I will be watching this at least 20 times to absorb it all and have it stick!! LOL this I find wicked KOOL! The older I get the more science I want to learn, keep up the good work!
@@JasonWrightArt Ken's quite a dude... he had one particularly great idea yesterday he shared with me... but I'm not allowed to share... let's just say ... BIG things ... BIG plans...
Wow, I love this video so much. This pulling back the curtain on WHY low carb diets work at the cellular level is so satisfying. Thanks for putting this together!
Wow..for me personally!!?? It explains A LOT!! I'm turning 55 next month. I feel like I'm 30. I went through chemo a year ago for breast cancer and did keto all through...went carnivore for about 4 weeks here recently. I am a new person. I am fascinated by this. I am living this. Thank you! You Rock.. seriously no joke. I love your stuff. Keep explaining like I'm 5yoa. I SO appreciate you!
@@nicknorwitzPhD Claude Shannon and information theory is rumored to have said "The amount of information in a thing corresponds to it's ability to surprise. If you weren't surprised, you got confirmation, not unique information." Wrong answers always surprise me. Sad story. We lost him way too soon to early onset Alzheimer's.
Hey Nick... I watched this one and the one before with your revamped format and style. I think you had a good balance of TLDR and teasers for us science nerds. Keep it up! I think you are making a difference
You're not the only one who has come to this conclusion. A couple years ago, I watched a presentation by ... someone. I thought it was Benjamin Bikman, but have never been able to find the lecture since. Even tho I can't remember precisely who presented it, I recall the summary rather clearly. Higher insulin caused mitochondrial fragmentation vs lower insulin. Smaller, more numerous mitochondria were less capable of producing energy and less capable of utilizing fatty acids as fuel. Shifting metabolic function inside the mitochondria was an important step along the pathway to reversing obesity, and reducing one's insulin plays a critical multifaceted role in this process.
@@johnfinnell4814 I'm not sure. You'd have to dig into a little more detail to answer that question. In the context of this video, the higher insulin was a direct cause of mitochondrial fragmentation, but I think disfunction is a step beyond that. The fragmentation mostly has an effect on the Uncoupling Proteins and how much the mitochondria are willing to waste excess fuel vs more rigidly conserving it.
I love your style of scientific communication. There are too many people online who will quote a paper without fully understanding it or cherry pick information and never actually give you a source. This is clear and consice without being needlessly dumbed down. I hope you don't ever sacrifice your scientific accuracy for easier comprehension. I might have to watch some parts multiple times and do some of my own research, but I would rather do that than get sugarcoated nonsense. Great video.
Thank-you for visually showing us these two clear variations of mitochondria. I am post menopausal and have been eating healthy low carb for over 20 years (think back to the Zone days). I have no so called ‘symptoms of menopause’ whatsoever and tons of energy. I’m definitely a LMHR. Your channel is helping me understand my own physiology. Please keep going (and posting) where no scientist seems have gone before. It’s life changing!
Love your take on this. No wild claims without caveat or clarification. Clear that it was in mice but show the human data too and clarifying it's not the whole picture. This is more of the type of analysis the low carb and carnivore community needs!
The coolest thing is that all these things seem to coalesce and the patterns start to emerge. We are starting to see the forest despite the trees that has distracted a lot of people's thinking.
The difference between a slow and fast metabolism only accounts for 100-300 calories at most, but so many people believe it is a difference of 1000's of calories. Still 100-300 can make a big difference especially in the lower weight range.
Absolutely loved the information presented in this video! Great material and I think I speak for many of us when I thank you for this metabolic breakdown!
Thank you, Dr. Norwitz! Like a lot of people not steeped in the world of biology, many times being confronted by all the acronyms and lengthy terminology inherent in the subject can make things incomprehensible. You really did a great job in explaining this in a way that a layperson, like myself, can understand it. I have always wondered about the mechanism behind the metabolic advantage of low carb diets, and now there seems to be a plausible explanation for it. This RALA and DRP phenomenon would go a long way to also explaining the common experience that low carb dieters speak about of having a reduced appetite. If a low carb diet is better at producing a hormonal milieu that engenders the mitochondria to work better, the low carb dieter doesn't feel as lethargic and starved of energy, thus leading to lower caloric intake. This mechanistic explanation harmonizes the hormonal model of weight control with CICO.
*My thoughts after warching:* 1) Can the smaller mitochondria that have been split be acted upon again by the Ral-a interaction and be forced to split into even small mitochondria? 2) Does mitochondrial size affect their ability to handle oxidative stress? 3) Does mitochondrial size affect the rate of mitochondrial replication? Does the Ral-a interaction - inducing mitochondrial splitting and decreased power output potential - feed into a generational downward spiral of mitochondrial performance? Something like: 1) Ral-a induces mitochondrial splitting 2) Smaller mitochondria are more susceptible to oxidative stress and reproduce faster than large mitochondria 3) The fractured mitochondria reproduce small, frail mitochondria. 4) The cycle repeats causing each mitocondial generation to be less effective
Very insetting hypothesis about a 'vicious cycle' ... I like the way you think, although I can't say they provided data to support that downward spiral in the paper
@@nicknorwitzPhD Right; this paper seems confined to one fission event (or at least doesn't include information related to generational fission). I was just applying the idea of Ral-a induced mitochondrial change to the idea that some cancers might be the result of multi-generational mitochondrial degeneration. The hypothesis is that mitochondria exposed to enough oxidative stress to reduce their function (but not enough to trigger apoptosis) end up producing inferior generations of mitochondria until a point is reached that mitochondria can no longer produce energy via oxidation but are forced to rely on fermentation to survive. Once this state is reached, cells are essitially no longer able to interface with other cells and begin to behave as cancers - existing out of sync with other cells, deriving energy by fermentation, replicating without regulation, etc. So I just mashed the concept of generational mitochondrial decay with the concept of Ral-a induced mitochondrial change (and loss of power output).
If insulin is the key driver then this mitochondrial and metabolic rate theory would also be supported by a fasting hypothesis in addition to a low carb diet.
@@johncalla2151because fasting restricts all nutrients not just insulin production and it happens probably because it's a survival mechanism to preserve the backup fuel you have for as long as possible
Would it have been vastly different if you had learned this at 70? It's assuredly better then learning this when you are 80. The past is the past. At the rate we are getting new and better information you will see many benefits that the previous generations did not. Take any advantage you can get and take it as a positive.
@@johncalla2151 the transition to keto had a few consequences. My b p would spike in the morning, sometimes quite high. Cortisol was my guess, but the doctors had no explanation. I’ve lost most of my middle fat, and actually gained muscle. I’m clearer mentally and my stamina is much better. Not going back to carbs. After almost 25 years of heart disease I no feel better than anytime since my 30’s.
