This leptin theory has been all the rage since at least the 90s and is one of the big parts of mainstream obesity science right now. Stephan Guyenet's The Hungry Brain is all about this.
I think while most of the stuff they talk about is true, it's also not the major cause of the obesity epidemic in most people. It's only one half of the equation, and they don't have any solutions for it.
E.g. you probably also read that while you can restore "slimness" by injecting mice with leptin, this doesn't work in humans? Leptin therapy was thought to be the cure for obesity in the 90s or so, and has turned out to be completely useless.
I'd call this the "signaling defect" theory of obesity. I'm more of a believer in the "fuel partitioning" part.
Signaling theory says there is enough fat, and you can get to it, but the signal is broken. Most fat people make enough leptin, huge amounts in fact, so maybe the brain's leptin receptors are broken.
Fuel partitioning theory says: there is enough fat physically in your body, but you somehow can't ACTUALLY get to it, so you are, in a sense, literally starving - the signal isn't wrong!
I don't deny all the leptin research, I just wonder if it's that relevant. If leptin/signaling theory was the whole deal, then we would see that people who actually just ate less with willpower lost weight and kept it off. But that's not what we see. We'd see me overeat by thousands of calories, but I don't. I actually undereat (both by expected TEE of 3,300 and measured of 4,600), and still I currently am not losing weight.
So I think leptin is a cute mouse experiment, and might explain the circus man/woman from 1830 or whatever, but not the obesity epidemic. At least it's not the major factor I'd say, although leptin resistance probably doesn't help.
Oh that's just the CICO snarl. I bet if you just didn't eat anything for two weeks you'd lose weight just fine. And as soon as you started eating ad lib again it would come straight back.
The interesting thing would be why ex150 unbreaks this mechanism. I think it's the protein restriction part.
I bet that burning excess protein is using the same pathway as burning PUFAs, or interfering somehow. Mumble mumble peroxisomes mumble vaults?
So on ex150 you're constantly releasing PUFAs from stores, but they're getting used and so don't block the leptin. You do your 'protein refeed' and suddenly you're starving hungry again.
I cite your ex150-salmon experiment as further evidence. You betrayed the faith by flirting with the polyunsaturated whore-of-Babylon and the vengeance of the Lord fell upon you in quantifiable form.
Do it again! Fish oil supplements! I hear 'Golden Calf' is a good brand.
No, it's not. There are many anecdotes on the reddit about it.
Even in myself. First, you can't "just" not eat anything for 2 weeks. Almost nobody can, especially not the metabolically fucked.
If you locked me in a cage for 2 weeks without food, I'd be insane by day 5 or so (estimate) and would start biting my fingers off by day 6.
So in a sense I would "lose weight" but at what cost?
I have done 2 months of weekday fast/weekend feast, i.e. 5 day fasts every week 8 times in a row.
I only lost a bit of water weight while not eating, and it was always back literally after my first morning meal on Saturday. I.e., I did not lose any fat.
This part of "CICO obviously being true" is already false and has been disproven many times.
You can disguise this obvious fact by saying "just" and "weight" instead of fat and "just fine" but it's simply not true if you consider fat, not water weight.
I seriously don't believe leptin is important. You seem to assume that it plays a causal role here, I think that's wrong. It just doesn't explain my 2 decades of personal experience well at all.
> I only lost a bit of water weight while not eating, and it was always back literally after my first morning meal on Saturday. I.e., I did not lose any fat.
> This part of "CICO obviously being true" is already false and has been disproven many times.
I really don't want to disbelieve you, but I am having huge trouble with this. It takes a vast amount of energy to maintain your body temperature. And if your core temperature drops then you'll die. Your basal metabolic rate can't fall much.
That energy has to be coming from somewhere. Water-weight sure, you carry about 2000kcal of glycogen so you can burn that and lose 2kg of glycogen and associated water.
And there'll be food in your guts that you're still digesting. But the rest of the needed energy must also be coming from somewhere. 2000kcal plus gut contents probably won't keep a man going for five days.
So I have a dilemma, disbelieve my friend who does not lie, break my faith in the conservation of energy, or find the extra energy source I have forgotten about. Which would you recommend?
