Well, being back online is one thing. Having the time to actually do any posting appears to be quite another... At the moment I'm actually sleeping until 6am, well after the time I'm usually writing posts. Life is exceedingly busy with life type things, especially the house, garden, work and emergency patching up of our elderly Miata. As life settles down I'll get back to posting again but for the next few weeks it's just not a practical proposition!
Thanks to all for the comments about the family on the last post and for links emailed.
Peter
Showing posts with label High Fat. Show all posts
Showing posts with label High Fat. Show all posts
Friday, August 5, 2011
Tuesday, August 2, 2011
Low-carb, high-fat diets add no arterial health risks to obese
Good news, I would say:
Low-carb dieters showed no harmful vascular changes but also on average dropped 10 pounds in 45 days, compared to an equal number of study participants randomly assigned to a low-fat diet. The low-fat group, whose diets consisted of no more than 30 percent from fat and 55 percent from carbs, took on average 70 days, nearly a month longer, to lose the same amount of weight. [...]
However, Stewart does contend that an overemphasis on low-fat diets has likely contributed to the obesity epidemic in the United States by encouraging an overconsumption of foods high in carbohydrates. He says that high-carb foods are, in general, less filling and that people tend to get carried away with how much low-fat food they can eat. More than half of American adults are estimated to be overweight, with a body mass index of 26 or higher; a third are considered to be obese, with a BMI of 30 or higher.Full article here.
Fasting insulin and weight loss and calories-in vs calories-out
I had this exchange in the comments on a previous post:
Frank said...
Hi Peter. I'd say that I pretty much agree with your post. Insulin and caloric deficit are not mutually exclusive, ie, low-insulin could enhance fat loss on a caloric deficit or, looked from another perspective, a caloric deficit could enhance fat loss if someone has low insulin level. I have only one question for you. For the sake of it lets make thing black and white. What do you believe is the most important thing to do, in order to achieve weight/fat loss a) be in a caloric deficit (your insulin level does not matter much) b) having a low-insulin level (it does not matter much if you're in a caloric deficit or not). Again, in real life, I don't believe they exclude each other, but if you could fix only one to have a weight loss, which one would you fix? Calories or insulin? The way I see it is that, as you stated, insulin inhibits lipolysis, but more lipolysis does not equal more oxidation. It still has to be matched to energy expenditure. In that case, calories would be the most important factor. That's my point of view and it could be wrong. I'm just wondering if you agree to some degree with it, because reading your post, I get the idea that you do. Thanks for your time.
Peter said...
Ah Frank, now there is a question. Without caloric deficit (and I want uncoupling proteins, sleeping metabolic rate, spontaneous movements, etc, etc, etc, everything, accounted for) there will be no weight loss. But, in real life, if I could only alter just one, it would be insulin. I would expect no weight loss but I would expect improved health. What else matters?
There is a flaw in the answer I gave to this question. It's working at the Noddy level of calories-in vs calories-out.
The Noddy approach is perfectly adequate to explain the findings of GnK's paper (PR's weight loss excepted, if she genuinely ate all she was asked to), but embarrassingly stupid in the real world.
Let's look at calories-in vs calories-out in the fixed caloric phase of the Abredeen study.
Calories-in is total calories in to metabolism. There are two sources. Those from the diet, let's assume (incorrectly) these are genuinely all of the 2000kcal/d on offer. Then there is the supply of free fatty acids metered out from adipocytes under the regulation of insulin. Maybe a little glycogen, but I'll ignore that for the discussion.
Under LCHF conditions more FFAs are accessible due to lower insulin levels. More get used and, from Table 1, only 1930kcal of food are needed to supplement those calories-in from adipocytes in order to meet total metabolic needs. Hunger is low. Calories supplied are clearly able to meet voluntary calories out. Demand is within the limits of supply. Some food is refused.
Under MCMF conditions the higher insulin level allows less calories to be supplied from fat in to metabolism (adipose derived calories-in fall), so calories-in accepted from food spontaneously increase to the full 2000kcal/d. Under the study conditions we cannot tell if 2000kcal plus reduced adipose FFA supply is enough for as much metabolic activity as was possible under low insulin conditions. What if it is not? Now the real question is: Does lipolysis automatically increase to supply all needs for calories out? Why should it? Lipolysis is controlled by insulin. Insulin is high, lipolysis restrained.