Great work Nick, the explanations and graphics are perfect illustrations. I kept thinking at some point my attention will drift off and id need to rewatch it again 😂 Dont forget, exercise also promotes insulin sensitivity which can help for those who aren't on keto. I like to extend my fasting like Huberman does till 10am or 11am, and according to his oral health vid, it's great for miniralizing teeth, another nod to IF.
Really good video. I like the level of detail you go to although I have to admit I don't understand some of it (the really geeky stuff). You're very thorough and articulate. Keep up the good work.
Good point. Just as some people have higher polygenetic risks for diabetes, maybe so too their overall risk of being affected by carbohydrates. I would expect at a calorie surplus anyone would have weight gain
Interesting but we shouldn't mistake mechanisms for outcomes. Intermittent fasting also decreases insulin, I'm not sure if the literature suggests higher energy expenditure for them too.
I try to bring enthusiasm and be clear where I'm puzzling pieces and speculating. I am NOT sure that this accounts for any fraction of the TEE benefit seen in LCD vs HCD RCTs. It's speculation, as I state. You're right.
I would appreciate if you did a deep dive on insulin plus glucose response to protein consumption. Recently I’ve seen some discussions that are very pertinent to how I feel, which basically feels like not having enough energy to walk across a room, with unregulated emotions and brain fog. Some women are solving this with much higher fat to protein meals while following carnivore. I would like to understand why we get that dysfunctional and how this macro change fixes it.
Great video Nick. Could you do a day of eating vlog or a week. I think you would help alot of people see what it actually looks like and the how not just the why of all the science.
Loved this video! Thanks for your content. Im going through menopause and want to be metabolically fit to lose weight and feel better. I believe in keto and carnivore and hearing the science behind it is awesome.
Fascinating pointing out a mechanism by which Low Carb diets may speed up metabolism and give Low Carb diets an advantage over high carb diets. All roads towards chronic disease seem paved with high Insulin. Low Carb diets lower Insulin.
Isn't there a question of measuring metabolic rate? I keep hearing from the CICO people that low-carb diets bias RQ measurements, but they claim that doubly labeled water is still accurate? My layman take-home interpretation of all of this was that if there is a metabolic effect it is small (maybe 15%) but it doesn't even have to be true because of how satiating the diet is, more protein etc. Definitely cool that we can see a potential mechanism if the metabolic difference is real
There are people who dispute the calorie out side of low carb metabolism, Nick and other Insulin model of obesity proponents (David Ludwig) think there is an effect, others say there is none.@@henrikmadsen2176
Bro if your skinny and eat alot be grateful because you can basically eat anything you want without getting fat its really a blessing in diguise if you think about
Yesterday was my first visit to my doctor-recommended diabetes nutrition counseling specialist after beginning keto in February 2024. I’ve lost 30 lbs in two months, and feel better than ever. But the diabetes nutrition counselor says that my weight loss is too fast, and is primarily a loss of subcutaneous fat and lean muscle. She also stated that my metabolism is slowing/will slow, and that longer-term I will not loose weight and will have less muscle - which I will be unable to regain. So she wants a Mediterranean 100-150 carb/day diet instead of my keto 20--50 carb/day diet. It’s now my job to figure out if she’s correct. I turn 70 next week and recently retired, so I have an increasing interest in my nutrition, and time to explore that. Unfortunately there is so much contradictory information, including from reasonably reputable sources (like the American Diabetes Association, which publishes the guidelines that my local diabetes nutrition specialist uses). I wish I knew who to trust and what to do, but I don’t. So I’m starting to revisit some/many of the videos I’ve seen over the past several months, including Nick’s. I find Nick’s videos to be among the most interesting and helpful for me, but it’s my responsibility to learn more about nutrition for over-70 diabetic men from a variety of sources and apply what I learn to my life. I never expected my retirement years to be spent doing this, but that’s the hand I dealt to myself by not paying attention to my nutrition for many years. Any suggestions regarding additional resources would be appreciated, I’ve been looking at stuff from Ben Bikman, Eric Westman, David Perlmutter, Nadir Ali and others, and understand that this is not an easy process. I have an undergraduate degree in chemistry (more than 40 years ago) and was a patent lawyer for 35 years so I’m comfortable with science, but am pretty low down the ladder on these subjects.
Why not consider getting a dexa body composition scan? That way you don't have to guess about lean/fat mass. Then repeat in 6 months and see what has happened.
@nicknorwitzPhD I'll leave that for you! I've got other things to accomplish! I'll never have your brain or memory... But I am carnivore and killing it! Down over 100 💯 😝
Regarding the "metabolic advantage" illustration (controlled studies on humans): Why is it even labelled an "advantage" ? 1. How is the increase in "energy expenditure" measured ?? is it via the oxygen-usage? An increased oxygen-consumption could be from: A. Moving around more? og B. Needing to use more oxygen for an unchanged amount of movement, because fat for fuel is less efficient than carbs? (in the latter case the graph actually illustrate the inefficiency of fat for fuel). 2. What was the state of the participants (the study subjects)? I will NOT expect to see the same outcome/graph if one make the experiment with well trained individuals (a bunch of you Nick) - because I believe well trained lean you, will be able to switch between "highcarb-lowfat" and "lowcarb-highfat" without any significant change in oxygen-consumption (unless put on long sessions of zone 3-4 cardio), because people in shape are better (more efficient) at burning fat for fuel, than are people out of shape! I have seen studies saying up to 30% better at burning fat for fuel, because of a larger density of "fat for fuel mobilizing enzymes" in the body of well trained individuals. Any comments on my speculations Nick ?
Do you think this mitochondrial fission could be an adaptive response by the cell to avoid additional oxidative stress that would be caused by producing energy? I think it's likely that fat cells in obese people are highly stressed by reactive oxygen species accumulation, which would cause those cells to become insulin resistant to protect against further stress. Could mitochondrial fission be another mechanism to protect the cell? It would also be interesting to see how this whole process differs in an obesogenic low carb diet.
Hey, first of all: incredibly good video, I have to watch it several times. And second I have a question: what is your opinion on an "animal based diet" or whatever you want to call it. So the intake of high amounts of saturated fats AND carbohydrates at the same time. Basically a keto/carnivore diet where you implement carbs from fruits and some plants (e.g. sweet potato), especially on training days
I prefer Brad Marshal’s idea of winter mode/human torpor; long saturated FA promote fission while UFA cause IR to preserve energy for winter/lower body temperature etc
I think that a year on a low-carb diet should have been long enough to recover from the effects of having been put on prednisone for 2 months! It hasn't. You didn't give me anything I could use that would help and if you had I probably already gone there. This is great news because it tells us something about the mechanism.
