I was really looking forward to a physiological conclusion. So many questions! Eating saturated fat leads to more immediate energy but could also overloaded mitochondria in an overfed state? Olive oil creates stored fat which could be good for a fasting person later or an athlete that works out fasted but bad for an obese person? Is the palmatic acid creating mitogenesis through uncoupling? Will these small mitochondria with less atp elongate and merge in a fasted state? This research creates more questions than answers.
Ig I'm going with: I don't want my cells dying so I'm avoiding saturated fat. I have avacado w/EV olive oil for breakfast most days. The slower burn of unsaturated fat may be why I don't get very hungry throughout the day.?
Reduced intracellular fat storage with saturated fat against higher storage with unsaturated fat. Why doesn't this , partly, explain some of the current weight problems people are having with 'healthy' foods compared to ancestral diets?
Or is it that the cell rejects the unsaturated fat as an energy source, but it is so similar to animal fats which are used for energy that it is stored away, but it is always rejected as an energy source, and so remains as fat?
Our body differentiates the type of fat by the length of its carbon chain, avoid the long chains, choose unrefined medium chain fat. The body chose to store fat in saturated form due to its stability. Avoid putting any PUFA or MUFA such as olive oil that will turn rancid at the blink of an eye.
30:53 increased fission/drp 1 is probably a marker of mitochondrial growth. In cells it would be cell division. That goes together with the growth of the saturated fat translocators. Given that greater mitochondrial activity is usually a good thing, not sure why you were throwing out there that you see a lot of cellular death, uncharacteristically without support. Just a few examples: universal drop in body temperatures over decades (lower metabolic rate), metabolic disorders are all related to reduction in mitochondrial energy production. So to have something that actually increases it seems to be pretty noteworthy, regardless of other things we know what too much saturated fat can do. You might even speculate that saturated fat is a great energy source for us. High ldl might not mean the fat is to blame, but that you are either taking in excessive amounts, or that the liver is too damaged to clear enough ldl, which then oxidizes leading to problems.
Finally someone with an informative conclusion proposal! All other comments are just writing how great the guy doing these vids is, no substance. Corny. Yes, what you say is to the point. Unsaturated fats are toxic, saturated fats are great. Its the frying oils that make people obese, not sugars, not to the same degree.
It makes me wonder about context. As you say in this video, an increase in palmatate (saturated fat) will increase the mitochondrial fragmentation. In other videos, you mentioned how fasting or nutrient depravation can elongate small mitochondria. If we look at this from the point of view of our distant ancestors who were perhaps regularly subjected to forced periods of feasting and fasting (hunt & kill an animal, scarf it down, might be several days before you eat again). Maybe in the long run if used in this context it's a net positive, where the sudden intake of palmatate during the feasting period causes an increase of mitochondria with perhaps subpar health, but then over the next day or two their morphology improves during the fasting period.
@@LenkaSaratogaTbh, I don't apply it to my eating style. It's just something I thought was curious. If I were going to apply it somehow, it would probably be by eating a very large meal containing almost exclusively of fatty meats, then not eating again for another 48 or 72 hours.
Thanx Thomas. as is my goal as social scientist and anthropologist that the real sciences in all its doubts and searching should be presented to everybody, I follow your presentations. They are much more informative then the Gurus who take every study as granted and base complete life styles on it. We see things but don’t know what it means is still the level I work on in my anthropological work. Keep on doing the good stuff and don’t forget the dissertation. My dissertation started with a conversation I had with a Maribou from the Gambia. He asked me, what is the main part of our knowledge an I said. I dont know. And he said, you are right, that is the main part.
Thanks for the video. Biggest immediate takeaway is that definitely there is a huge difference in mitochondrial response to saturated vs unsaturated fat in this experiment. Let's not forget that dna of these cells does not guarantee the same behaviour in all humans, since they have a variety of human dna of various origins. By that, I mean that in human genome there are many traits, some from Neanderthal people, some from ice age people, some from ice age people that lived on equator and were spared of the long winter climate during that ice age. Ice conditioned most of the globe in period when sapiens sapiens evolved. Their foods' fats were mostly saturated ones, if they lived in these harsh winterish conditions. So, a quick conclusion (rather hypothesis with high likelyhood to be confirmed): humans are evolutionary adapted to saturated fats, and since unsaturated fats perform differently, it might be wise to avoid unsaturated fats.
*Radovan:* _"... in period when sapiens sapiens evolved."_ Life didn't evolve. The notion that all life evolved from a microbe is 19th century mythology that can 𝘰𝘯𝘭𝘺 be believed by faith with no support from modern molecular biology.
Evolution’s Bite is a great book by Peter Ungar which shows the (much less clear cut) beautiful picture of human diets over time. It’s not strongly tending towards high animal or non-animal saturated fatty acid consumption, though. But let’s grant that’s true. A big part of evolutionary biology is antagonistic pleiotropy- specifically, as a theory of aging based on competing gene expressions. In short, it actually comes to the opposite conclusion: all else equal, if two foods are of the same health-promoting value in the reproductive window, one ancestral and one novel, we should favor the novel food for longevity purposes. It’s tempting to think what we evolved to must be good, but that’s far from necessarily the case; it took me a while to grasp this one, so I’d be happy to clarify more if ya want 👍
At the end before your conclusions discussion, I had been thinking that the "increasing" activity would actually lead to a shorter cell life resulting from mitochondria degradation due to increase ROS production in a shorter period and hence less time for the cell/mitochondria anti-oxidation processes to mitigate the effects of the higher concentrations of ROS. When you said increase "cell death" I think you were implying something similar to my thinking. This would lead me to think that the unsaturated fats being sequestered, and I assumed eventually consumed by mitochondria slowly over a longer period of time means less ROS stress (peaking stress) and hence heathier and longer-lived mitochondria/cell. - Mechanical/Naval Engineer here and I love this mechanistic stuff. Good informative video!
40:04 _"So, can we apply this to the real world? No."_ Well darn it! I listened to this in anticipation that you'd tell us saturated fats are more healthy than unsaturated.
Yes, saturated fats are good, unsaturated are plain toxic, no matter what this guy has or has no courage to admit. He is a conformist and has hard time to break out of the fog of dogma. The reason cells still don't live long even on saturated fats, is that fat is a bad source of energy for a cell, period. Cells like glucose. Douhhh! But the author still deserves the credit for bringing this topic up.
Watched half. Thx for this. Really useful. I guess having mentioned what a mitochondria is, u could have explained the difference between saturated and unsaturated fats as well. Saturated will be solid at room temp. So much disinformation on good Vs bad fats even if one Googles images...
Thank you. Please make talk practical to ordinary people to help us understand to eat saturated fat or not? If we need to eat , how much per day ? Make your knowledge how is applicable to our daily lives? I am a consultant surgeon and fade up with too many jargon names. What I want is what is the effect of saturated fat, other fats we eat on mitochondria. The talk is typical of young scientists who live in their own minds.Please make talk more practical to our lives.
hey!! Great coverage. That is really interesting... I'm trying to check mitochondrial functions in obese patients in my masters, which they all have increased levels of FFA... This article gave me some ideas to what analyse.
So great! For this purpose of obesity study, it would absolutely wonderful to have the same 3 or 4 slides/studies integrating carbohydrates. It would enable us to compare and hierarchy the impact of both glucose and fat on mitochondria. Thank you for this rich sharing.