If there is any shortfall in the calories from fat plus 2000kcal, there are only limited calories available to burn. You can't burn what you don't have. Calories-out would drop because they simply cannot exceed the supply available. I would expect the participants to automatically reduce their calories-out. There is no free lunch. Calories-out = calories-in. All need to be accounted for.
Is it be possible to force lipolysis in the face of hyperinsulinaemia to increase FFAs from fat to a higher level without lowering insulin?
Of course it is. There are other hormones in addition to insulin. You can throw around adrenaline, growth hormone, glucagon and probably a truckload of others I've not thought about. You can add in direct sympathetic nervous system innervation of adipocytes to effect lipolysis if you like. But these mechanisms come with a price. The price is hunger.
I think it's called working up an appetite.
In the Aberdeen study the attempt to maintain caloric intake failed during the LCHF phase because low insulin increased caloric supply from fat. Higher insulin in the MCMF phase limited calories-in derived from adipose tissue and may well have set a cap on total calories available for use during this higher insulin phase.
In Frank's thought experiment it might be easy to fix dietary calories-in, but people might refuse some of them if insulin was low enough for adipose tissue derived FFAs to be available.... If they ate all of their calories but wriggled in their chair a bit more because they had more calories available then the concept of calories-out being fixed is lost....
I'll just finish with a clarification of this phrase from another commenter:
"lipolysis is not beta oxidation"
This is, ultimately, accurate. That doesn't stop it being bollocks.
A rather more perceptive view is the situation comes from, of all places, the lipophobic cardiologists who published on FFAs and myocardial ischaemia:
"The rate of fatty-acid uptake and oxidation by the heart is controlled by their availability [33]"
Oh, interesting. Availability. A supply led system. Hmmmmmm. I would guess most FFA burning tissue would follow cardiac muscle. Now I can't quite remember what effect insulin has on lipolysis and FFA availability. Silly me.
Peter
Frank said...
Hi Peter. I'd say that I pretty much agree with your post. Insulin and caloric deficit are not mutually exclusive, ie, low-insulin could enhance fat loss on a caloric deficit or, looked from another perspective, a caloric deficit could enhance fat loss if someone has low insulin level. I have only one question for you. For the sake of it lets make thing black and white. What do you believe is the most important thing to do, in order to achieve weight/fat loss a) be in a caloric deficit (your insulin level does not matter much) b) having a low-insulin level (it does not matter much if you're in a caloric deficit or not). Again, in real life, I don't believe they exclude each other, but if you could fix only one to have a weight loss, which one would you fix? Calories or insulin? The way I see it is that, as you stated, insulin inhibits lipolysis, but more lipolysis does not equal more oxidation. It still has to be matched to energy expenditure. In that case, calories would be the most important factor. That's my point of view and it could be wrong. I'm just wondering if you agree to some degree with it, because reading your post, I get the idea that you do. Thanks for your time.
Peter said...
Ah Frank, now there is a question. Without caloric deficit (and I want uncoupling proteins, sleeping metabolic rate, spontaneous movements, etc, etc, etc, everything, accounted for) there will be no weight loss. But, in real life, if I could only alter just one, it would be insulin. I would expect no weight loss but I would expect improved health. What else matters?
There is a flaw in the answer I gave to this question. It's working at the Noddy level of calories-in vs calories-out.
The Noddy approach is perfectly adequate to explain the findings of GnK's paper (PR's weight loss excepted, if she genuinely ate all she was asked to), but embarrassingly stupid in the real world.
Let's look at calories-in vs calories-out in the fixed caloric phase of the Abredeen study.
Calories-in is total calories in to metabolism. There are two sources. Those from the diet, let's assume (incorrectly) these are genuinely all of the 2000kcal/d on offer. Then there is the supply of free fatty acids metered out from adipocytes under the regulation of insulin. Maybe a little glycogen, but I'll ignore that for the discussion.
Under LCHF conditions more FFAs are accessible due to lower insulin levels. More get used and, from Table 1, only 1930kcal of food are needed to supplement those calories-in from adipocytes in order to meet total metabolic needs. Hunger is low. Calories supplied are clearly able to meet voluntary calories out. Demand is within the limits of supply. Some food is refused.