Well, what about a different lever: build up muscles? Doesn't muscles soak up glucose from the bloodstream, especially after training? Shouldn't a good amount of muscles have the same effect as a low carb diet (while the real diet in fact is "normal carb")?
Totally makes sense.... However, picture around min 6 mark, the one that illustrates the waterfall metaphor. Is it just me or the mitochondria in both cases kinda look the same size? Which kinda contradicts the previous statements about fusion vs fision?
Isnt it the evolutionary mechanism that allows us to burn fat more efficiently? Like, oxidizing fat is more complicated and required maybe more space for mitochondria to work in? Therefore, thats why they are bigger on low carb diet.
Hi Nick, this information is terrific! Do you think this Ral-a topic could be somehow related to the work of Joslin and Benedict on untreated T1D's high bmr and how it drops as soon as insulin is injected?
A little depressing. I have to have dessert. I have a major sugar craving after meals. Sometimes fruit will suffice, but other times it won't stop until I get sugar.
It's because you're addicted to sugar. You'll have to quit sugar for a couple weeks to stop the craving. What's wild is you'll have sugar again after weeks without and it'll be disgustingly sweet.
Amazing video!! One thing I couldn't understand is why in the purple stain image, why the RalA KO mitochondria don't look much larger than in the control image?
comment noted... honestly haven't seen much on a true metabolic advantage of begging fat in humans... at least not with any reasonable exposures... there are data on increased metabolic rates in people who, say, swim in cold water for a couple hours... but I don't think most of us are doing that daily. In terms of cold showers and ice baths, I don't think it increases metabolic rate much after the exposure, but there may be other (neurological) benefits.
Well, hell's bells! We've stumbled our way through this damn mess and arrived at the end of this nine-minute nightmare, and I’m left with nothing but a profound ignorance of what the hell any of it was supposed to mean. Good job, I suppose.
I prefer Brad Marshal’s idea of winter mode/human torpor; long saturated FA promote fission while UFA cause IR to preserve energy for winter/lower body temperature etc
Actually "We show here that C18:0 ingestion rapidly and robustly causes mitochondrial fusion in people within 3 h after ingestion" www.nature.com/articles/s41467-018-05614-6
I have also read something similar in the past with high carbohydrate low fat diets (less than 20g). I wonder if that is because in nature there wasn't any abundant sources of food that were both high carbohydrate and high fat.
I recommend everyone watch this video thru to the end. This is really solid! Here's a quick overview of what Nick covers in fast vs slow metabolism, re: mitochondrial function. - Mitochondria play an important role in energy production through oxidative phosphorylation. Their function and efficiency depends on the balance of fusion (joining together) and fission (breaking apart). - Research showed that obesity leads to more mitochondrial fragmentation due to increased activity of the protein DRP1, which promotes fission. DRP1 activity is controlled by the protein RalA. - RalA and DRP1 levels are higher in obesity, leading to more mitochondrial fission and reduced efficiency. Mice studies showed deletion of RalA prevented weight gain and increased energy expenditure. - Insulin stimulates RalA, so lower insulin levels from a low-carb diet may decrease RalA/DRP1 signaling, allowing more fusion and larger, more efficient mitochondria over time. This could explain the metabolic benefits seen in human low-carb diet studies.
Insulin-resistance (IR) (here measured by HOMA-IR). 1. What is actually being measured ?? 2. Does high IR result in high levels of insulin in the bloodstream ???
If DRP levels are linked to insulin levels, why do some people who are thin have a different insulin response than overweight people? If they've developed insulin resistance, why do some develop it and others don't yet both eat pretty much the same diet?
There are genetic factors that aren't that well understood. Why do Asians tend towards skinny-fat(visceral) and Africans tend towards more sub-cutaneous fat. It also has individual variability. Mates within a family of the same race that use glucose monitoring have found that certain foods won't spike one person's insulin but will very much spike the other ones. There are way too many confounders. Diet is just one of them. Of course, it could be one of them is just sneaking food or not declaring it.
@@Santa-ny1yp I think genetic factors are paramount. I went to a boarding school where we all ate the same food...there really wasn't the opportunity to eat other things or binge eat. Some kids were skinny ( me) , some were overweight and some were super muscular despite not supplementing themselves with protein etc . I'm middle aged now , eat whatever I like as I always have and weigh only a few pounds more than I did when I was 18....6ft and around 154Ilbs.
Love your content. I have been unable to locate your 1 page Google doc on lowering LDL on a low-carb diet. Would you provide a link if it's still available?
Well, without going to low carb this implies that eating lfrequency/meal sizing might have some effect on mretabolism on cellular level and beyond simplistic common sense view of having fuel available all the time.. But it remains unknown if smaller doses of insulin more frequently during the day or fewer bigger doses of insulin make more effect on those derps..
It's always humbling to see the effort required to prove seemingly simple concepts in biology. I would guess that going LCD is basically forcing adaptation onto your mitochondria because they have less glucose to burn. Perhaps ultimately this is because ATP synthesis is not 100% efficient, and changes in efficiency and quantity of mitochondria are always made with that in mind.
Mind. Blown. 🤯 (I think my energy expenditure doubled just *watching* this. I'm like, stupidly excited. I think I'm going to go run around the house now... 😅)
From the research and months-long reading of the literature I've done (and admittedly my research is still ongoing), it appears the "high carb" approach creates this fission-prone mitochondrial state under two and only two conditions: when fat is ingested along with the "high carbs", and when the body is (as a result) turned into Randle Cycle City... and... when the "high carbs" apparoach is low in caloric intake. However, "high carb" in sufficiently large quantities, and in the near-absense of fat intake - with the body left to upregulate _de novo lipogenesis_ for its fat needs (and that's the best kind of fat; fat that does not have concentrated industrial chemicals such as found in cattle) - creates very high metabolism and T3 production, along with all the benefits that come with it; muscle-retention, higher testosterone, etc. Yet I think the most important caveate with this "high carb low fat" approach is it has to involve a LOT of food per day. Many raw vegans (for example) suffer here because of their dismally low-caloric approach to their "high carb" meals. But those that eat in excess of 3000-4000 calories of carbs per day appear to metabolically thrive. Anyway, it's all quite interesting!
I'm just being curious! What I didn't hear but wonder is how did they turn off the RalA in the mice? Whatever they did to turn it off sounds to me like the basis for replacing GLP-1 agonists like Wegovy and become the next overpriced wonder drug. Side effects to follow.