Just thinking... Since palmitate is the "gold standard" of fatty acid synthase (from any macronutrient oxidation surplus), it would be more prone to obligatory oxidation in mithocondria. Oleate (or other unsaturated fats) is nobler. Maybe the reason why cells store it in lipid droplets or in order to restore membrane phospholipids. 🤔
Well if palmitate is what cells produce upon surplus of sugar oxidation, then probably that's what cells will prefer to metabolise best and safest again when calories are needed. Douhh! Fat oxidation is what turns them into CO2, water and energy, a good thing. Unsaturated fats staying in droplets are maybe ... rejected as useless toxic garbage, the cell don't want to touch with a 10' pole. Cell membrane needing high quantities of uns. oils is a big myths.
Found your channel about a week ago. Love it. I've been watching this kind of stuff for many years, and into it long before youtube itself. In this era of so much bs/bad information people just eat up because they don't have 'base' knowledge, just go on this guy sounds smart. You really dive in and get to the heart of matters. Love it. Follower for sure.
Firstly, your's truly is appreciative of the in depth nature of the video itself, as currently Keto-Kid here does need to keep abreast with research, be it positive or negative. If you can even make that distinction in this case. Secondly, on the Henrietta Lax topic, a decent 10 minute overview can be found on the World Service. Namely under the Witness-History podcast series. For in death, humanity owes her a great debt. Rarely does a specific cancer bring about such a bountiful source of research potential. All told, useful video indeed.
I don't think we can say either way whether these findings are good or not. More cell deaths also don't mean anything bad, as cell deaths are often desirable, it can very well be a mechanism by which the body protects itself. To leap to conclusions from this would be a mechanistic speculation and bad logic. You are right to withhold from making a statement outright. It's still interesting nonetheless to see how this all works together. What I know about Palmitate metabolism in humans is that in rat studies humans have a gene to prevent certain deleterious effects of palmitate, while rats don't(As you can imagine, they don't get nearly as much as humans do in their diet). So all of these factors have to be accounted for, but we really don't know as much as some people might claim to know.
How did they separate out the potential for the mitochondria to use the sugar solution, control plus was the the base to which they added fat? How do they control which path of the Krebs cycle is used for energy production? This is critical since they measure O2, which varies by what energy source is used and how (glycolis vs oxphos). How "fat adapted" is the cell line? is fat adaption really about how much CPT1 is produced by cells?
For the last four years I have focused on maximizing autophagy. All my research on this topic keeps leading me back to the mitochondria. I did everything that triggers autophagy, on the same day, and every mole on my body dried up and fell off. Eating crushed broccoli sprouts seem to really make the effect go exponential.
I am new to your channel, and for me this is extremely interesting. 😘 For consumers wanting to make an informed choice between the available foods and fats, it would be very interesting to know what happens with the refined seed oils (PUFAs) and margarine in their mitochondria. Refined seed oils have reportedly no nutritional value and are readily oxidized. Personally I made the choice for grass fed butter and saturated oils for baking and cooking and bam all processed PUFAs from my kitchen.. I think that I get enough unsaturated fats from meat and fish. To ask my question: what is known about refined poly unsaturated fats and the mitochondria? If you already posted a video about the subject, I apologize.
What is the potential fate of thr lipid dropplets? They are in triglyceride form? Futue oxidation in the cell? Or storage in fat cells? Thanks. Excellent long form info👍
Great video. A paper came in out a few years ago that, if I recall, showed that palmitate specifically really amped up cancer growth, and this cell line is a cervical cancer. Might a non-cancerous cell process fats differently? Also is there any evidence that oleate is permanently stored in the droplets? You would think that it would eventually be beoken down. Awfully wasteful if not.
Humans have a gene to deal with the negative effects of Palmitate. Conversely, the rats they study on don't have this gene because rats don't have to deal with palmitate often. They took out this gene and put it in rats and found that it decrease negative effects of Palmitate significantly, also confirming that they got the right gene. Of course, this isn't the result they wanted so they have to spin it to make it sound like a bad thing. Like no, the gene did what it was supposed to do, because humans consume a lot of Palmitate, like other highly carnivorous animals. If you isolate Palmitate from the effects of this gene, of course you will see bad things occur. And epidemiology showing a 10-30% increase in incidence based on levels of palmitate consumption is not enough to convince anyone of a negative effect of Palmitate on humans.
Or is it a case of animal fats being preferentially used by animals, and vegetable fats not being so suitable for use by animals get preferentially stored as fat?
2023 and we are still asking the basic question about fat, saturated vs unsaturated? Society that built robots and spacecraft.. 😂 I need no arrogant degree in mol. biology to tell you from evidence in society that unsaturated fats are darn toxic and fattening for the population. Inuits who are unassimilated in western lifestyle eating predominantly animal fat are much better off. Yes their life span is rel. short, but then again, they don't get any sun, healthy carbs, vitamins etc.
Something interesting to look at with regard to this is the exceptional longevity of naked mole rats and their extremely high levels of monounsaturated fat in there cell walls… hmmm maybe a connection to the Mediterranean diet and health?
This is interesting. I'm going to keep listening and see what conclusions you come to. Are you planning to compare your findings with the unsaturated fats?
So palmitic acid causes mitochondrial fission? But there was another study showing stearic acid causes mitochondrial fusion. So all saturated fats don't act the same?
You have shown and proven sth groundbreaking, to my mind... Mitochondria are really greatly troubled by saturated fat, so they end up fragmenting and dying. And so does the cell after them. Non-saturated fat is much easier on the mitochondria, therefore it does not get first- line preference for processing - it can get stored in fat droplets and wait to be taken care of, while saturated fat is so dangerous, that it has to be processed immediately. And the cell 'hopes' that no more of this burden is coming so as not to burn out the mitochondria through overloading, then (sharing the heavy workload) fragmentation and, finally, disintegration. TY
One question, was there any studies comparing long chain saturated fats versus medium or short chain saturated fats? C16:0 versus C12:0 versus C8:0? And in terms of unsaturated fats ...mono unsaturated versus poly unsaturated versus oxidized polyunsaturated fats... since the poly unsaturated fats are the most likely to oxidize. Note that my comments (all of them) were typed as I was still listening so some of my questions were partially answered.
This is not a subject we learn about in our daily lives, so I appreciate the video and content, just to add to my base knowledge and feel I am actually getting introduced to such different world and fascinating one at that! Thank you!
Holy Crap! a lot of cell death with palmatate. Palm oil is all over the place in the processed food chain. I get my fats from lard , butter, meat and fish. I am 70 and I have the energy of a 40 year old.
LOL. That was inconclusive. Cell death is not necessarily a bad thing. Proliferation and cell survival in senescence are bad things. I think what can be concluded is that unsaturated fats have more tendency to be stored and saturated fats burned. This would seem to be adaptive if one assumes that saturated fat from animal sources is a marker of prosperous times and plant source fats an indicator of lean times. In times of abundance usage of energy would be okay while conservation/storage would be requisite in lean ones. I am curious whether oleate usage similarly leads to a lot of cell death. Certainly, high carb intake favours proliferation.
Wow. That was a fantastic video. One that I could actually understand. I'm not a scientist but I am trying to understand fats more. My take away from this is that a diet high in saturated fats may lead to higher and faster cell senescence. Whereas a diet higher in unsaturated fats would lead to more of a stockpile in the lipids storage of the cell and a slower use of that energy. Does that sound about right?