Under MCMF conditions the higher insulin level allows less calories to be supplied from fat in to metabolism (adipose derived calories-in fall), so calories-in accepted from food spontaneously increase to the full 2000kcal/d. Under the study conditions we cannot tell if 2000kcal plus reduced adipose FFA supply is enough for as much metabolic activity as was possible under low insulin conditions. What if it is not? Now the real question is: Does lipolysis automatically increase to supply all needs for calories out? Why should it? Lipolysis is controlled by insulin. Insulin is high, lipolysis restrained.
If there is any shortfall in the calories from fat plus 2000kcal, there are only limited calories available to burn. You can't burn what you don't have. Calories-out would drop because they simply cannot exceed the supply available. I would expect the participants to automatically reduce their calories-out. There is no free lunch. Calories-out = calories-in. All need to be accounted for.
Is it be possible to force lipolysis in the face of hyperinsulinaemia to increase FFAs from fat to a higher level without lowering insulin?
Of course it is. There are other hormones in addition to insulin. You can throw around adrenaline, growth hormone, glucagon and probably a truckload of others I've not thought about. You can add in direct sympathetic nervous system innervation of adipocytes to effect lipolysis if you like. But these mechanisms come with a price. The price is hunger.
I think it's called working up an appetite.
In the Aberdeen study the attempt to maintain caloric intake failed during the LCHF phase because low insulin increased caloric supply from fat. Higher insulin in the MCMF phase limited calories-in derived from adipose tissue and may well have set a cap on total calories available for use during this higher insulin phase.
In Frank's thought experiment it might be easy to fix dietary calories-in, but people might refuse some of them if insulin was low enough for adipose tissue derived FFAs to be available.... If they ate all of their calories but wriggled in their chair a bit more because they had more calories available then the concept of calories-out being fixed is lost....
I'll just finish with a clarification of this phrase from another commenter:
"lipolysis is not beta oxidation"
This is, ultimately, accurate. That doesn't stop it being bollocks.
A rather more perceptive view is the situation comes from, of all places, the lipophobic cardiologists who published on FFAs and myocardial ischaemia:
"The rate of fatty-acid uptake and oxidation by the heart is controlled by their availability [33]"
Oh, interesting. Availability. A supply led system. Hmmmmmm. I would guess most FFA burning tissue would follow cardiac muscle. Now I can't quite remember what effect insulin has on lipolysis and FFA availability. Silly me.
Peter
Palmitic acid: the horror never ends
Chris forwarded me a link to this study. Read about inflammasones in tissue culture and quake. Here is the relevant line:
"These findings provide insights into the association of inflammation, diet and T2D."
It gets even better. Here is the best line from the press release:
"These results support the idea that inflammation plays a role in chronic disease," says Ting. "The simple message is to avoid fatty foods as much as possible."
OK, you take isolated cells, bathe them in 2mmol palmitic acid and they become unhappy. This is supposed to have something to do with eating a high fat diet?????
Just for fun I'm going, in my head, to eat some (gasp, horror) palmitic acid. Please don't do this at home, you probably don't want to inflame your inflammasomes.
I'm looking through my refrigerator for some palmitic acid but I notice that all there is in my fridge is Food. Bugger. What comes closest? Maybe butter??? Butter is undoubtedly Food, but it does have rather a lot of palmitic acid. Let's give it a try.
Half a pound of butter, here I come. Mmmmmmm. Nice. Yummie.
Now let's measure my blood palmitic acid levels . OOOOOh, post prandial triglycerides are up! Right on, I'm gonna die, some time soon. But what about the acid, the pamitic acid?
Ah, FFAs are also up up up. Success! 500, 600, 700, yes, 800micromol/l. If I really am in luck I might make that 2000micomol/l hit and drop right in to the inflammasome mediated diabetes zone. You know, that palmitic acid trip to nowhere.
Oh, but except for feeling a bit nauseous from all that butter in one go, I feel fine. Perhaps because I don't really have 2mmol/l palmitate in my blood stream after all. Double bugger. It seems like there is major, like MAJOR, contamination of my blood palmitate with oleate. Some is from the butter, some is from my own bloody liver cocking up the experiment. Using delta 9 desaturase to drop the occasional double bond in to long chain saturated fats ensures normal physiology.
Now, if I wasn't such a cheapskate I'd shell out the ackers to see if Ting et al used mixes of palmitate and oleate as well as either fatty acid in isolation. We know from the abstract that oleate does not inflame your inflammasomes... But I am a cheapskate, so I won't. Instead I'll go to this study:
"Low concentrations of oleate (0.1mM) completely inhibited palmitate-induced oxidative stress, SAPK activation, and apoptosis."