Nick Question. Just your thoughts. If you’re on a keto diet. And let’s say the past 5 days zero carbs, and you have a CGM in juts monitoring blood sugar. If you drink a Celsius drink with 5 calories but it really spikes your blood sugar. And you drink it before a workout. Is it really a bad thing. Is it stimulating the fat burning into glucose into the blood stream. Will this help burn more fat. Or are we doing more harm potentially. Just thoughts, not medical advice. Thx. You think outside the box.
Great summary and video! I wonder what your take on Dr. Gundrys view of mitochondrial uncoupling (he views it as positive and how they divide to 'share' the load to produce energy) and if there is a relation to the fusion/fission function you talk about here. His method is to eat in a way to stimulate mitochondrial uncoupling. Thoughts?
Love the improvements to the video presentation! Also awesome paper. Do you think it would be advantageous to go low carb once in a while to increase mitochondrial fusion? If so how long do you think it would take? Carbs are too useful for my strength training to remove completely at the moment.
I think I was boen insulin resistant. At 8 months the doctor told my mother to take away fruit. The low fat, high fibre death diet they called the semi vegan food pyramid was a disaster for me.
I was not born insulin resistant; I had to work hard for many years to build that. The number of Cokes I had to drink, and the number of pretzels I had to eat . . . . But now, at 70, I’m finally on a better path. I hope it’s not too late.
@@jaro6985 fiber is terrible for everyone, not indicated in the human diet. You've been fooled by dogma and cereal companies and vegan propoganda. World journal of gastroenterology 2012, fiber removed, 100% resolution of symptoms. Fiber causes constipation, diverticulosis, autoimmune conditions, Crohn's, UC.
@@jaro6985 @jaro6985 fiber is terrible for everyone, not indicated in the human diet. You've been fooled by dogma, religion propoganda, cereal industry. World journal of gastroenterology 2012, fiber removed, 100% resolution of symptoms. Fiber causes constipation, diverticulosis, autoimmune conditions, Crohn's, UC.
I think excessive protein or fat or carbohydrate is going to cause cellular damage. I think low levels of any of these would cause cellular damage too. Moderate levels of nutrients and staying at 15 to 19% bodybat with a decent amount of muscle content seems to be optimal. It would appear if you feed two groups of people one excess fat and one excess carbohydrate the carbohydrate group will gain less fat by a considerable margin. I guess it has to do with NEAT. I guess the problem with excess carbohydrate is that its tends to lead to more overconsumption. Which is habitual. Most of this really comes down to psychology and if diet is a factor, its how your diet effects your psychology
I love that there are so many good educational videos out there like this. Funny thing is, when I was a kid, and I don’t know how I got to this assumption, but I thought “metabolism” was how fast food passed through your bowels 😂
So here is what I get out of this. Fat people tend to be more DRPy. If they stop going to so many RALAs, they can stop or slow the DRP. If they control insulin spikes they can stop going to RALAs. Even if people don't want to or have a hard time controlling carbs, they can still blunt the spiking by ordered eating. The best order I've found is eating in this order, fiber, protein, fat, carbs. If fiber inflames your gut and/or you can cut out carbs, then do so.
9:11 Wouldnt it indicate more of an advantage to those already at lower weight (or more accurately better body composition) regardless of diet type? If obesity and fat accumulation around the pancreas cells are what drives diabetes and IR, I was under the impression that the overall amount of insulin circulating exposure has more to do with that. I could be misremembering but i thought most research has shown comparable testing of homa IR, fasting glucose, a1c, etc. between groups regardless of diet composition so long as participants are comparably metabolically healthy? Also do you have a link for the meta analysis cited?
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I will be watching this at least 20 times to absorb it all and have it stick!! LOL this I find wicked KOOL! The older I get the more science I want to learn, keep up the good work!
LOVE THIS!
@@richardmitchell7836 20 times??? Come on, 17 times at most! 😄
DRP!
DRP!
KB in the HOUSE!!
@@JasonWrightArt Ken's quite a dude... he had one particularly great idea yesterday he shared with me... but I'm not allowed to share... let's just say ... BIG things ... BIG plans...
@@nicknorwitzPhDMy guess is you’re both going to test your invincibility to ultraviolet light.
@@nicknorwitzPhD it would be awesome to watch you two chat
Wow, I love this video so much. This pulling back the curtain on WHY low carb diets work at the cellular level is so satisfying. Thanks for putting this together!
Love back!
Wow..for me personally!!?? It explains A LOT!! I'm turning 55 next month. I feel like I'm 30. I went through chemo a year ago for breast cancer and did keto all through...went carnivore for about 4 weeks here recently. I am a new person. I am fascinated by this. I am living this. Thank you! You Rock.. seriously no joke. I love your stuff. Keep explaining like I'm 5yoa. I SO appreciate you!
I appreciate you! This is amazing!!!
Even before I watch this I have to say that I don't always agree with your answers but you ask damn good questions.
I'll take that. I'd rather ask good questions... get the answer a bit wrong... and adapt my answer overtime than the alternative.
@@nicknorwitzPhD Claude Shannon and information theory is rumored to have said "The amount of information in a thing corresponds to it's ability to surprise. If you weren't surprised, you got confirmation, not unique information."
Wrong answers always surprise me.
Sad story. We lost him way too soon to early onset Alzheimer's.
@@paulpladin9590 Thanks. great quote!
Thanks a lot NIck, I am a nutritional therapist with training in low carb/ ketogenic diet and I learn so much with your videos.
Hey Nick... I watched this one and the one before with your revamped format and style. I think you had a good balance of TLDR and teasers for us science nerds. Keep it up! I think you are making a difference
Awesome, thank you! 🙏🏻
You're not the only one who has come to this conclusion. A couple years ago, I watched a presentation by ... someone. I thought it was Benjamin Bikman, but have never been able to find the lecture since. Even tho I can't remember precisely who presented it, I recall the summary rather clearly. Higher insulin caused mitochondrial fragmentation vs lower insulin. Smaller, more numerous mitochondria were less capable of producing energy and less capable of utilizing fatty acids as fuel. Shifting metabolic function inside the mitochondria was an important step along the pathway to reversing obesity, and reducing one's insulin plays a critical multifaceted role in this process.
Is higher insulin the cause or the symptom of mitochondrial dysfunction?
@@johnfinnell4814 I'm not sure. You'd have to dig into a little more detail to answer that question. In the context of this video, the higher insulin was a direct cause of mitochondrial fragmentation, but I think disfunction is a step beyond that. The fragmentation mostly has an effect on the Uncoupling Proteins and how much the mitochondria are willing to waste excess fuel vs more rigidly conserving it.