Thanks, Rick. These take quite some planning. I'm really happy to hear its understandable, though - it helps me figure out if I'm communicating correctly. I think your point could be correct. In that case, it would have been cool to measure some genes of senescence (usually those are downstream genes that are targeted by the protein called p53). I think no matter what, high levels of fat ultimately leads to detriment to the cells, regardless of the type, but the mechanism differs between them. I don't think we can conclude anything on senescence from this data, but it would be a cool thing to further this research with.
My take on this is that saturated fat is an efficient fuel source for mitochondria, and unsaturated is not, no one is eating so much fat that the cells are bathed in it. And over nutrition of any kind will cause mitochondrial fragmentation. So the fact that unsaturated fat mimics a fasted state to mitochondria, while the cell is storing it, is concerning. I'd like to see longer term what the cell ends up doing with the stored unsaturated fats. Does the mitochondria eventually use it?
Butter: more ATP but could be bad due to cell death. Olive oil: less ATP but less cell death (but more lipids in the cell - even fatty liver)? Then add age and metabolic issues including not enough CPT1. Good luck figuring all out!!
Thanks for making these videos. I find this very interesting but absolutely do not have the ability to understand these papers if I were to just try and read them on my own.
As someone who worked in the formulation side of anti-cancer drugs, I do remember that the HeLa immortal cancer cell line caused a major issue in the 1990's... when they started doing genetic testing of the various cell lines, they learned that about 90% of the human cell lines had been contaminated and replaced with the HeLa cells, thus invalidating much of the past 30 years of cancer drug research. So the drug screening they would do using various human cancer cell lines from various organs turned out to have been tested on HeLa cells that had contaminated and wiped out what they thought were the carefully stored cancer cells for different organs. My work consisted on developing safe formulations for clinical trials -- did not mean the drugs tested were safe, only that the formulation used to provide the dosages they wanted were... they usually picked drugs that did not dissolve well, so a lot of formulation work was needed to get the dosages they wanted. I also developed analytical tests for raw material, in-process, finished product and stability testing of the product. Several times I was able to develop a lyophilized formulation that could be stored at normal freezer temperatures for at least 2 years, when the drug raw material itself had to be stored in a -80C freezer. That was necessary because we had to account for every milligram of the material because of the 3 years to gather and purify about 40 grams of material, and then due to the difference in how different countries package and handle deep frozen material, they lost half of the material when they thawed a container that the shipping country had packed at -80 C. Different standard operating procedures caused the pressure to build up in the container as the material was brought up to room temperaure before opening... POOF!!!! a big dust cloud in the safety hood upon opening the container.
Don't get me wrong, I appreciate the knowledge nuggets. Can you maybe have something more conclusive. So, say this is what this nutrient does to your cells. Conclusion, good or bad and why.
I appreciate the input, methanial. The way I have things organized is that I cover each study in depth so people can sink their teeth into the details, and with each study on a topic, the body of literature grows until I can release a video giving more concrete "advice" with answers as to why. On this topic, I'll be releasing just such a video in several weeks, stay tuned.
Not the way science actually works. This study was done on a particular cancer cell line and may or may not tell you anything abput what happens in humans on average, let alone any particular human specifically; and there is almost certainly a bunch of tradeoffs and confounders. These cells are used because they are easy to grow and study.
I remember DRP1 being my biochem prof's favourite protein...except he called it "derp" and proceeded to include many appropriately "derpy" cat pictures in the lecture slides to match...it was pretty cringe in hindsight, but I guess scientists have to make their own fun where they can 😂
Could the experiment shown at 6;06 mins, not be negatively/inaccurately effected by the sugar content that’s there? Sugar and fat don’t really mix well.
Great video! Very informative, thanks. I know you didn't want to make any extrapolations from this to everyday life for people wrt nutrition, etc. However recently i saw a video from FireInaBottle where he discussed how squirrels eating large amounts of acorns, etc, that contained high amounts of oleic acid gained weight. Perhaps trees benefited from producing these fats to help fatten up animals who collected their seeds for the winter to spread further across territory, etc. Many human populations never had oleic acid heavy diets and are now significantly obese on a modern diet higher in vegetable oils when traditionally it would have comprised of only small amounts of animal fats (butter, lean pork, etc). Even the ancient Greeks knew of obesity (there are sources), considering their more recent adoption of olive oil at the time might have been why. Just speculation but interesting none the less.
Interesting. This is good feedback. Even when I say “if you look here” and things of that nature, you still feel the audio only podcast is helpful to you?
so short term palmitate is good but long term causes cell death, but you still haven't tested oleate long enough to see if it also causes cell death? I don't need a definitive conclusion but would love a few hypothesis. drp is splitting mitochondria more when exposed to palmitate that seems good as its an indicator of mitochondrial biogenesis..
Am I wrong, or both the fat intakes came as extra calories above the base glycosis supply from the media? Would this be related to the perceived fat toxicity?
I like the thought process, R. You may have a point there. It is possible the added fat increases the energy availability, which it certainly does, and that has an effect, itself. The media is different from cell to cell, but in this case, it tends to be a high glucose media, which could exacerbate the issue.
Thank you for all the information😊 Please can you do a video about physiological effects too with respect to cell biology. Lots of love and regards(India)
fragmentation = reduction on mitochondrial energy generation to reduce excessive oxidative stress, also enables autophagy of broken mitochondrias. Might indicate too much fuel reserve. elongation = increases energy generation efficiency and also disallow autophagy. Might indicate lack of available fuel
Love your videos dude, they're all super informative. I wanted to take your opinion on my confusion related to nutrition. I'm underweight at the moment with a BMI of 17.5 but repugnant to gain weight because I can't do strength training for an year or maybe more. I was on the receiving end of a L1 burst fracture which restrains me from lifting weights. Now, I don't wanna gain a lot of fat just to get on the ideal side of a subjective metric which is kind of inevitable without strength training. Any ideas what steps I can take next? On a side note, I'm eating 1300-1400 calories only on a daily basis which I do understand is inadequate.
Well, if you're already struggling to eat enough, I wouldn't worry too much about gaining fat. If anything, I'd focus on a healthy diet that's still full of calories. I would just keep an eye out on your weight over time as you eat healthy fats, carbohydrates, and moderate protein. If you gain 10 lbs or so, I'd say that's a benefit. You don't strike me as someone who will suddenly become overweight, so I'd just do things in moderation, keep up light physical activity to the best of your ability. I don't think there's much else to be done until you've healed up. On that note, I hope you have a speedy recovery, HH.
@@tunneling-nanotubes Thanks a ton sir...I'm myself looking to crank up my vitamins and minerals' intake which at the moment is substandard to say the least. But exposure to sunlight isn't toiling and I should be doing it, albeit my laziness (kind of) has prevented me from doing that. I hope to change that very soon.
Many thanks for the fascinating video - it seems saturated fats are preferred, for building new membranes, and maybe also for fuel. Mitochondria prefer the fuels and building blocks they evolved to use. Unsaturated fats are like fake lego, dont quite fit and compromise the integrity of the construction.
Unsaturated fats are important as well because they help the cell membrane have some fluidity/flexibility which impacts its receptors function. Saturated fats I think of as the scaffolding that provides a solid frame for cell membrane structure. A balance of both is needed to maintain structure integrity of the cell membrane that is neither too fluid or rigid.