That's it, one tenth of one millimole of oleate completely negates the adverse effects of isolated palmitate.
Maybe check this one:
"Oleate alone did not cause mtROS generation and mtDNA damage, and its addition to palmitate prevented palmitate-induced mtDNA damage, increased total ATP levels and cell viability, and prevented palmitate-induced apoptosis and inhibition of insulin-stimulated Akt (Ser(473)) phosphorylation."
I could go on. No one, ever, at any time, has 2mmol/l of isolated palmitate in their bloodstream. A whiff of oleate is completely protective against the evil intentions of a researcher with a block of palmitate when viewed from the bottom of a test tube. It's called physiology. We are evolved to work this way. Knock out delta 9 desaturase and things become quite fun, but that's another story!
Citing the existing literature doesn't get you a Nature publication. Nor does it allow you to write press releases of utter stupidity to support low fat eating while simultaneously keeping yourself off the dole.
Peter
"These findings provide insights into the association of inflammation, diet and T2D."
It gets even better. Here is the best line from the press release:
"These results support the idea that inflammation plays a role in chronic disease," says Ting. "The simple message is to avoid fatty foods as much as possible."
OK, you take isolated cells, bathe them in 2mmol palmitic acid and they become unhappy. This is supposed to have something to do with eating a high fat diet?????
Just for fun I'm going, in my head, to eat some (gasp, horror) palmitic acid. Please don't do this at home, you probably don't want to inflame your inflammasomes.
I'm looking through my refrigerator for some palmitic acid but I notice that all there is in my fridge is Food. Bugger. What comes closest? Maybe butter??? Butter is undoubtedly Food, but it does have rather a lot of palmitic acid. Let's give it a try.
Half a pound of butter, here I come. Mmmmmmm. Nice. Yummie.
Now let's measure my blood palmitic acid levels . OOOOOh, post prandial triglycerides are up! Right on, I'm gonna die, some time soon. But what about the acid, the pamitic acid?
Ah, FFAs are also up up up. Success! 500, 600, 700, yes, 800micromol/l. If I really am in luck I might make that 2000micomol/l hit and drop right in to the inflammasome mediated diabetes zone. You know, that palmitic acid trip to nowhere.
Oh, but except for feeling a bit nauseous from all that butter in one go, I feel fine. Perhaps because I don't really have 2mmol/l palmitate in my blood stream after all. Double bugger. It seems like there is major, like MAJOR, contamination of my blood palmitate with oleate. Some is from the butter, some is from my own bloody liver cocking up the experiment. Using delta 9 desaturase to drop the occasional double bond in to long chain saturated fats ensures normal physiology.
Now, if I wasn't such a cheapskate I'd shell out the ackers to see if Ting et al used mixes of palmitate and oleate as well as either fatty acid in isolation. We know from the abstract that oleate does not inflame your inflammasomes... But I am a cheapskate, so I won't. Instead I'll go to this study:
"Low concentrations of oleate (0.1mM) completely inhibited palmitate-induced oxidative stress, SAPK activation, and apoptosis."
That's it, one tenth of one millimole of oleate completely negates the adverse effects of isolated palmitate.
Maybe check this one:
"Oleate alone did not cause mtROS generation and mtDNA damage, and its addition to palmitate prevented palmitate-induced mtDNA damage, increased total ATP levels and cell viability, and prevented palmitate-induced apoptosis and inhibition of insulin-stimulated Akt (Ser(473)) phosphorylation."
I could go on. No one, ever, at any time, has 2mmol/l of isolated palmitate in their bloodstream. A whiff of oleate is completely protective against the evil intentions of a researcher with a block of palmitate when viewed from the bottom of a test tube. It's called physiology. We are evolved to work this way. Knock out delta 9 desaturase and things become quite fun, but that's another story!
Citing the existing literature doesn't get you a Nature publication. Nor does it allow you to write press releases of utter stupidity to support low fat eating while simultaneously keeping yourself off the dole.
Peter
Palmitic acid: the horror never ends addendum
Okay, Victoria sent me the full pdf.
This group used 0.2mmol/l or 0.5mmol/l palmitate conjugated to bovine serum albumin. All other fatty acids were completely excluded. No semblance of physiological mixtures were involved.
But guess what, they had a living mouse model too!