Actually I do think that we must have a way of storing protein that we haven't found out about yet, so maybe that will get us all the way to five days without food or metabolising fat?
1. My basal metabolic rate has fallen to around 1,000kcal in the past, as I stayed weight stable for 2 months of ~1,000kcal/day OMAD. Maybe it can get even lower in the short term via buffers like glycogen. I've also LOST weight at 4,200kcal/day for a month. So we know my flexibility spans at least 3,200kcal/day for the range of 1-2 months.
2. I just disproved naive CICO nominally and hypothetically: ate 2,890kcal, allegedly burned 4,600kcal, on average by LBM should burn 3,300. You can argue "DLW was wrong" but then you need to argue that my metabolic rate is below expected when RMR also confirms it's normal or slightly high. Starting to be a lot of gymnastics here.
> I seriously don't believe leptin is important. You seem to assume that it plays a causal role here, I think that's wrong.
Well, it's doing *something*. And it's doing it in all vertebrates, and it does seem to be a total fat-levels measuring hormone.
Like I say, it seems to have worked exactly as expected for me for most of my life, and it seems to have gone a bit wrong recently, and it seems to be badly broken in a lot of younger people and particularly Americans. That's why I got interested in PUFAs in the first place.
Your systems may be hopelessly broken. But actually I don't think they are as long as you're doing ex150.
You get your cement-truck satiety (which I always called 'not feeling hungry' or 'feeling full'), and as long as you stay on ex150 your weight seems to be under homeostatic control, albeit your set point is too high.
Your weight doesn't just random walk according to the whims of sloth and gluttony, or hyper-palatability or whatever. It's pretty stable (on ex150).
I think we're actually agreeing pretty hard here. I see what happens to you and think 'broken homeostat'. You see what happens to you and think 'no homeostat'. But we're seeing the same things.
1. You don't know that what's gone wrong is leptin. It might be your leptin is working fine and something else is off. There are various mechanisms of what could be wrong, and there are even various seed oil-induced ones. Leptin seems to be one of them, but we don't know it's The One or even participating. It could, of course, just like ECS and ROS and phospholipid omega balance or or or..
2. I think cement-truck satiety & ex150 and other "miracle" diets seem to disprove leptin theory, at least as I understand it. At least the supply part. When I was 300lbs a day before ex150, I presumably excreted the same amount of leptin as I did at 300lbs a day into ex150. Yet, somehow, I started losing fat very rapidly. I suppose something about the demand/downstream effects of leptin could be involved, but it's a similar data point to giving people leptin treatment having 'very modest' results. The total level of serum leptin doesn't seem to be a problem in almost anyone (human).
3. Yea, we're seeing the same things. It's interesting how that leads people to jump to very different (or slightly different) conclusions intuitively.
> If you locked me in a cage for 2 weeks without food, I'd be insane by day 5 or so (estimate) and would start biting my fingers off by day 6.
I can believe this, especially if you had a bit of protein in your cage. But I think it would be your system doing what it's supposed to do. Making you seek food as an overwhelming matter of extreme urgency because it thinks you're starving.
> E.g. you probably also read that while you can restore "slimness" by injecting mice with leptin, this doesn't work in humans? Leptin therapy was thought to be the cure for obesity in the 90s or so, and has turned out to be completely useless.
So I *do* remember reading this, and I think that's why I thought it must be more complicated, but I couldn't find it when I was looking, got any links?
I think I'm just remembering it from Guyenet's The Hungry Brain. The entire book is essentially about this, so you might enjoy it. I found it a bit long and tedious, in a Malcom Gladwell pop science without any real content way.
It is always difficult when more than one thing can be wrong. Mega doses of PUFA especially seed oil were not in the food supply until recently (1970’s?). I think seed oil was the oil in oil based paint.
Maybe I can get an NIH grant to see if adoption of latex paints causes obesity. You know P=.05.
For my own self PUFA but mostly corn oil trigger my arthritis. I have dialed out and burned off enough PUFA stores, that a small dose of French Fries or Chips gives me global joint pain for about 1.5 days.
