I certainly shall!
Lumen - let the conversation begin đ
Status Update:
Hi Michael,
Thank you for your patience.
The super early bird and early bird backers will be shipped in two batches, the first of which started in September and will continue until the end of November. The second batch will begin shipping during December until the end of January.
Based on your pledge and region, your Lumen is included in the second batch of shipping.
We know that for many of our backers, the wait to receive their Lumen device has been long. While new users will need to pay a subscription fee, as a token of our appreciation for the faith in Lumen as an early backer, we announced that all Lumen Indiegogo backers will be provided with a FREE lifetime membership to the Lumen app.
If you have any other questions, please do not hesitate to reach out to us.
Have a happy and healthy day,
Lexi
Mike's Excellent Zero Carb Beer Adventure :beer:
I was wondering about thisâŚwas thinking about asking for it as a Christmas present from my husband, but on their website after you click âbuyâ it says âDue to high demand, orders made today will ship in Marchâ
Iâm curious to hear about it when you get it. I was a little confused about how it works. I thought that in order to get your RQ and know if you are burning fat or glucose you need to know the ratio of how much oxygen is going into your lungs vs CO2 out. Their website seems to only talk about measuring CO2 out, so Iâm not sure how they calibrate it to you as an individual. Looking forward to your review!
Iâm not really sure I understand the use case for this if someone is on keto. I own an indirect calorimeter that also measures RER/RQ but I never bother to use for function. All Iâm interested in is RMR and VO2 max. Also, the RQ readings during extended fasts were nonsense; the algorithms werenât programmed for that.
If youâve been on keto for a while youâre pretty much burning fat. You already know your RQ! Iâm not an expert on the subject obviously; what am I missing? Is it for keto athletes that do carb cycling or something?
Fat burn. Ketones are only an indirect measure of fat burn and fat adaptation. They donât tell you how much and how efficiently youâre utilizing fats for fuel. I think using RER/RQ is probably a better way to determine both fat burn and efficiency. There is also a wide range of opinions and claims on this forum about how much carbs one can consume and remain in ketosis/fat burn. The device will help to pin down that controversy, I think.
Yes, but the more important ratio to measure is CO2 : O2 out. Since burning fat produces less CO2 per unit of O2 the ratio of both in exhaled air can be used to determine RER. See this:
If you"ve been on keto for at least a week your RER is between .7 and .8, and it stays there until you fall off the wagon. The chart would basically be a squigly line between .7 and .8 for as long as you stay under 20g carbs per day wouldnât it?
The other problem is that the algorithm will probably have been programmed with an emphasis around an RER of 1.0 under the assumption that people eat carbs. My indirect calorimeter has this problem. Iâve gotten back readings over .8 while 80hrs into an extended fast. Not humanly possible. It cost $12k and had just been recertified by the lab. Even so, I donât think the results are reliable at the lower end of the scale. Maybe the Lumen will be better, if so that would be very interesting.
My understanding is that the utility of RER increases as carbs do. If youâre a DASH diet carb burner and fat is 5% of your dietary calories, and youâre trying to lose weight, RER will tell you a little. If youâre on keto, it wonât be able to tell you whether consuming bodyfat, muscle or dietary fat & dietary protein. Or does the Lumen claim to do so? Is there some other biomarker it tests for that allows this?
That would definitely be interesting. What calculation would you use to do this? Iâm a bit of an RER noob, but I do love to experiment. Is there a paper you can link?
This is what I would like to find out. You would think that if one is eating 70 or 75% of calories from fat for an extended period of time that they would be burning fat for fuel a majority of the time, but I think there are other confounding factors. For example, cortisol or the presence of an immune response could create a demand for glucose. I would like to know if itâs possible for gluconeogenesis to create enough glucose to cause the body to switch itâs main fuel source to carbohydrates even in the absence of dietary carbs. I donât have any evidence of this, and maybe Iâm misunderstanding something, but I think it might be possible. It would be really interesting if, for example, I were to try this product and find that despite eating less than 20 grams of carbs per day my RER was closer to 1.0 than .7 or .8 while being sick with a cold, for example, or after eating something that caused an inflammatory response.
Anything is possible. All the research Iâve read and my own n=1 supports what I said above, but I didnât mean to suggest that universal.
It sounds like at least part of your n=1 might support my hypothesis Iâm mostly kidding because I obviously donât know the whole story, but I suspect it is possible for your RER to be over .8 while 80 hours into a fast. Everyone talks about autophagy during fasting, so you could be turning old proteins into glucose to provide some energy for your brain and red blood cells. Certain hormones like human growth hormone go up during fasting and I think this might also create a demand for glucose.