This IS cool! 😎 I am living proof! Thanks Nick!! Loving the new style videos.
WELCOME!
you are the one thats frickin cool! thanks a bunch Nic, great work as usual. Keep it up!
AWE!! Thanks!
I love your style of scientific communication. There are too many people online who will quote a paper without fully understanding it or cherry pick information and never actually give you a source. This is clear and consice without being needlessly dumbed down. I hope you don't ever sacrifice your scientific accuracy for easier comprehension. I might have to watch some parts multiple times and do some of my own research, but I would rather do that than get sugarcoated nonsense. Great video.
Thanks. I appreciate this. I do my best to balance within and across videos. Some will be more simple and some a bit deeper…
Thank-you for visually showing us these two clear variations of mitochondria. I am post menopausal and have been eating healthy low carb for over 20 years (think back to the Zone days). I have no so called ‘symptoms of menopause’ whatsoever and tons of energy. I’m definitely a LMHR. Your channel is helping me understand my own physiology. Please keep going (and posting) where no scientist seems have gone before. It’s life changing!
Yes! This is super cool! I loved it, please keep doing this type of videos, applied science all the way...
Thanks!
Yes that is absolutely as cool as you think it is!!!
Thanks Nick!
glad you agree!
Love your take on this. No wild claims without caveat or clarification. Clear that it was in mice but show the human data too and clarifying it's not the whole picture. This is more of the type of analysis the low carb and carnivore community needs!
The coolest thing is that all these things seem to coalesce and the patterns start to emerge. We are starting to see the forest despite the trees that has distracted a lot of people's thinking.
The difference between a slow and fast metabolism only accounts for 100-300 calories at most, but so many people believe it is a difference of 1000's of calories. Still 100-300 can make a big difference especially in the lower weight range.
Absolutely loved the information presented in this video! Great material and I think I speak for many of us when I thank you for this metabolic breakdown!
Thank you, Dr. Norwitz! Like a lot of people not steeped in the world of biology, many times being confronted by all the acronyms and lengthy terminology inherent in the subject can make things incomprehensible. You really did a great job in explaining this in a way that a layperson, like myself, can understand it. I have always wondered about the mechanism behind the metabolic advantage of low carb diets, and now there seems to be a plausible explanation for it. This RALA and DRP phenomenon would go a long way to also explaining the common experience that low carb dieters speak about of having a reduced appetite. If a low carb diet is better at producing a hormonal milieu that engenders the mitochondria to work better, the low carb dieter doesn't feel as lethargic and starved of energy, thus leading to lower caloric intake. This mechanistic explanation harmonizes the hormonal model of weight control with CICO.
I'm glad you like the video :)
Happy Easter everyone. I think I’ve fragmented my mitochondria at the Easter buffet! I’m full of DRP!
Lolol 🍫🍫🍫
Quite interesting. Even if just a theory or a hypothesis, definitely thought provoking!
*My thoughts after warching:*
1) Can the smaller mitochondria that have been split be acted upon again by the Ral-a interaction and be forced to split into even small mitochondria?
2) Does mitochondrial size affect their ability to handle oxidative stress?
3) Does mitochondrial size affect the rate of mitochondrial replication?
Does the Ral-a interaction - inducing mitochondrial splitting and decreased power output potential - feed into a generational downward spiral of mitochondrial performance?
Something like:
1) Ral-a induces mitochondrial splitting
2) Smaller mitochondria are more susceptible to oxidative stress and reproduce faster than large mitochondria
3) The fractured mitochondria reproduce small, frail mitochondria.
4) The cycle repeats causing each mitocondial generation to be less effective
Very insetting hypothesis about a 'vicious cycle' ... I like the way you think, although I can't say they provided data to support that downward spiral in the paper
@@nicknorwitzPhD Right; this paper seems confined to one fission event (or at least doesn't include information related to generational fission).
I was just applying the idea of Ral-a induced mitochondrial change to the idea that some cancers might be the result of multi-generational mitochondrial degeneration.
The hypothesis is that mitochondria exposed to enough oxidative stress to reduce their function (but not enough to trigger apoptosis) end up producing inferior generations of mitochondria until a point is reached that mitochondria can no longer produce energy via oxidation but are forced to rely on fermentation to survive.
Once this state is reached, cells are essitially no longer able to interface with other cells and begin to behave as cancers - existing out of sync with other cells, deriving energy by fermentation, replicating without regulation, etc.
So I just mashed the concept of generational mitochondrial decay with the concept of Ral-a induced mitochondrial change (and loss of power output).
@@monnoo8221 I didn't make any conclusions. Thanks for responding, though.
@@monnoo8221we have uncoupled mitochondria in our brown fat.
The drum roll punchline was great. Thanks Doc.
you're welcome! glad you enjoyed
If insulin is the key driver then this mitochondrial and metabolic rate theory would also be supported by a fasting hypothesis in addition to a low carb diet.
And it obviously isn't as fasting dramatically lowers metabolic rate.
@@johncalla2151because fasting restricts all nutrients not just insulin production and it happens probably because it's a survival mechanism to preserve the backup fuel you have for as long as possible
After 6+ months of very low carb, my energy is vastly improved. Wish I had known this before turning 71
Would it have been vastly different if you had learned this at 70? It's assuredly better then learning this when you are 80. The past is the past. At the rate we are getting new and better information you will see many benefits that the previous generations did not. Take any advantage you can get and take it as a positive.
@@Santa-ny1yp I’m not complaining. People think I’m in my 50’s. However, 20+ years of cardiovascular disease is the issue. I’m working to reverse it.
Never too late! GO YOU!
Is it actual energy or is it stress hormones cortisol and adrenaline?
@@johncalla2151 the transition to keto had a few consequences. My b p would spike in the morning, sometimes quite high. Cortisol was my guess, but the doctors had no explanation. I’ve lost most of my middle fat, and actually gained muscle. I’m clearer mentally and my stamina is much better. Not going back to carbs. After almost 25 years of heart disease I no feel better than anytime since my 30’s.
Great work Nick, the explanations and graphics are perfect illustrations. I kept thinking at some point my attention will drift off and id need to rewatch it again 😂
Dont forget, exercise also promotes insulin sensitivity which can help for those who aren't on keto. I like to extend my fasting like Huberman does till 10am or 11am, and according to his oral health vid, it's great for miniralizing teeth, another nod to IF.
"exercise also promotes insulin sensitivity" --I'm very pro exercise!
Good work Nick.
TYVM
well presented. thanks
thanks for listening! I had extra fun with this one.