Interesting that it's mostly corn oil. Corn oil is significantly higher (58%) in omega-6 linoleic acid than even soybean oil (51%). Or something else in it?
Seems true or at the very least plausible since TPTB feed PUFA to cattle to fatten the cattle for market. We share highly conserved pathways and such with our bovine friends.
I don't even pretend to know the chemistry, but I do know that grass fed beef and corn/soy fed beef taste completely different. Grass fed tastes clean and corn/soy quite greasy. Which leads me to believe that even if the corn/soy beef is PUFA free, it's still not 'right'. It can actually give me a stomach ache. So I stick to grass fed 98% of the time.
Could be, I think most British beef is grass-fed anyway so I may not have ever tasted whatever passes for beef in the States. The best thing to do might be to look at the PUFA percentages on the labels. Ours are usually about 0.3g/100g.
I understand that there's a certain level of creativity allowed with labels, but since most people think PUFAs are the dog's, any error is likely to be upwards.
Don't think we have PUFA labels on our beef in the USA. At least I've never seen one.
The thought behind my post is that I tend to believe that PUFAs and their oxidation are not the only reason dairy products and meat from cows force-fed seeds are not good for us. Cows evolved to eat grass, not seeds so their body's chemistry changes when they are force-fed seeds. And these changes are imo not good for us, regardless of the PUFA ratios.
All of the above is totally amateur and not science-based, but the difference in taste alone is enough to make me think the issue goes beyond PUFAs.
I've noticed after forswearing the damned things for a year or so, that 'greasy' is an excellent description of the taste of rancid PUFAs. Like you say, most of the natural fats taste great. Vegetable oils that have oxidised are 'greasy' and form strange solids.
I'm sure that's right, and if there's a difference in taste there is certainly a difference in chemistry. But the interesting questions are about what the magnitude (and direction) of the various effects are.
E.g. Bees visiting lavender plants will produce funny tasting honey, and that lavender taste is probably psychoactive, calming down people's anxiety, but is it a big effect?, and what does it do to people who aren't over-anxious in the first place?, and what else does it do?
Can we blame all the diseases of modernity on lavender? Or just some mental effects in people who deliberately eat lavender-flavoured things? Or should we not worry about it at all?
Bees naturally visit lavender plants; cows do not naturally eat corn or soybeans. That's the key difference. Plus there are no lavender plant 'feed lots' where bees are forced to consume nothing but lavender. :)
This is a nitpick, but I think force-feeding is a misleading term here; as much as I've seen, cattle love seeds. When a bucket of vitamin-fortified flour is placed in the pasture, all the sheep come and stick their noses into the bucket, then the ox comes, scatters them with a slight head movement and sticks his own head in. It's like fast food for them, tasty.
Counter-nitpick, what do cattle on good grass do if you give them a bucket of rape seeds? I mean, I already know the answer, the local cows eat bikes. But do they prefer them to grass given a free choice?
And cows deal quite elegantly with rapeseed cake, what about pigs and chickens, that deal with it about as badly as we do?
Actually what we need to test is wild boar and jungle fowl on butter vs. sunflower oil. For which we are going to need a supply of obese, yet brave, Dothraki maidens.
Agreed, I feed the local ducks porridge oats and they love them. I have to do it carefully or the fights get quite nasty. Honestly, mothers stealing oats from their own ducklings. Animals.
I stopped feeding the swans after they started pecking on the hull at six o'clock in the morning wanting breakfast. Scrounging white bastards can fuck off and get jobs if they want to eat that early.
Hi Claudiney, I stuck the numbers into a spreadsheet.
The control mice seem to do quite well on their diets, They don't seem to be making much leptin at all, their values are about the same size as the variance. And I figure they're just growing as mice are supposed to do, with little body fat.
This despite omega-6/omega-3 ratios of 468:1 and 10:1, which you'd think would make some difference.
Differences between the control groups seem small compared to the variance of the measurements.
I assume they're getting enough of both types of the essential fatty acids, not too much, and either using them correctly or disposing of them, as you'd expect.
The DIO (diet induced obesity) mice are all getting about twice as much PUFA in the same amount of food as the control mice. The differences are the omega-6/omega-3 ratios of the various diets, which range from 187:1 to 3:1.