@@powerliftingpremedcrafter473... The issue with PUFA polyunsaturated fatty acids is the current dose being injested. It's stored and can't be burned, essentially becoming a poison to the system.
As I understand it, when the cell burns saturated fat, it will promote reverse electron transport and emit ROS, signalling the cell to become insulin resistant, protecting it from taking in more fat, so is rate limiting.(fat cells may function differently) I also thought this does not happen with unsaturated fats, and shorter chain saturated fats, which avoid this limiting mechanism. *What are your thoughts on this, and how it may relate to your comment that extended exposure to palmitate causing increased mitochondria activity, leading to cell death long term?*
I really, really want to know the outcome of this research. Fat is very important, and we need to do fat correctly. There is so much false data and half truths. I am so eager to get to the truth, especially about saturates. Aarre Peltomaa p.s. The extreme curiosity to be resolved, is whether we can boost fat metabolism with those enzymes or not.
Does the increase in mitochondria due to fragmentation also increase the degree mitochondrial uncoupling. There is an assumption that uncoupling results in an overall increase in efficiency and a reduction in ROS. If true, this could be important for health. Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases www.ncbi.nlm.nih.gov/pmc/articles/PMC6721602/#:~:text=Mitochondrial%20uncoupling%20can%20be%20defined,for%20mitochondria%2Ddependent%20ATP%20synthesis.
Hey Mark - that's a brilliant point. I love the way you're thinking, and you're absolutely right that generally when mitochondria fragment, they upregulate UCP, which does reduce the burden on the ETC and thereby reduces ROS. However, counterintuitively, although the mechanism is exactly right, the studies I've seen have shown palmitate increase fragmentation, yet an *increase* in ROS. Exactly why is tough to say, but I believe one of the mechanisms is through the activation of the JNK pathway. Great point!
Holy Shitake Mushrooms and Gosh Dang ! I wish I could just... read a summary of all your videos... What a freaking treasure chest of information, holy shitake! Man!! Maybe chatgpt will summarize your videos for me, I need to understand what you know ASAP! I've been eating high saturated/animal fat for years now, but have varied the amount of carbs I eat. I almost completely avoided vegetable fats, wheat, corn, and processed for 10 years.. though I'm now experimenting with wheat products(sourdough, pasta).
Yes, but cut out the carbs too. Burning dietry fat trains your body to burn body fat, but sugar is so toxic that it has to be controlled within very tight limits, and will be used first - then you get hungry after the elevated insulin creates a sugar crash, so consume more carbs, and repeat.
Less fat is better for weight loss than more fat. But yes, saturated fats have shown to increase weight less than unsaturated fats, or at least in mice studies. I'm not sure of a human trial that has tested this.
Hahaha. Had a look at the show notes to see, if I could skip any of the sciency stuff: Conclusions/results [you will be lost, if you skip to this]: Oh well then. Let's see, if my poor, little brain can make sense of this.
Totally excellent point, but I’ll keep this short. There was an experiment that was done by Oswell , I think. Anyways it was how much sawdust could be added to rice crispy without being notice. My point to all of this is to reference the difference between saturated fat and unsaturated. The process to extract unsaturated fat/ oils is unnatural and very oxidative on their own. Saturated fat isn’t the same it is very stable to oxidation. The cells are organic, saturated fat is organic. I would proposed that any inorganic fats would increase oxygen, the reasons are an invader of very similar make up, but the cells, the mitochondria knows the difference between them. I think the first reported heart attack was 1912, I think I’m writing and could be off a bit. Before 1912 Americans were eating saturated fats. Once linolenics were introduced, the rate of cardiovascular disease was increased.
So that means that it's actually the other way around! So, You store unsaturated fat (getting fatter) and USE The saturated fat for energy (for physical activity and more) Right??! So that means that we have been scammed of years of life by W.H.O. Saying that saturated fats are bad, and that unsaturated fats are the good ones...
Think of the unsaturated fat going into the gas tank to be used when needed, while the saturated fats go directly into the fuel-injection system. Recall at the end in the conclusions discussion he mentioned that "increased cell death"? Yes, the mitochondria is burning the unsaturated fat faster, but that also means the concentration of the ROS (reactive oxygen species) the byproduct of burn the fat has a higher peak concentration in the mitochondria. Higher concentration/density of ROS means the cell/mitochondria's antioxidants gets overwhelmed resulting in more damage otherwise would have occurred. - The stored "unsaturated" does get used but over an extended period of time, so the negative effect of ROS are more easily managed by the cell.
That's correct, Richard - they're both unsaturated. No, not all fats behave the same, there is some difference, but the wide spread effects *seem* to be about similar (exception being trans fats).
A key thing is also length of fatty acids. Short and medium chained fats are absorbed very differently and AFAIK not really stored as-is anywhere but oxidized preferentially or used to build longer fats if not needed.
Love your work, but having trouble seeing the forest for the trees... looking for insights into the real-world choices that confront us in the supermarket, and in reference to all the expert opinions floating around about food and diet....
TMI ⚠. BUT I do listen to my body, my normal. Any changes, WTF!! I don't chase test results, how I FEEL is more important. I'm 6 fucking 8 years old. BTW. 😮💪
Sòunds like a lot of assumptions, built on a lot of vague images and explained using some dodgy statistics.....When are you going to say anything about the bacteria, who are actually doing all the work?
I was really looking forward to a physiological conclusion. So many questions! Eating saturated fat leads to more immediate energy but could also overloaded mitochondria in an overfed state? Olive oil creates stored fat which could be good for a fasting person later or an athlete that works out fasted but bad for an obese person? Is the palmatic acid creating mitogenesis through uncoupling? Will these small mitochondria with less atp elongate and merge in a fasted state? This research creates more questions than answers.
Ig I'm going with: I don't want my cells dying so I'm avoiding saturated fat.
I have avacado w/EV olive oil for breakfast most days. The slower burn of unsaturated fat may be why I don't get very hungry throughout the day.?
Reduced intracellular fat storage with saturated fat against higher storage with unsaturated fat.
Why doesn't this , partly, explain some of the current weight problems people are having with 'healthy' foods compared to ancestral diets?
Or is it that the cell rejects the unsaturated fat as an energy source, but it is so similar to animal fats which are used for energy that it is stored away, but it is always rejected as an energy source, and so remains as fat?
Our body differentiates the type of fat by the length of its carbon chain, avoid the long chains, choose unrefined medium chain fat. The body chose to store fat in saturated form due to its stability. Avoid putting any PUFA or MUFA such as olive oil that will turn rancid at the blink of an eye.
Man I am gonna learn so much from this channel. Thanks Physionic!
30:53 increased fission/drp 1 is probably a marker of mitochondrial growth. In cells it would be cell division. That goes together with the growth of the saturated fat translocators.
Given that greater mitochondrial activity is usually a good thing, not sure why you were throwing out there that you see a lot of cellular death, uncharacteristically without support. Just a few examples: universal drop in body temperatures over decades (lower metabolic rate), metabolic disorders are all related to reduction in mitochondrial energy production. So to have something that actually increases it seems to be pretty noteworthy, regardless of other things we know what too much saturated fat can do.
You might even speculate that saturated fat is a great energy source for us. High ldl might not mean the fat is to blame, but that you are either taking in excessive amounts, or that the liver is too damaged to clear enough ldl, which then oxidizes leading to problems.
Finally someone with an informative conclusion proposal! All other comments are just writing how great the guy doing these vids is, no substance. Corny.