Really good video. I like the level of detail you go to although I have to admit I don't understand some of it (the really geeky stuff). You're very thorough and articulate. Keep up the good work.
But you tried and are trying by virtue of listening and that's what matters!
It did not answer why some people do not gain weight despite eating high carb.
Probably because they are not in a calorie surplus and maintain good insulin sensitivity thanks to that. Insulin is not a bad hormone at all.
Good point. Just as some people have higher polygenetic risks for diabetes, maybe so too their overall risk of being affected by carbohydrates. I would expect at a calorie surplus anyone would have weight gain
Interesting but we shouldn't mistake mechanisms for outcomes. Intermittent fasting also decreases insulin, I'm not sure if the literature suggests higher energy expenditure for them too.
I try to bring enthusiasm and be clear where I'm puzzling pieces and speculating. I am NOT sure that this accounts for any fraction of the TEE benefit seen in LCD vs HCD RCTs. It's speculation, as I state. You're right.
Beautifully explained. You made so much improvement in talking to public.
Actually awesome !!! This started out to potentially be confusing but ended up amazing
LOVE THIS!
I would appreciate if you did a deep dive on insulin plus glucose response to protein consumption. Recently I’ve seen some discussions that are very pertinent to how I feel, which basically feels like not having enough energy to walk across a room, with unregulated emotions and brain fog. Some women are solving this with much higher fat to protein meals while following carnivore. I would like to understand why we get that dysfunctional and how this macro change fixes it.
This is soooo cool, Nicholas! My nerdy heart!
Let's go!
Great video Nick. Could you do a day of eating vlog or a week. I think you would help alot of people see what it actually looks like and the how not just the why of all the science.
Loved this video! Thanks for your content. Im going through menopause and want to be metabolically fit to lose weight and feel better. I believe in keto and carnivore and hearing the science behind it is awesome.
Love you're investing in your health and excited to learn!
Fascinating pointing out a mechanism by which Low Carb diets may speed up metabolism and give Low Carb diets an advantage over high carb diets. All roads towards chronic disease seem paved with high Insulin. Low Carb diets lower Insulin.
Extremely cool. Thank you!!
You're very welcome!
Isn't there a question of measuring metabolic rate? I keep hearing from the CICO people that low-carb diets bias RQ measurements, but they claim that doubly labeled water is still accurate? My layman take-home interpretation of all of this was that if there is a metabolic effect it is small (maybe 15%) but it doesn't even have to be true because of how satiating the diet is, more protein etc. Definitely cool that we can see a potential mechanism if the metabolic difference is real
“CICO-people” … are there people that believe otherwise? People that believe you can gain weight in a caloric deficit ??
There are people who dispute the calorie out side of low carb metabolism, Nick and other Insulin model of obesity proponents (David Ludwig) think there is an effect, others say there is none.@@henrikmadsen2176
@@henrikmadsen2176Yes, because you can, and you can lose weight in a surplus.
Bro if your skinny and eat alot be grateful because you can basically eat anything you want without getting fat its really a blessing in diguise if you think about
Yesterday was my first visit to my doctor-recommended diabetes nutrition counseling specialist after beginning keto in February 2024. I’ve lost 30 lbs in two months, and feel better than ever. But the diabetes nutrition counselor says that my weight loss is too fast, and is primarily a loss of subcutaneous fat and lean muscle. She also stated that my metabolism is slowing/will slow, and that longer-term I will not loose weight and will have less muscle - which I will be unable to regain. So she wants a Mediterranean 100-150 carb/day diet instead of my keto 20--50 carb/day diet. It’s now my job to figure out if she’s correct.
I turn 70 next week and recently retired, so I have an increasing interest in my nutrition, and time to explore that. Unfortunately there is so much contradictory information, including from reasonably reputable sources (like the American Diabetes Association, which publishes the guidelines that my local diabetes nutrition specialist uses). I wish I knew who to trust and what to do, but I don’t. So I’m starting to revisit some/many of the videos I’ve seen over the past several months, including Nick’s. I find Nick’s videos to be among the most interesting and helpful for me, but it’s my responsibility to learn more about nutrition for over-70 diabetic men from a variety of sources and apply what I learn to my life. I never expected my retirement years to be spent doing this, but that’s the hand I dealt to myself by not paying attention to my nutrition for many years.
Any suggestions regarding additional resources would be appreciated, I’ve been looking at stuff from Ben Bikman, Eric Westman, David Perlmutter, Nadir Ali and others, and understand that this is not an easy process. I have an undergraduate degree in chemistry (more than 40 years ago) and was a patent lawyer for 35 years so I’m comfortable with science, but am pretty low down the ladder on these subjects.
Apparently the American Diabetes Association are corrupt!
th-cam.com/video/r_6obZSMvk4/w-d-xo.htmlsi=NbBxVzLJBvW6VtI5
Why not consider getting a dexa body composition scan? That way you don't have to guess about lean/fat mass. Then repeat in 6 months and see what has happened.
Who wished they paid more attention or remembered college biology and chemistry?
Never too late to learn! Thanks for listening, commenting and joining in on the scientific fun!
@nicknorwitzPhD I'll leave that for you! I've got other things to accomplish! I'll never have your brain or memory... But I am carnivore and killing it! Down over 100 💯 😝
@@jenjabba6210 WOW!
That study showing the increase in energy expenditure as % of calories from carbs goes down is a cool study to look at
Ludwig 2018 in BMJ… classic
Regarding the "metabolic advantage" illustration (controlled studies on humans): Why is it even labelled an "advantage" ?
1. How is the increase in "energy expenditure" measured ?? is it via the oxygen-usage? An increased oxygen-consumption could be from: A. Moving around more? og B. Needing to use more oxygen for an unchanged amount of movement, because fat for fuel is less efficient than carbs? (in the latter case the graph actually illustrate the inefficiency of fat for fuel).
2. What was the state of the participants (the study subjects)? I will NOT expect to see the same outcome/graph if one make the experiment with well trained individuals (a bunch of you Nick) - because I believe well trained lean you, will be able to switch between "highcarb-lowfat" and "lowcarb-highfat" without any significant change in oxygen-consumption (unless put on long sessions of zone 3-4 cardio), because people in shape are better (more efficient) at burning fat for fuel, than are people out of shape!
I have seen studies saying up to 30% better at burning fat for fuel, because of a larger density of "fat for fuel mobilizing enzymes" in the body of well trained individuals.
Any comments on my speculations Nick ?