They're all clearly deranged, eating more and ending up weighing about twenty percent more than the control mice. Probably they're overwhelmed, and the PUFAs are circulating freely in the blood, causing chaos.
It seems suspicious that all the DIO mice gain roughly the same amount of weight, in spite of these differences. I wonder if that's just because they were all eating all the food they were given. The 187:1 mice might be eating a bit more than the other groups and end up weighing a bit more, but the effect size is close to the measurement variance.
The big differences are in the amount of leptin they're making. That should be similar since they're at similar weights, but it's not, the 137:1 mice are making about twice as much as the 3:1 mice.
It looks to me like the omega-3 in the diets is suppressing leptin production more than the omega-6 does.
Probably both types of PUFA are interfering with leptin reception in the brain somehow, and that's why they're getting so hungry
I think that's about all I'm prepared to take away from this study, and it agrees with the interpretation I gave in the essay above.
The DIO 137:1 mice might be eating a bit more, but they're also getting slightly more total PUFA.
The authors seem to agree about the omega-3 effect, since they say:
Compared to mice fed the control diets, the expression of leptin in fat tissue and leptin-R and POMC in the hypothalamus was higher in the diet-induced obesity (DIO) mice, and the n-3 PUFAs in the diets reversed these elevated expression levels.
This leptin theory has been all the rage since at least the 90s and is one of the big parts of mainstream obesity science right now. Stephan Guyenet's The Hungry Brain is all about this.
I think while most of the stuff they talk about is true, it's also not the major cause of the obesity epidemic in most people. It's only one half of the equation, and they don't have any solutions for it.
E.g. you probably also read that while you can restore "slimness" by injecting mice with leptin, this doesn't work in humans? Leptin therapy was thought to be the cure for obesity in the 90s or so, and has turned out to be completely useless.
I'd call this the "signaling defect" theory of obesity. I'm more of a believer in the "fuel partitioning" part.
Signaling theory says there is enough fat, and you can get to it, but the signal is broken. Most fat people make enough leptin, huge amounts in fact, so maybe the brain's leptin receptors are broken.
Fuel partitioning theory says: there is enough fat physically in your body, but you somehow can't ACTUALLY get to it, so you are, in a sense, literally starving - the signal isn't wrong!
I don't deny all the leptin research, I just wonder if it's that relevant. If leptin/signaling theory was the whole deal, then we would see that people who actually just ate less with willpower lost weight and kept it off. But that's not what we see. We'd see me overeat by thousands of calories, but I don't. I actually undereat (both by expected TEE of 3,300 and measured of 4,600), and still I currently am not losing weight.
So I think leptin is a cute mouse experiment, and might explain the circus man/woman from 1830 or whatever, but not the obesity epidemic. At least it's not the major factor I'd say, although leptin resistance probably doesn't help.
> If leptin/signaling theory was the whole deal, then we would see that people who actually just ate less with willpower lost weight and kept it off.
Why would we see that? Once the willpower failed it would come straight back on!
Yea, but it would work until then. But in many of us, it doesn't even come off!
Oh that's just the CICO snarl. I bet if you just didn't eat anything for two weeks you'd lose weight just fine. And as soon as you started eating ad lib again it would come straight back.
The interesting thing would be why ex150 unbreaks this mechanism. I think it's the protein restriction part.
I bet that burning excess protein is using the same pathway as burning PUFAs, or interfering somehow. Mumble mumble peroxisomes mumble vaults?
So on ex150 you're constantly releasing PUFAs from stores, but they're getting used and so don't block the leptin. You do your 'protein refeed' and suddenly you're starving hungry again.
I cite your ex150-salmon experiment as further evidence. You betrayed the faith by flirting with the polyunsaturated whore-of-Babylon and the vengeance of the Lord fell upon you in quantifiable form.
Do it again! Fish oil supplements! I hear 'Golden Calf' is a good brand.
No, it's not. There are many anecdotes on the reddit about it.
Even in myself. First, you can't "just" not eat anything for 2 weeks. Almost nobody can, especially not the metabolically fucked.