Yes, what you say is to the point. Unsaturated fats are toxic, saturated fats are great. Its the frying oils that make people obese, not sugars, not to the same degree.
It makes me wonder about context. As you say in this video, an increase in palmatate (saturated fat) will increase the mitochondrial fragmentation. In other videos, you mentioned how fasting or nutrient depravation can elongate small mitochondria. If we look at this from the point of view of our distant ancestors who were perhaps regularly subjected to forced periods of feasting and fasting (hunt & kill an animal, scarf it down, might be several days before you eat again). Maybe in the long run if used in this context it's a net positive, where the sudden intake of palmatate during the feasting period causes an increase of mitochondria with perhaps subpar health, but then over the next day or two their morphology improves during the fasting period.
Read your comment.
It’s good!
May I ask? How do personally apply this understanding to your eating style?
@@LenkaSaratogaTbh, I don't apply it to my eating style. It's just something I thought was curious. If I were going to apply it somehow, it would probably be by eating a very large meal containing almost exclusively of fatty meats, then not eating again for another 48 or 72 hours.
@@craigslitzer4857thank you for detailed response
Thanx Thomas. as is my goal as social scientist and anthropologist that the real sciences in all its doubts and searching should be presented to everybody, I follow your presentations. They are much more informative then the Gurus who take every study as granted and base complete life styles on it. We see things but don’t know what it means is still the level I work on in my anthropological work. Keep on doing the good stuff and don’t forget the dissertation. My dissertation started with a conversation I had with a Maribou from the Gambia. He asked me, what is the main part of our knowledge an I said. I dont know. And he said, you are right, that is the main part.
Thanks for the video. Biggest immediate takeaway is that definitely there is a huge difference in mitochondrial response to saturated vs unsaturated fat in this experiment. Let's not forget that dna of these cells does not guarantee the same behaviour in all humans, since they have a variety of human dna of various origins. By that, I mean that in human genome there are many traits, some from Neanderthal people, some from ice age people, some from ice age people that lived on equator and were spared of the long winter climate during that ice age. Ice conditioned most of the globe in period when sapiens sapiens evolved. Their foods' fats were mostly saturated ones, if they lived in these harsh winterish conditions. So, a quick conclusion (rather hypothesis with high likelyhood to be confirmed): humans are evolutionary adapted to saturated fats, and since unsaturated fats perform differently, it might be wise to avoid unsaturated fats.
*Radovan:* _"... in period when sapiens sapiens evolved."_
Life didn't evolve. The notion that all life evolved from a microbe is 19th century mythology that can 𝘰𝘯𝘭𝘺 be believed by faith with no support from modern molecular biology.
Evolution’s Bite is a great book by Peter Ungar which shows the (much less clear cut) beautiful picture of human diets over time. It’s not strongly tending towards high animal or non-animal saturated fatty acid consumption, though. But let’s grant that’s true. A big part of evolutionary biology is antagonistic pleiotropy- specifically, as a theory of aging based on competing gene expressions. In short, it actually comes to the opposite conclusion: all else equal, if two foods are of the same health-promoting value in the reproductive window, one ancestral and one novel, we should favor the novel food for longevity purposes. It’s tempting to think what we evolved to must be good, but that’s far from necessarily the case; it took me a while to grasp this one, so I’d be happy to clarify more if ya want 👍
At the end before your conclusions discussion, I had been thinking that the "increasing" activity would actually lead to a shorter cell life resulting from mitochondria degradation due to increase ROS production in a shorter period and hence less time for the cell/mitochondria anti-oxidation processes to mitigate the effects of the higher concentrations of ROS. When you said increase "cell death" I think you were implying something similar to my thinking. This would lead me to think that the unsaturated fats being sequestered, and I assumed eventually consumed by mitochondria slowly over a longer period of time means less ROS stress (peaking stress) and hence heathier and longer-lived mitochondria/cell. - Mechanical/Naval Engineer here and I love this mechanistic stuff. Good informative video!
40:04 _"So, can we apply this to the real world? No."_
Well darn it! I listened to this in anticipation that you'd tell us saturated fats are more healthy than unsaturated.
Yes, saturated fats are good, unsaturated are plain toxic, no matter what this guy has or has no courage to admit. He is a conformist and has hard time to break out of the fog of dogma. The reason cells still don't live long even on saturated fats, is that fat is a bad source of energy for a cell, period. Cells like glucose. Douhhh!
But the author still deserves the credit for bringing this topic up.
Thanks. I look forward to further information about your work. Cell biology is fascinating!
Watched half. Thx for this. Really useful.
I guess having mentioned what a mitochondria is, u could have explained the difference between saturated and unsaturated fats as well. Saturated will be solid at room temp.
So much disinformation on good Vs bad fats even if one Googles images...
Thank you. Please make talk practical to ordinary people to help us understand to eat saturated fat or not? If we need to eat , how much per day ? Make your knowledge how is applicable to our daily lives? I am a consultant surgeon and fade up with too many jargon names. What I want is what is the effect of saturated fat, other fats we eat on mitochondria. The talk is typical of young scientists who live in their own minds.Please make talk more practical to our lives.
hey!! Great coverage. That is really interesting... I'm trying to check mitochondrial functions in obese patients in my masters, which they all have increased levels of FFA... This article gave me some ideas to what analyse.
That's great to hear, Hugo. An unexpected benefit of doing this particular video, I love it. All the best with your graduate work.
So great! For this purpose of obesity study, it would absolutely wonderful to have the same 3 or 4 slides/studies integrating carbohydrates. It would enable us to compare and hierarchy the impact of both glucose and fat on mitochondria. Thank you for this rich sharing.
Just thinking... Since palmitate is the "gold standard" of fatty acid synthase (from any macronutrient oxidation surplus), it would be more prone to obligatory oxidation in mithocondria. Oleate (or other unsaturated fats) is nobler. Maybe the reason why cells store it in lipid droplets or in order to restore membrane phospholipids. 🤔
Well if palmitate is what cells produce upon surplus of sugar oxidation, then probably that's what cells will prefer to metabolise best and safest again when calories are needed. Douhh! Fat oxidation is what turns them into CO2, water and energy, a good thing. Unsaturated fats staying in droplets are maybe ... rejected as useless toxic garbage, the cell don't want to touch with a 10' pole. Cell membrane needing high quantities of uns. oils is a big myths.
Found your channel about a week ago. Love it.
I've been watching this kind of stuff for many years, and into it long before youtube itself. In this era of so much bs/bad information people just eat up because they don't have 'base' knowledge, just go on this guy sounds smart.
You really dive in and get to the heart of matters. Love it. Follower for sure.
Welcome aboard!
Firstly, your's truly is appreciative of the in depth nature of the video itself, as currently Keto-Kid here does need to keep abreast with research, be it positive or negative. If you can even make that distinction in this case.
Secondly, on the Henrietta Lax topic, a decent 10 minute overview can be found on the World Service. Namely under the Witness-History podcast series. For in death, humanity owes her a great debt. Rarely does a specific cancer bring about such a bountiful source of research potential.
All told, useful video indeed.
I don't think we can say either way whether these findings are good or not. More cell deaths also don't mean anything bad, as cell deaths are often desirable, it can very well be a mechanism by which the body protects itself. To leap to conclusions from this would be a mechanistic speculation and bad logic. You are right to withhold from making a statement outright. It's still interesting nonetheless to see how this all works together.
