) #29

That’s just a choice. Some people feel better in ketosis.