If you locked me in a cage for 2 weeks without food, I'd be insane by day 5 or so (estimate) and would start biting my fingers off by day 6.
So in a sense I would "lose weight" but at what cost?
I have done 2 months of weekday fast/weekend feast, i.e. 5 day fasts every week 8 times in a row.
I only lost a bit of water weight while not eating, and it was always back literally after my first morning meal on Saturday. I.e., I did not lose any fat.
This part of "CICO obviously being true" is already false and has been disproven many times.
You can disguise this obvious fact by saying "just" and "weight" instead of fat and "just fine" but it's simply not true if you consider fat, not water weight.
I seriously don't believe leptin is important. You seem to assume that it plays a causal role here, I think that's wrong. It just doesn't explain my 2 decades of personal experience well at all.
> I only lost a bit of water weight while not eating, and it was always back literally after my first morning meal on Saturday. I.e., I did not lose any fat.
> This part of "CICO obviously being true" is already false and has been disproven many times.
I really don't want to disbelieve you, but I am having huge trouble with this. It takes a vast amount of energy to maintain your body temperature. And if your core temperature drops then you'll die. Your basal metabolic rate can't fall much.
That energy has to be coming from somewhere. Water-weight sure, you carry about 2000kcal of glycogen so you can burn that and lose 2kg of glycogen and associated water.
And there'll be food in your guts that you're still digesting. But the rest of the needed energy must also be coming from somewhere. 2000kcal plus gut contents probably won't keep a man going for five days.
So I have a dilemma, disbelieve my friend who does not lie, break my faith in the conservation of energy, or find the extra energy source I have forgotten about. Which would you recommend?
Actually I do think that we must have a way of storing protein that we haven't found out about yet, so maybe that will get us all the way to five days without food or metabolising fat?
1. My basal metabolic rate has fallen to around 1,000kcal in the past, as I stayed weight stable for 2 months of ~1,000kcal/day OMAD. Maybe it can get even lower in the short term via buffers like glycogen. I've also LOST weight at 4,200kcal/day for a month. So we know my flexibility spans at least 3,200kcal/day for the range of 1-2 months.
2. I just disproved naive CICO nominally and hypothetically: ate 2,890kcal, allegedly burned 4,600kcal, on average by LBM should burn 3,300. You can argue "DLW was wrong" but then you need to argue that my metabolic rate is below expected when RMR also confirms it's normal or slightly high. Starting to be a lot of gymnastics here.
> I seriously don't believe leptin is important. You seem to assume that it plays a causal role here, I think that's wrong.
Well, it's doing *something*. And it's doing it in all vertebrates, and it does seem to be a total fat-levels measuring hormone.
Like I say, it seems to have worked exactly as expected for me for most of my life, and it seems to have gone a bit wrong recently, and it seems to be badly broken in a lot of younger people and particularly Americans. That's why I got interested in PUFAs in the first place.
Your systems may be hopelessly broken. But actually I don't think they are as long as you're doing ex150.
You get your cement-truck satiety (which I always called 'not feeling hungry' or 'feeling full'), and as long as you stay on ex150 your weight seems to be under homeostatic control, albeit your set point is too high.
Your weight doesn't just random walk according to the whims of sloth and gluttony, or hyper-palatability or whatever. It's pretty stable (on ex150).
I think we're actually agreeing pretty hard here. I see what happens to you and think 'broken homeostat'. You see what happens to you and think 'no homeostat'. But we're seeing the same things.
1. You don't know that what's gone wrong is leptin. It might be your leptin is working fine and something else is off. There are various mechanisms of what could be wrong, and there are even various seed oil-induced ones. Leptin seems to be one of them, but we don't know it's The One or even participating. It could, of course, just like ECS and ROS and phospholipid omega balance or or or..
2. I think cement-truck satiety & ex150 and other "miracle" diets seem to disprove leptin theory, at least as I understand it. At least the supply part. When I was 300lbs a day before ex150, I presumably excreted the same amount of leptin as I did at 300lbs a day into ex150. Yet, somehow, I started losing fat very rapidly. I suppose something about the demand/downstream effects of leptin could be involved, but it's a similar data point to giving people leptin treatment having 'very modest' results. The total level of serum leptin doesn't seem to be a problem in almost anyone (human).