Do you think this mitochondrial fission could be an adaptive response by the cell to avoid additional oxidative stress that would be caused by producing energy? I think it's likely that fat cells in obese people are highly stressed by reactive oxygen species accumulation, which would cause those cells to become insulin resistant to protect against further stress. Could mitochondrial fission be another mechanism to protect the cell? It would also be interesting to see how this whole process differs in an obesogenic low carb diet.
Hey, first of all: incredibly good video, I have to watch it several times.
And second I have a question: what is your opinion on an "animal based diet" or whatever you want to call it. So the intake of high amounts of saturated fats AND carbohydrates at the same time. Basically a keto/carnivore diet where you implement carbs from fruits and some plants (e.g. sweet potato), especially on training days
I prefer Brad Marshal’s idea of winter mode/human torpor; long saturated FA promote fission while UFA cause IR to preserve energy for winter/lower body temperature etc
I think that a year on a low-carb diet should have been long enough to recover from the effects of having been put on prednisone for 2 months! It hasn't. You didn't give me anything I could use that would help and if you had I probably already gone there. This is great news because it tells us something about the mechanism.
Well, what about a different lever: build up muscles? Doesn't muscles soak up glucose from the bloodstream, especially after training? Shouldn't a good amount of muscles have the same effect as a low carb diet (while the real diet in fact is "normal carb")?
Totally makes sense.... However, picture around min 6 mark, the one that illustrates the waterfall metaphor. Is it just me or the mitochondria in both cases kinda look the same size? Which kinda contradicts the previous statements about fusion vs fision?
Maybe look again... they are definitely different in size on the TEM
Isnt it the evolutionary mechanism that allows us to burn fat more efficiently?
Like, oxidizing fat is more complicated and required maybe more space for mitochondria to work in? Therefore, thats why they are bigger on low carb diet.
Hi Nick, this information is terrific! Do you think this Ral-a topic could be somehow related to the work of Joslin and Benedict on untreated T1D's high bmr and how it drops as soon as insulin is injected?
A little depressing. I have to have dessert. I have a major sugar craving after meals. Sometimes fruit will suffice, but other times it won't stop until I get sugar.
It's because you're addicted to sugar. You'll have to quit sugar for a couple weeks to stop the craving. What's wild is you'll have sugar again after weeks without and it'll be disgustingly sweet.
Amazing video!! One thing I couldn't understand is why in the purple stain image, why the RalA KO mitochondria don't look much larger than in the control image?
Please do a video on the benefits of the beiging of white fat.
comment noted... honestly haven't seen much on a true metabolic advantage of begging fat in humans... at least not with any reasonable exposures... there are data on increased metabolic rates in people who, say, swim in cold water for a couple hours... but I don't think most of us are doing that daily. In terms of cold showers and ice baths, I don't think it increases metabolic rate much after the exposure, but there may be other (neurological) benefits.
it definitely tastes better browned.
Well, hell's bells! We've stumbled our way through this damn mess and arrived at the end of this nine-minute nightmare, and I’m left with nothing but a profound ignorance of what the hell any of it was supposed to mean. Good job, I suppose.
As I math lecturer in a college used to say to us: "If it's not impressive, then I don't know what is."
I prefer Brad Marshal’s idea of winter mode/human torpor; long saturated FA promote fission while UFA cause IR to preserve energy for winter/lower body temperature etc
Actually "We show here that C18:0 ingestion rapidly and robustly causes mitochondrial fusion in people within 3 h after ingestion" www.nature.com/articles/s41467-018-05614-6
I have also read something similar in the past with high carbohydrate low fat diets (less than 20g).
I wonder if that is because in nature there wasn't any abundant sources of food that were both high carbohydrate and high fat.
I recommend everyone watch this video thru to the end. This is really solid!
Here's a quick overview of what Nick covers in fast vs slow metabolism, re: mitochondrial function.
- Mitochondria play an important role in energy production through oxidative phosphorylation. Their function and efficiency depends on the balance of fusion (joining together) and fission (breaking apart).
- Research showed that obesity leads to more mitochondrial fragmentation due to increased activity of the protein DRP1, which promotes fission. DRP1 activity is controlled by the protein RalA.
- RalA and DRP1 levels are higher in obesity, leading to more mitochondrial fission and reduced efficiency. Mice studies showed deletion of RalA prevented weight gain and increased energy expenditure.
- Insulin stimulates RalA, so lower insulin levels from a low-carb diet may decrease RalA/DRP1 signaling, allowing more fusion and larger, more efficient mitochondria over time. This could explain the metabolic benefits seen in human low-carb diet studies.
Oh really good information here regarding the benefits of low carb. Go team Mitochondria.
Insulin-resistance (IR) (here measured by HOMA-IR).
1. What is actually being measured ??
2. Does high IR result in high levels of insulin in the bloodstream ???
Thank you. Extremely helpful and interesting
You're very welcome!
thanks Nick so cool
YW!
If DRP levels are linked to insulin levels, why do some people who are thin have a different insulin response than overweight people? If they've developed insulin resistance, why do some develop it and others don't yet both eat pretty much the same diet?
There are genetic factors that aren't that well understood. Why do Asians tend towards skinny-fat(visceral) and Africans tend towards more sub-cutaneous fat. It also has individual variability. Mates within a family of the same race that use glucose monitoring have found that certain foods won't spike one person's insulin but will very much spike the other ones. There are way too many confounders. Diet is just one of them. Of course, it could be one of them is just sneaking food or not declaring it.
@@Santa-ny1yp I think genetic factors are paramount. I went to a boarding school where we all ate the same food...there really wasn't the opportunity to eat other things or binge eat. Some kids were skinny ( me) , some were overweight and some were super muscular despite not supplementing themselves with protein etc . I'm middle aged now , eat whatever I like as I always have and weigh only a few pounds more than I did when I was 18....6ft and around 154Ilbs.
I think epigenetic factors are paramount but obviously genetic factors play a role
Love your content. I have been unable to locate your 1 page Google doc on lowering LDL on a low-carb diet. Would you provide a link if it's still available?
Well, without going to low carb this implies that eating lfrequency/meal sizing might have some effect on mretabolism on cellular level and beyond simplistic common sense view of having fuel available all the time.. But it remains unknown if smaller doses of insulin more frequently during the day or fewer bigger doses of insulin make more effect on those derps..
Excellent, thanks a lot 👌
You're welcome!
It's always humbling to see the effort required to prove seemingly simple concepts in biology. I would guess that going LCD is basically forcing adaptation onto your mitochondria because they have less glucose to burn. Perhaps ultimately this is because ATP synthesis is not 100% efficient, and changes in efficiency and quantity of mitochondria are always made with that in mind.