What I know about Palmitate metabolism in humans is that in rat studies humans have a gene to prevent certain deleterious effects of palmitate, while rats don't(As you can imagine, they don't get nearly as much as humans do in their diet). So all of these factors have to be accounted for, but we really don't know as much as some people might claim to know.
How did they separate out the potential for the mitochondria to use the sugar solution, control plus was the the base to which they added fat? How do they control which path of the Krebs cycle is used for energy production? This is critical since they measure O2, which varies by what energy source is used and how (glycolis vs oxphos). How "fat adapted" is the cell line? is fat adaption really about how much CPT1 is produced by cells?
For the last four years I have focused on maximizing autophagy. All my research on this topic keeps leading me back to the mitochondria. I did everything that triggers autophagy, on the same day, and every mole on my body dried up and fell off. Eating crushed broccoli sprouts seem to really make the effect go exponential.
Ave you tried taking pure Asprin? It has autophagic affects without having to do the fasting.
Also, If has been shown to enhance tumor growth.
@@rebeccajane3532don’t you mean impede tumor growth, rather than enhance?
@@i.ehrenfest349 no it is not a typo.
Let me see if I can get the research for you
I am new to your channel, and for me this is extremely interesting. 😘
For consumers wanting to make an informed choice between the available foods and fats, it would be very interesting to know what happens with the refined seed oils (PUFAs) and margarine in their mitochondria.
Refined seed oils have reportedly no nutritional value and are readily oxidized.
Personally I made the choice for grass fed butter and saturated oils for baking and cooking and bam all processed PUFAs from my kitchen..
I think that I get enough unsaturated fats from meat and fish.
To ask my question: what is known about refined poly unsaturated fats and the mitochondria?
If you already posted a video about the subject, I apologize.
Search tip: How Seed Oils Destroy Your Mitochondria and Lead To Chronic Disease
What is the potential fate of thr lipid dropplets? They are in triglyceride form? Futue oxidation in the cell? Or storage in fat cells? Thanks. Excellent long form info👍
Great video. A paper came in out a few years ago that, if I recall, showed that palmitate specifically really amped up cancer growth, and this cell line is a cervical cancer. Might a non-cancerous cell process fats differently? Also is there any evidence that oleate is permanently stored in the droplets? You would think that it would eventually be beoken down. Awfully wasteful if not.
Humans have a gene to deal with the negative effects of Palmitate. Conversely, the rats they study on don't have this gene because rats don't have to deal with palmitate often. They took out this gene and put it in rats and found that it decrease negative effects of Palmitate significantly, also confirming that they got the right gene. Of course, this isn't the result they wanted so they have to spin it to make it sound like a bad thing. Like no, the gene did what it was supposed to do, because humans consume a lot of Palmitate, like other highly carnivorous animals.
If you isolate Palmitate from the effects of this gene, of course you will see bad things occur. And epidemiology showing a 10-30% increase in incidence based on levels of palmitate consumption is not enough to convince anyone of a negative effect of Palmitate on humans.
Or is it a case of animal fats being preferentially used by animals, and vegetable fats not being so suitable for use by animals get preferentially stored as fat?
2023 and we are still asking the basic question about fat, saturated vs unsaturated? Society that built robots and spacecraft.. 😂 I need no arrogant degree in mol. biology to tell you from evidence in society that unsaturated fats are darn toxic and fattening for the population. Inuits who are unassimilated in western lifestyle eating predominantly animal fat are much better off. Yes their life span is rel. short, but then again, they don't get any sun, healthy carbs, vitamins etc.
Fuel for cancer is glucose
Something interesting to look at with regard to this is the exceptional longevity of naked mole rats and their extremely high levels of monounsaturated fat in there cell walls… hmmm maybe a connection to the Mediterranean diet and health?
This is interesting. I'm going to keep listening and see what conclusions you come to. Are you planning to compare your findings with the unsaturated fats?
The findings of my dissertation? No, although I’ve pushed for it, it doesn’t look like it’s going to happen.
We can't evaluate cell response to fat without evaluating the glucose and insulin context.
So palmitic acid causes mitochondrial fission? But there was another study showing stearic acid causes mitochondrial fusion. So all saturated fats don't act the same?
You have shown and proven sth groundbreaking, to my mind...
Mitochondria are really greatly troubled by saturated fat, so they end up fragmenting and dying. And so does the cell after them. Non-saturated fat is much easier on the mitochondria, therefore it does not get first- line preference for processing - it can get stored in fat droplets and wait to be taken care of, while saturated fat is so dangerous, that it has to be processed immediately. And the cell 'hopes' that no more of this burden is coming so as not to burn out the mitochondria through overloading, then (sharing the heavy workload) fragmentation and, finally, disintegration. TY
Doh.
Lipid droplets are implicated in a lot of pathology.
cardston medical research canada -lovin every minute of it!
One question, was there any studies comparing long chain saturated fats versus medium or short chain saturated fats? C16:0 versus C12:0 versus C8:0? And in terms of unsaturated fats ...mono unsaturated versus poly unsaturated versus oxidized polyunsaturated fats... since the poly unsaturated fats are the most likely to oxidize. Note that my comments (all of them) were typed as I was still listening so some of my questions were partially answered.
These deep dives are the best, keep it up💪
Thank you for your brilliant content.
This is not a subject we learn about in our daily lives, so I appreciate the video and content, just to add to my base knowledge and feel I am actually getting introduced to such different world and fascinating one at that! Thank you!
Holy Crap! a lot of cell death with palmatate. Palm oil is all over the place in the processed food chain. I get my fats from lard , butter, meat and fish. I am 70 and I have the energy of a 40 year old.
32:22 man casually shit on their microscopes, respectfully LMAO 💀
Thank you so much for sharing your work 🙏
Thanks we really need this
LOL. That was inconclusive.
Cell death is not necessarily a bad thing. Proliferation and cell survival in senescence are bad things.
I think what can be concluded is that unsaturated fats have more tendency to be stored and saturated fats burned. This would seem to be adaptive if one assumes that saturated fat from animal sources is a marker of prosperous times and plant source fats an indicator of lean times.
In times of abundance usage of energy would be okay while conservation/storage would be requisite in lean ones.
I am curious whether oleate usage similarly leads to a lot of cell death. Certainly, high carb intake favours proliferation.
Wow. That was a fantastic video. One that I could actually understand. I'm not a scientist but I am trying to understand fats more. My take away from this is that a diet high in saturated fats may lead to higher and faster cell senescence. Whereas a diet higher in unsaturated fats would lead to more of a stockpile in the lipids storage of the cell and a slower use of that energy. Does that sound about right?
Thanks, Rick. These take quite some planning. I'm really happy to hear its understandable, though - it helps me figure out if I'm communicating correctly. I think your point could be correct. In that case, it would have been cool to measure some genes of senescence (usually those are downstream genes that are targeted by the protein called p53). I think no matter what, high levels of fat ultimately leads to detriment to the cells, regardless of the type, but the mechanism differs between them. I don't think we can conclude anything on senescence from this data, but it would be a cool thing to further this research with.
My take on this is that saturated fat is an efficient fuel source for mitochondria, and unsaturated is not, no one is eating so much fat that the cells are bathed in it. And over nutrition of any kind will cause mitochondrial fragmentation. So the fact that unsaturated fat mimics a fasted state to mitochondria, while the cell is storing it, is concerning. I'd like to see longer term what the cell ends up doing with the stored unsaturated fats. Does the mitochondria eventually use it?