3. Yea, we're seeing the same things. It's interesting how that leads people to jump to very different (or slightly different) conclusions intuitively.
> If you locked me in a cage for 2 weeks without food, I'd be insane by day 5 or so (estimate) and would start biting my fingers off by day 6.
I can believe this, especially if you had a bit of protein in your cage. But I think it would be your system doing what it's supposed to do. Making you seek food as an overwhelming matter of extreme urgency because it thinks you're starving.
Sure, my point is that "I bet if you just didn't eat anything for two weeks you'd lose weight just fine" is an invalid statement.
It's kinda like saying "I bet if you just doubled your velocity every day, you would quickly reach the speed of light just fine."
The word "just" and "fine" are doing a lot of work here.
> E.g. you probably also read that while you can restore "slimness" by injecting mice with leptin, this doesn't work in humans? Leptin therapy was thought to be the cure for obesity in the 90s or so, and has turned out to be completely useless.
So I *do* remember reading this, and I think that's why I thought it must be more complicated, but I couldn't find it when I was looking, got any links?
I think I'm just remembering it from Guyenet's The Hungry Brain. The entire book is essentially about this, so you might enjoy it. I found it a bit long and tedious, in a Malcom Gladwell pop science without any real content way.
> I found it a bit long and tedious, in a Malcom Gladwell pop science without any real content way.
High praise indeed!
It is always difficult when more than one thing can be wrong. Mega doses of PUFA especially seed oil were not in the food supply until recently (1970’s?). I think seed oil was the oil in oil based paint.
Maybe I can get an NIH grant to see if adoption of latex paints causes obesity. You know P=.05.
For my own self PUFA but mostly corn oil trigger my arthritis. I have dialed out and burned off enough PUFA stores, that a small dose of French Fries or Chips gives me global joint pain for about 1.5 days.
> Maybe I can get an NIH grant to see if adoption of latex paints causes obesity. You know P=.05.
I for one am happy to predict that drinking latex paint has metabolic effects. You might even find a way of reducing bad cholesterol!
Interesting that it's mostly corn oil. Corn oil is significantly higher (58%) in omega-6 linoleic acid than even soybean oil (51%). Or something else in it?
Seems true or at the very least plausible since TPTB feed PUFA to cattle to fatten the cattle for market. We share highly conserved pathways and such with our bovine friends.
I'm not sure that PUFAs ever get into cows. They get eaten by bacteria in cows' stomachs which is why beef and milk are still PUFA free.
I don't even pretend to know the chemistry, but I do know that grass fed beef and corn/soy fed beef taste completely different. Grass fed tastes clean and corn/soy quite greasy. Which leads me to believe that even if the corn/soy beef is PUFA free, it's still not 'right'. It can actually give me a stomach ache. So I stick to grass fed 98% of the time.
Could be, I think most British beef is grass-fed anyway so I may not have ever tasted whatever passes for beef in the States. The best thing to do might be to look at the PUFA percentages on the labels. Ours are usually about 0.3g/100g.
I understand that there's a certain level of creativity allowed with labels, but since most people think PUFAs are the dog's, any error is likely to be upwards.
Don't think we have PUFA labels on our beef in the USA. At least I've never seen one.
The thought behind my post is that I tend to believe that PUFAs and their oxidation are not the only reason dairy products and meat from cows force-fed seeds are not good for us. Cows evolved to eat grass, not seeds so their body's chemistry changes when they are force-fed seeds. And these changes are imo not good for us, regardless of the PUFA ratios.
All of the above is totally amateur and not science-based, but the difference in taste alone is enough to make me think the issue goes beyond PUFAs.
I've noticed after forswearing the damned things for a year or so, that 'greasy' is an excellent description of the taste of rancid PUFAs. Like you say, most of the natural fats taste great. Vegetable oils that have oxidised are 'greasy' and form strange solids.
Vegetable oils don't have to have oxidized to taste wrong, at least for me.
I'm sure that's right, and if there's a difference in taste there is certainly a difference in chemistry. But the interesting questions are about what the magnitude (and direction) of the various effects are.