Now you have to be wondering exactly how they managed to get a mouse to have 0.5mmol/l of palmitate in its bloodstream, to the exclusion of all other fatty acids, during a glucose tolerance test. After all, their test tube model used pure palmitate, surely they used the same conditions in their mice? This is a Nature paper after all.
How did they perform this near miracle? Well the methods section (when you finally find it tacked on to the end of the paper, an afterthought down beyond the references) doesn't mention any attempt to measure live mouse fatty acids at all. They didn't. WTF, this got published in Nature!
The diet used was good old commercial 5TJN. When I downloaded the composition pdf from the Test Diet website to my laptop it said I'd already downloaded it some time before..... It's popular!
Here's the link, it won't embed:
www.testdiet.com/PDF/5TJN.pdf
How much sugar would you like with your Crisco? Remember, always ask for your favourite lipotoxin by name...
NO NO NO.
JUST SAY NO.
Say no to Crisco.
As so often happens, this paper details feats of molecular and cellular manipulation of breathtaking complexity. How can anyone be capable of doing this and yet be so stupid? Awesome!
Peter
And it gets worse. The stats were done on "Prism 5.0 for Macintosh". OMG they're Mac users. It shouldn't be allowed. Their laptops should be confiscated forthwith. Now. I'll have them please.
This group used 0.2mmol/l or 0.5mmol/l palmitate conjugated to bovine serum albumin. All other fatty acids were completely excluded. No semblance of physiological mixtures were involved.
But guess what, they had a living mouse model too!
Now you have to be wondering exactly how they managed to get a mouse to have 0.5mmol/l of palmitate in its bloodstream, to the exclusion of all other fatty acids, during a glucose tolerance test. After all, their test tube model used pure palmitate, surely they used the same conditions in their mice? This is a Nature paper after all.
How did they perform this near miracle? Well the methods section (when you finally find it tacked on to the end of the paper, an afterthought down beyond the references) doesn't mention any attempt to measure live mouse fatty acids at all. They didn't. WTF, this got published in Nature!
The diet used was good old commercial 5TJN. When I downloaded the composition pdf from the Test Diet website to my laptop it said I'd already downloaded it some time before..... It's popular!
Here's the link, it won't embed:
www.testdiet.com/PDF/5TJN.pdf
How much sugar would you like with your Crisco? Remember, always ask for your favourite lipotoxin by name...
NO NO NO.
JUST SAY NO.
Say no to Crisco.
As so often happens, this paper details feats of molecular and cellular manipulation of breathtaking complexity. How can anyone be capable of doing this and yet be so stupid? Awesome!
Peter
And it gets worse. The stats were done on "Prism 5.0 for Macintosh". OMG they're Mac users. It shouldn't be allowed. Their laptops should be confiscated forthwith. Now. I'll have them please.
Palmitic acid: the horror never ends speculation
Back in her PhD days my wife attended a seminar presented by a visiting researcher on some aspect of the inflammatory cascade. It was very technical and focused around the interaction of a certain ligand with its receptor at some critical juncture in whatever process they had devoted the last n years of their life to studying.
The ligand was all-cis-docosa-4,7,10,13,16,19-hexa-enoic acid. No one in the room had any idea what this stuff was, certainly not the extremely intelligent presenter, other than as a molecular key to a molecular lock. It's a stock lab reagent purchased in research grade purity from any one of a number of suppliers. You could equally order cervonic acid.
At the level of reductionism these people can work at there is no need to be aware that all-cis-docosa-4,7,10,13,16,19-hexa-enoic acid is available in gel caps from Holland and Barrett or is present in the nearest can of sardines as the more familiar DHA.
So imagine you are some newbie PhD student. You walk in to the lab and are handed a reading list a mile long. The lab has certain research lines you are going to slot in to, particularly focused around inflammasome activation by fatty acids. You got the post because you had picked up extensive experience with cell culture and inflammation research based around both endotoxin and asbestos, plus a track record of multiple Nature publications from your undergraduate work.
The lab you walk in to has cells in culture which go ballistic on exposure to utterly physiological concentrations of palmitic acid. At least six widely differing cell types behave in exactly the same way. This looks like a generic effect and puts palmitic acid up there with asbestos as a proinflammatory agent. You switch to Flora that very lunch time, and spread it thinly too.