Thank you for all the nice videos!! Please find out about omega 3 vs omega 6, effect. an glucose vs ketone! Thank you!!
Butter: more ATP but could be bad due to cell death. Olive oil: less ATP but less cell death (but more lipids in the cell - even fatty liver)? Then add age and metabolic issues including not enough CPT1. Good luck figuring all out!!
Thanks for making these videos. I find this very interesting but absolutely do not have the ability to understand these papers if I were to just try and read them on my own.
"The Immortal Life of Henrietta Lacks" is a great, great book on HeLa, her life, and medical ethics.
As someone who worked in the formulation side of anti-cancer drugs, I do remember that the HeLa immortal cancer cell line caused a major issue in the 1990's... when they started doing genetic testing of the various cell lines, they learned that about 90% of the human cell lines had been contaminated and replaced with the HeLa cells, thus invalidating much of the past 30 years of cancer drug research. So the drug screening they would do using various human cancer cell lines from various organs turned out to have been tested on HeLa cells that had contaminated and wiped out what they thought were the carefully stored cancer cells for different organs.
My work consisted on developing safe formulations for clinical trials -- did not mean the drugs tested were safe, only that the formulation used to provide the dosages they wanted were... they usually picked drugs that did not dissolve well, so a lot of formulation work was needed to get the dosages they wanted. I also developed analytical tests for raw material, in-process, finished product and stability testing of the product. Several times I was able to develop a lyophilized formulation that could be stored at normal freezer temperatures for at least 2 years, when the drug raw material itself had to be stored in a -80C freezer. That was necessary because we had to account for every milligram of the material because of the 3 years to gather and purify about 40 grams of material, and then due to the difference in how different countries package and handle deep frozen material, they lost half of the material when they thawed a container that the shipping country had packed at -80 C. Different standard operating procedures caused the pressure to build up in the container as the material was brought up to room temperaure before opening... POOF!!!! a big dust cloud in the safety hood upon opening the container.
Medical ethics would be nice to have.
Keep it up. You always have great content
Wah nic has 70k subscribers now nice. Been here since hundreds. Keep up the good work bro
Appreciate the support!
I’m certainly not going to read too much into this, as he states in his conclusion. I already know saturated fat sends my cholesterol though the roof.
Don't get me wrong, I appreciate the knowledge nuggets. Can you maybe have something more conclusive. So, say this is what this nutrient does to your cells. Conclusion, good or bad and why.
I appreciate the input, methanial. The way I have things organized is that I cover each study in depth so people can sink their teeth into the details, and with each study on a topic, the body of literature grows until I can release a video giving more concrete "advice" with answers as to why. On this topic, I'll be releasing just such a video in several weeks, stay tuned.
@@Physionic Great! Thanks for the response!
Not the way science actually works. This study was done on a particular cancer cell line and may or may not tell you anything abput what happens in humans on average, let alone any particular human specifically; and there is almost certainly a bunch of tradeoffs and confounders. These cells are used because they are easy to grow and study.
I remember DRP1 being my biochem prof's favourite protein...except he called it "derp" and proceeded to include many appropriately "derpy" cat pictures in the lecture slides to match...it was pretty cringe in hindsight, but I guess scientists have to make their own fun where they can 😂
Are we burning fatty acids or actually ketones which are derived from fatty acids? Or both?
Could the experiment shown at 6;06 mins, not be negatively/inaccurately effected by the sugar content that’s there? Sugar and fat don’t really mix well.
Im catching up on your videos. I love to know the details behind the scenes when it comes to how my body works..
"Who am I?" I thought you were going to say "I am a hunky-looking medicine nerd with a silky deep voice that lulls you into watching my content".
Should I watch this video if I’m deciding whether to eat a cheesesteak(saturated fats) or an avocado(unsaturated fats)?
No.
So you get inflammation with the saturated fat?
This is not true but not all SFA are made the same. Good SFA lowers C-RP, TRG/HDL ratio and eventually the LDL level.
Please, more videos like this!
Great video! Very informative, thanks. I know you didn't want to make any extrapolations from this to everyday life for people wrt nutrition, etc. However recently i saw a video from FireInaBottle where he discussed how squirrels eating large amounts of acorns, etc, that contained high amounts of oleic acid gained weight. Perhaps trees benefited from producing these fats to help fatten up animals who collected their seeds for the winter to spread further across territory, etc. Many human populations never had oleic acid heavy diets and are now significantly obese on a modern diet higher in vegetable oils when traditionally it would have comprised of only small amounts of animal fats (butter, lean pork, etc). Even the ancient Greeks knew of obesity (there are sources), considering their more recent adoption of olive oil at the time might have been why. Just speculation but interesting none the less.
i like having the podcast available LOL bc i watch like 5 mins of these and get distracted
Interesting. This is good feedback. Even when I say “if you look here” and things of that nature, you still feel the audio only podcast is helpful to you?
so short term palmitate is good but long term causes cell death, but you still haven't tested oleate long enough to see if it also causes cell death? I don't need a definitive conclusion but would love a few hypothesis. drp is splitting mitochondria more when exposed to palmitate that seems good as its an indicator of mitochondrial biogenesis..
There are better representatives of SFA than palmitate, wonder why it was chosen and not the others.
Am I wrong, or both the fat intakes came as extra calories above the base glycosis supply from the media?
Would this be related to the perceived fat toxicity?
I like the thought process, R. You may have a point there. It is possible the added fat increases the energy availability, which it certainly does, and that has an effect, itself. The media is different from cell to cell, but in this case, it tends to be a high glucose media, which could exacerbate the issue.
@@Physionic Thank you
@@PhysionicRandle cycle?
thanks for educating.
More about effect of saturated fat on leaky gut syndrome please.
Thank you for all the information😊
Please can you do a video about physiological effects too with respect to cell biology.
Lots of love and regards(India)
What's the significance of mitochondrial fragmentation vs elongation?
fragmentation = reduction on mitochondrial energy generation to reduce excessive oxidative stress, also enables autophagy of broken mitochondrias. Might indicate too much fuel reserve.
elongation = increases energy generation efficiency and also disallow autophagy. Might indicate lack of available fuel
Thank you
Awesome video👏
Love your videos dude, they're all super informative. I wanted to take your opinion on my confusion related to nutrition. I'm underweight at the moment with a BMI of 17.5 but repugnant to gain weight because I can't do strength training for an year or maybe more. I was on the receiving end of a L1 burst fracture which restrains me from lifting weights. Now, I don't wanna gain a lot of fat just to get on the ideal side of a subjective metric which is kind of inevitable without strength training. Any ideas what steps I can take next? On a side note, I'm eating 1300-1400 calories only on a daily basis which I do understand is inadequate.
Well, if you're already struggling to eat enough, I wouldn't worry too much about gaining fat. If anything, I'd focus on a healthy diet that's still full of calories. I would just keep an eye out on your weight over time as you eat healthy fats, carbohydrates, and moderate protein. If you gain 10 lbs or so, I'd say that's a benefit. You don't strike me as someone who will suddenly become overweight, so I'd just do things in moderation, keep up light physical activity to the best of your ability. I don't think there's much else to be done until you've healed up. On that note, I hope you have a speedy recovery, HH.
@@Physionic Thanks a lot, I really appreciate it.👍
@@adityaaryan942 sure thing.