E.g. Bees visiting lavender plants will produce funny tasting honey, and that lavender taste is probably psychoactive, calming down people's anxiety, but is it a big effect?, and what does it do to people who aren't over-anxious in the first place?, and what else does it do?
Can we blame all the diseases of modernity on lavender? Or just some mental effects in people who deliberately eat lavender-flavoured things? Or should we not worry about it at all?
Bees naturally visit lavender plants; cows do not naturally eat corn or soybeans. That's the key difference. Plus there are no lavender plant 'feed lots' where bees are forced to consume nothing but lavender. :)
"cows force-fed seeds"
This is a nitpick, but I think force-feeding is a misleading term here; as much as I've seen, cattle love seeds. When a bucket of vitamin-fortified flour is placed in the pasture, all the sheep come and stick their noses into the bucket, then the ox comes, scatters them with a slight head movement and sticks his own head in. It's like fast food for them, tasty.
Counter-nitpick, what do cattle on good grass do if you give them a bucket of rape seeds? I mean, I already know the answer, the local cows eat bikes. But do they prefer them to grass given a free choice?
And cows deal quite elegantly with rapeseed cake, what about pigs and chickens, that deal with it about as badly as we do?
Actually what we need to test is wild boar and jungle fowl on butter vs. sunflower oil. For which we are going to need a supply of obese, yet brave, Dothraki maidens.
Agreed, I feed the local ducks porridge oats and they love them. I have to do it carefully or the fights get quite nasty. Honestly, mothers stealing oats from their own ducklings. Animals.
I stopped feeding the swans after they started pecking on the hull at six o'clock in the morning wanting breakfast. Scrounging white bastards can fuck off and get jobs if they want to eat that early.
thank you - clear, concise BUT with a storytellers detail. GREAT, well written article.
So kind, thank you Joan!
"That'll do. Omega-3s both prevent the production of leptin and prevent it getting into the brain."
From Table 3 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3117679/) it does not appear to be the case.
Mices that have more leptin and are deficient in Omega-3 eat more.
Hi Claudiney, I stuck the numbers into a spreadsheet.
The control mice seem to do quite well on their diets, They don't seem to be making much leptin at all, their values are about the same size as the variance. And I figure they're just growing as mice are supposed to do, with little body fat.
This despite omega-6/omega-3 ratios of 468:1 and 10:1, which you'd think would make some difference.
Differences between the control groups seem small compared to the variance of the measurements.
I assume they're getting enough of both types of the essential fatty acids, not too much, and either using them correctly or disposing of them, as you'd expect.
The DIO (diet induced obesity) mice are all getting about twice as much PUFA in the same amount of food as the control mice. The differences are the omega-6/omega-3 ratios of the various diets, which range from 187:1 to 3:1.
They're all clearly deranged, eating more and ending up weighing about twenty percent more than the control mice. Probably they're overwhelmed, and the PUFAs are circulating freely in the blood, causing chaos.
It seems suspicious that all the DIO mice gain roughly the same amount of weight, in spite of these differences. I wonder if that's just because they were all eating all the food they were given. The 187:1 mice might be eating a bit more than the other groups and end up weighing a bit more, but the effect size is close to the measurement variance.
The big differences are in the amount of leptin they're making. That should be similar since they're at similar weights, but it's not, the 137:1 mice are making about twice as much as the 3:1 mice.
It looks to me like the omega-3 in the diets is suppressing leptin production more than the omega-6 does.
Probably both types of PUFA are interfering with leptin reception in the brain somehow, and that's why they're getting so hungry
I think that's about all I'm prepared to take away from this study, and it agrees with the interpretation I gave in the essay above.
The DIO 137:1 mice might be eating a bit more, but they're also getting slightly more total PUFA.
The authors seem to agree about the omega-3 effect, since they say:
Compared to mice fed the control diets, the expression of leptin in fat tissue and leptin-R and POMC in the hypothalamus was higher in the diet-induced obesity (DIO) mice, and the n-3 PUFAs in the diets reversed these elevated expression levels.
Can you read it differently?
Ooh that's interesting! Thank you so much, these are my favourite kinds of comments. I'll read that carefully and try again.