Mind. Blown. 🤯 (I think my energy expenditure doubled just *watching* this. I'm like, stupidly excited. I think I'm going to go run around the house now... 😅)
"stupidly excited" is the best kind!
From the research and months-long reading of the literature I've done (and admittedly my research is still ongoing), it appears the "high carb" approach creates this fission-prone mitochondrial state under two and only two conditions: when fat is ingested along with the "high carbs", and when the body is (as a result) turned into Randle Cycle City... and... when the "high carbs" apparoach is low in caloric intake.
However, "high carb" in sufficiently large quantities, and in the near-absense of fat intake - with the body left to upregulate _de novo lipogenesis_ for its fat needs (and that's the best kind of fat; fat that does not have concentrated industrial chemicals such as found in cattle) - creates very high metabolism and T3 production, along with all the benefits that come with it; muscle-retention, higher testosterone, etc.
Yet I think the most important caveate with this "high carb low fat" approach is it has to involve a LOT of food per day. Many raw vegans (for example) suffer here because of their dismally low-caloric approach to their "high carb" meals. But those that eat in excess of 3000-4000 calories of carbs per day appear to metabolically thrive.
Anyway, it's all quite interesting!
Yes, very cool…☺️
I'm just being curious! What I didn't hear but wonder is how did they turn off the RalA in the mice? Whatever they did to turn it off sounds to me like the basis for replacing GLP-1 agonists like Wegovy and become the next overpriced wonder drug. Side effects to follow.
Nick Question. Just your thoughts. If you’re on a keto diet. And let’s say the past 5 days zero carbs, and you have a CGM in juts monitoring blood sugar. If you drink a Celsius drink with 5 calories but it really spikes your blood sugar. And you drink it before a workout. Is it really a bad thing. Is it stimulating the fat burning into glucose into the blood stream. Will this help burn more fat. Or are we doing more harm potentially. Just thoughts, not medical advice. Thx. You think outside the box.
Cool. Though I'm already convinced that low carb is "fricking cool" because I enjoy it's benefits.
Glad to hear 👂 it
7:11 Isn't "less efficient at generating energy" good? Means more calories are burned to produce a unit of energy.
Nick , that is awesome. Keep it up.
I'll be like anti-gravity
Thank you Nick! What a fascinating lecture. Always enjoy your fun way of presenting the science. With cookies. 😂
🍪 🤓
Great summary and video! I wonder what your take on Dr. Gundrys view of mitochondrial uncoupling (he views it as positive and how they divide to 'share' the load to produce energy) and if there is a relation to the fusion/fission function you talk about here. His method is to eat in a way to stimulate mitochondrial uncoupling. Thoughts?
Really cool! Can you share your thoughts on how this is connected to LMHR and LEM? Thanks!
Love the improvements to the video presentation!
Also awesome paper.
Do you think it would be advantageous to go low carb once in a while to increase mitochondrial fusion? If so how long do you think it would take?
Carbs are too useful for my strength training to remove completely at the moment.
From an evolutionary standpoint, would increasing your energy expenditure be a metabolic advantage?
Big step up on the video 👍 great watch
Thank you! Trying!
I think I was boen insulin resistant. At 8 months the doctor told my mother to take away fruit.
The low fat, high fibre death diet they called the semi vegan food pyramid was a disaster for me.
I was not born insulin resistant; I had to work hard for many years to build that. The number of Cokes I had to drink, and the number of pretzels I had to eat . . . .
But now, at 70, I’m finally on a better path. I hope it’s not too late.
Modern food is so toxic, kids are getting type ii diabetes and fatty liver as young as 3 years old
High fiber is good for everyone, you are thinking high carb.
@@jaro6985 fiber is terrible for everyone, not indicated in the human diet. You've been fooled by dogma and cereal companies and vegan propoganda. World journal of gastroenterology 2012, fiber removed, 100% resolution of symptoms. Fiber causes constipation, diverticulosis, autoimmune conditions, Crohn's, UC.
@@jaro6985 @jaro6985 fiber is terrible for everyone, not indicated in the human diet. You've been fooled by dogma, religion propoganda, cereal industry. World journal of gastroenterology 2012, fiber removed, 100% resolution of symptoms. Fiber causes constipation, diverticulosis, autoimmune conditions, Crohn's, UC.
Would love to see you talk with Ben Bikman on this topic. He is a legend when it comes to insulin and mitochondria!
Know him well
I think excessive protein or fat or carbohydrate is going to cause cellular damage. I think low levels of any of these would cause cellular damage too. Moderate levels of nutrients and staying at 15 to 19% bodybat with a decent amount of muscle content seems to be optimal.
It would appear if you feed two groups of people one excess fat and one excess carbohydrate the carbohydrate group will gain less fat by a considerable margin. I guess it has to do with NEAT. I guess the problem with excess carbohydrate is that its tends to lead to more overconsumption. Which is habitual. Most of this really comes down to psychology and if diet is a factor, its how your diet effects your psychology
I love that there are so many good educational videos out there like this. Funny thing is, when I was a kid, and I don’t know how I got to this assumption, but I thought “metabolism” was how fast food passed through your bowels 😂
I mean ... not a terrible model for a kid...
Isn't it kind of understood that sugar intake results in a higher energy state?
When I have mouse findings in my house, I go on the hunt!!!
Thanks, Nick
LOL! good one 💩
So this is a mechanistic study of the benefits of Fasting, and other low insulin approaches.
So here is what I get out of this. Fat people tend to be more DRPy. If they stop going to so many RALAs, they can stop or slow the DRP. If they control insulin spikes they can stop going to RALAs. Even if people don't want to or have a hard time controlling carbs, they can still blunt the spiking by ordered eating. The best order I've found is eating in this order, fiber, protein, fat, carbs. If fiber inflames your gut and/or you can cut out carbs, then do so.
So what's the function of fission?
I think it’s freaking cool too!
YAS! You get it!
9:11 Wouldnt it indicate more of an advantage to those already at lower weight (or more accurately better body composition) regardless of diet type? If obesity and fat accumulation around the pancreas cells are what drives diabetes and IR, I was under the impression that the overall amount of insulin circulating exposure has more to do with that. I could be misremembering but i thought most research has shown comparable testing of homa IR, fasting glucose, a1c, etc. between groups regardless of diet composition so long as participants are comparably metabolically healthy?
Also do you have a link for the meta analysis cited?
It is frickin cool. What you are saying matches my life experience. Thank you nick for your interest in seeking truth.
Thanks for watching 😊
Thanks!
Welcome! And thank you back!
How does Urolithin A effect our mitochondria
Thanks!
Wahoo!
good info, but wouldn`t too little fission impede the process of mitophagy?