@@tunneling-nanotubes Thanks a ton sir...I'm myself looking to crank up my vitamins and minerals' intake which at the moment is substandard to say the least. But exposure to sunlight isn't toiling and I should be doing it, albeit my laziness (kind of) has prevented me from doing that. I hope to change that very soon.
Crucially here: when going for carbs (and you should), go for healthy carbs: Whole grains, beans, nuts, seeds and fruit.
Interesting.
Many thanks for the fascinating video - it seems saturated fats are preferred, for building new membranes, and maybe also for fuel. Mitochondria prefer the fuels and building blocks they evolved to use. Unsaturated fats are like fake lego, dont quite fit and compromise the integrity of the construction.
Unsaturated fats are important as well because they help the cell membrane have some fluidity/flexibility which impacts its receptors function. Saturated fats I think of as the scaffolding that provides a solid frame for cell membrane structure. A balance of both is needed to maintain structure integrity of the cell membrane that is neither too fluid or rigid.
@@powerliftingpremedcrafter473... The issue with PUFA polyunsaturated fatty acids is the current dose being injested. It's stored and can't be burned, essentially becoming a poison to the system.
As I understand it, when the cell burns saturated fat, it will promote reverse electron transport and emit ROS, signalling the cell to become insulin resistant, protecting it from taking in more fat, so is rate limiting.(fat cells may function differently)
I also thought this does not happen with unsaturated fats, and shorter chain saturated fats, which avoid this limiting mechanism.
*What are your thoughts on this, and how it may relate to your comment that extended exposure to palmitate causing increased mitochondria activity, leading to cell death long term?*
When would have humans seen increased saturated fats? During winter from their own stores? From animal kills?
Subscibed: All
I’m all in.
Thanks!
Thank you!
Nice thank you.
I really, really want to know the outcome of this research. Fat is very important, and we need to do fat correctly. There is so much false data and half truths. I am so eager to get to the truth, especially about saturates. Aarre Peltomaa
p.s. The extreme curiosity to be resolved, is whether we can boost fat metabolism with those enzymes or not.
lol
That was very informative.
Thank you very much, Matheus. I'm glad to hear it.
Does the increase in mitochondria due to fragmentation also increase the degree mitochondrial uncoupling. There is an assumption that uncoupling results in an overall increase in efficiency and a reduction in ROS. If true, this could be important for health.
Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases
www.ncbi.nlm.nih.gov/pmc/articles/PMC6721602/#:~:text=Mitochondrial%20uncoupling%20can%20be%20defined,for%20mitochondria%2Ddependent%20ATP%20synthesis.
Hey Mark - that's a brilliant point. I love the way you're thinking, and you're absolutely right that generally when mitochondria fragment, they upregulate UCP, which does reduce the burden on the ETC and thereby reduces ROS. However, counterintuitively, although the mechanism is exactly right, the studies I've seen have shown palmitate increase fragmentation, yet an *increase* in ROS. Exactly why is tough to say, but I believe one of the mechanisms is through the activation of the JNK pathway.
Great point!
Holy Shitake Mushrooms and Gosh Dang !
I wish I could just... read a summary of all your videos...
What a freaking treasure chest of information, holy shitake! Man!! Maybe chatgpt will summarize your videos for me, I need to understand what you know ASAP!
I've been eating high saturated/animal fat for years now, but have varied the amount of carbs I eat. I almost completely avoided vegetable fats, wheat, corn, and processed for 10 years.. though I'm now experimenting with wheat products(sourdough, pasta).
So eating saturated fat is better for fat loss than unsaturated??
Yes, but cut out the carbs too. Burning dietry fat trains your body to burn body fat, but sugar is so toxic that it has to be controlled within very tight limits, and will be used first - then you get hungry after the elevated insulin creates a sugar crash, so consume more carbs, and repeat.
Less fat is better for weight loss than more fat. But yes, saturated fats have shown to increase weight less than unsaturated fats, or at least in mice studies. I'm not sure of a human trial that has tested this.
Hahaha. Had a look at the show notes to see, if I could skip any of the sciency stuff:
Conclusions/results [you will be lost, if you skip to this]:
Oh well then. Let's see, if my poor, little brain can make sense of this.
Totally excellent point, but I’ll keep this short. There was an experiment that was done by Oswell , I think. Anyways it was how much sawdust could be added to rice crispy without being notice. My point to all of this is to reference the difference between saturated fat and unsaturated. The process to extract unsaturated fat/ oils is unnatural and very oxidative on their own. Saturated fat isn’t the same it is very stable to oxidation. The cells are organic, saturated fat is organic. I would proposed that any inorganic fats would increase oxygen, the reasons are an invader of very similar make up, but the cells, the mitochondria knows the difference between them. I think the first reported heart attack was 1912, I think I’m writing and could be off a bit. Before 1912 Americans were eating saturated fats. Once linolenics were introduced, the rate of cardiovascular disease was increased.
How do You find those images
Which ones?
@@Physionic the explantions ones
I make them.
So that means that it's actually the other way around! So, You store unsaturated fat (getting fatter) and USE The saturated fat for energy (for physical activity and more) Right??! So that means that we have been scammed of years of life by W.H.O. Saying that saturated fats are bad, and that unsaturated fats are the good ones...
Think of the unsaturated fat going into the gas tank to be used when needed, while the saturated fats go directly into the fuel-injection system. Recall at the end in the conclusions discussion he mentioned that "increased cell death"? Yes, the mitochondria is burning the unsaturated fat faster, but that also means the concentration of the ROS (reactive oxygen species) the byproduct of burn the fat has a higher peak concentration in the mitochondria. Higher concentration/density of ROS means the cell/mitochondria's antioxidants gets overwhelmed resulting in more damage otherwise would have occurred. - The stored "unsaturated" does get used but over an extended period of time, so the negative effect of ROS are more easily managed by the cell.
This is very interrenting iformation. Please do you have some information related to fat types and lysossomes?
Do you think saturated fat is healthy?
That's a broad question. I'd lean toward no, however, but I haven't made up my mind.
Aren't trans fats and PUFAs unsaturated? Do all unsaturated fats behave the same in the Mitochondria?
That's correct, Richard - they're both unsaturated. No, not all fats behave the same, there is some difference, but the wide spread effects *seem* to be about similar (exception being trans fats).
A key thing is also length of fatty acids. Short and medium chained fats are absorbed very differently and AFAIK not really stored as-is anywhere but oxidized preferentially or used to build longer fats if not needed.
love it
Love your work, but having trouble seeing the forest for the trees... looking for insights into the real-world choices that confront us in the supermarket, and in reference to all the expert opinions floating around about food and diet....
Wrong channel. You learn how your body works here, so you can use that knowledge to seek how to improve it.
Plenty of channels that do that
I don’t know why I listen to this when Dr Fauci can tell me the sole State-approved medical-science truth.
TMI ⚠. BUT I do listen to my body, my normal. Any changes, WTF!!
I don't chase test results, how I FEEL is more important. I'm 6 fucking 8 years old. BTW. 😮💪
Who else came to comment section for final takeaway lessons😂
Sòunds like a lot of assumptions, built on a lot of vague images and explained using some dodgy statistics.....When are you going to say anything about the bacteria, who are actually doing all the work?
Mono, great. Sat fat, great. Any significant dose of seed refined PUFA, scare me shitless.
So is meat fat bad?
Thanks!
Thank *you*, Richard. I appreciate the support.