Exercise can also cause your body to use glucose. If our evolutionary ancestors had to outrun a saber toothed tiger, theyâd have a jolt of cortisol and glucose to give them quick energy to run away. I assume they would use the glycogen in their muscles first, but then the extra glucose that had been created would go into the muscles to replace that loss. Often today when people experiences stress it is more chronic and doesnât necessarily involve physically running for oneâs life, so glucose is not depleted.
As much as I think keto is a great way to heal oneâs metabolism, I still have questions and the more n=1âs the better. I just think we should be careful that the cognitive dissonance that weâre all susceptible to doesnât get the better of us
RER or RQ is something they track closely during fasting studies. They use $$$ metabolic carts for this purpose. The RQ of a fasting subject is around ~0.7 after the first couple days, and it stays that way until fasting ceases regardless of whether itâs a few days or a few months. Every study done has had exactly the same result.
That said, there are exceptions due to genetic abnormalities but itâs pretty rare. One example is that fasting is lethal for most inuit and other folks indigeonus to the artic circle. They die very quickly if they donât have food. Read the article, itâs kind of fascinating!
That video was super interesting! I vaguely remember hearing about this genetic variation in Inuit populations and I liked the deep dive. Iâm not sure how much evidence there is to back up Chrisâs conclusion, though. Sounded like his theory was that Inuit populations developed this impaired ability to create ketones because of the threat of ketoacidosis. I think itâs just as likely that being in a constant state of ketosis might have made it hard to hold on to body fat, which would be bad in such a cold environment. I also think Inuit peoples must have been able to get enough glycogen from organ/muscle meat to keep their brain fueled, hence less need for ketones as fuel. Otherwise, if gluconeogensis and ketogenesis were both impaired, how would they feed their brains on a mostly meat diet?
I couldnât find the studies you were referring to regarding fasting RER/RQ, but would be interested to see them!
The âarctic variant of cpt1aâ take away: ketones are a byproduct of fat metabolism not the most important thing. Fat burning and fat adaptation are the most important things. We already know this. Defining âketosisâ as the production of ketones may not be applicable in this specific situation. These people are predominantly burning fat, not glucose. Because they do not have carbs to eat. They are producing sufficient glucose via gluconeogenesis. So Masterjohnâs conclusion is a non sequiter. It also illustrates why âchasing ketonesâ is a waste of time. The most important thing is fat burn (which hopefully the Lumen will help determine under all circumstances). When Masterjohn claims that our ancestors were not in ketosis most of the time, he has to explain what exactly they ate as an alternative to fat/protein. Plants of the Pleistocene were mostly indigestible cellulose and thus were not a viable alternative.
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What if, as I often do, you eat a higher percentage of protein (oh the horror!) rather than fat. That is, a âhighâ protein, âlow(er)â fat diet? And then compare that with lower protein, higher fat? If the same RER is achieved, does this mean Iâm burning more body fat while eating lower fat?
Even now, the Sami people (if they adhere to tradition) eat mainly reindeer, and only eat berries and roots for a short period, to fatten up for the winter. The vast majority of time, they will be in ketosis.
Iâm also wondering about the effect of protein/amino acid oxidation on RER. For that matter, also ethanol. This might be relevant to carbs, amino and fatty acids:
Apparently, ethanol does not oxidize to CO2 but to aldehyde and H2O. If so then it would not affect RER. Yet, I find that hard to accept. Something must happen to RER when youâre consuming ethanol. Maybe? Another question that Lumen may answer.
One thing that stood out in looking through that study was this: âMcCloy et al. (McCloy et al., 2004) found the cumulative oxidation of exogenous oleate and linolenate in humans to be 62% higher than exogenous linoleic acid.â This doesnât have anything to do with protein, but seems to further support what we already know about linoleic acid - that itâs bad, oxidizes slower than other fats, and probably stays around in the body longer.
My primary interest in Lumen would be to figure out if and when my body is producing amounts of endogenous glucose that are enough to trigger an insulin response that could switch me from burning fat to burning glucose. I think many here would agree that if they were to eat 60 grams of carbs that could trigger enough of an insulin response to switch their body from burning fat to glucose. I donât have any real proof of this, but Iâm fairly certain that the body can create at least 60 grams of endogenous glucose in a day and probably much more. Why would the body do this if it has plenty of fat to burn? One reason could be in response to inflammation. Itâs my understanding that an inflammatory response creates a demand for glucose. I have been obsessed with this topic because I think that having a better understanding of how certain immune responses affect metabolism could help answer a lot of my questions. For example, why do people with type 2 diabetes produce 3x more glucose than non-diabetic people? Why does 20 grams of carbs seem to be the limit when the brain requires probably around 40 grams per day even in ketosis? Is overeating carbs for an extended period of time really the main underlying cause of insulin resistance?