The lab also has an animal house in the basement. The rats are either fed a standard lab chow or a red coloured greasy type of pellet oozing fat. The lab techs feed and water the ratties. Your job is to compare molecular aspects of white blood cell inflammasome activation as the high fat rats get fatter over the weeks. Once a fortnight someone brings you a blood sample to work with but, apart from that, you will never see the rats again...
What do you question? EVERYONE knows that eating fat makes you fat. Fat is fat. Do you give a monkey's about EXACTLY what is in the pellets which stain the tech's hands red when they do the feeding? It's a standard obesogenic high fat diet from www.testdiets.com. All obesity research uses it or something similar...
Would you sit down and work out whether the hydrogen atoms on either side of the central double bond of one type of fatty acid in one constituent of the 5TJN are aligned on the same side or on opposite sides of the bond? You know, cis vs trans configuration...
It's sloppy. It's possible. People will really be able stand up and say, as Ting does:
"The simple message is to avoid fatty foods as much as possible."
They probably have no doubts. They believe. It's complete bollocks of course. But I have this concept of how things work...
Peter
The ligand was all-cis-docosa-4,7,10,13,16,19-hexa-enoic acid. No one in the room had any idea what this stuff was, certainly not the extremely intelligent presenter, other than as a molecular key to a molecular lock. It's a stock lab reagent purchased in research grade purity from any one of a number of suppliers. You could equally order cervonic acid.
At the level of reductionism these people can work at there is no need to be aware that all-cis-docosa-4,7,10,13,16,19-hexa-enoic acid is available in gel caps from Holland and Barrett or is present in the nearest can of sardines as the more familiar DHA.
So imagine you are some newbie PhD student. You walk in to the lab and are handed a reading list a mile long. The lab has certain research lines you are going to slot in to, particularly focused around inflammasome activation by fatty acids. You got the post because you had picked up extensive experience with cell culture and inflammation research based around both endotoxin and asbestos, plus a track record of multiple Nature publications from your undergraduate work.
The lab you walk in to has cells in culture which go ballistic on exposure to utterly physiological concentrations of palmitic acid. At least six widely differing cell types behave in exactly the same way. This looks like a generic effect and puts palmitic acid up there with asbestos as a proinflammatory agent. You switch to Flora that very lunch time, and spread it thinly too.
The lab also has an animal house in the basement. The rats are either fed a standard lab chow or a red coloured greasy type of pellet oozing fat. The lab techs feed and water the ratties. Your job is to compare molecular aspects of white blood cell inflammasome activation as the high fat rats get fatter over the weeks. Once a fortnight someone brings you a blood sample to work with but, apart from that, you will never see the rats again...
What do you question? EVERYONE knows that eating fat makes you fat. Fat is fat. Do you give a monkey's about EXACTLY what is in the pellets which stain the tech's hands red when they do the feeding? It's a standard obesogenic high fat diet from www.testdiets.com. All obesity research uses it or something similar...
Would you sit down and work out whether the hydrogen atoms on either side of the central double bond of one type of fatty acid in one constituent of the 5TJN are aligned on the same side or on opposite sides of the bond? You know, cis vs trans configuration...
It's sloppy. It's possible. People will really be able stand up and say, as Ting does:
"The simple message is to avoid fatty foods as much as possible."
They probably have no doubts. They believe. It's complete bollocks of course. But I have this concept of how things work...
Peter
Monday, August 1, 2011
Gary Taubes Interview on Underground Wellness
Excellent interview with Gary Taubes, author of Good Calories, Bad Calories. Originally broadcasted by Underground Wellness Radio.
Yesterdayday was first meat day
Edit: Today was fillet steak, OK so long as the piece is big enough to be sucked on without getting it all in her mouth at once...
Apparently babies are revolted by meat, just ask any vegan idiot
Peter
Apparently babies are revolted by meat, just ask any vegan idiot
Peter
Sunday, July 31, 2011
Now THAT is sustainable!
Amazing speech by Dan Barber, How I fell in Love with a Fish.
Barber speaks of a fish farm off the coast of Spain:
Barber speaks of a fish farm off the coast of Spain:
- Which does not feed their fish
- The fish feeds a population of 600 000 birds
- The farm acts as a huge water purifier
Nature is fantastic
Another speech by renowned chef Dan Barber. This time about foie gras, fat liver from duck or goose, which is considered to be an exquisite delicacy. The controversy of foie gras is gavage, or force feeding the animal. However, Barber's speech show that, if we cooperate with nature instead of try to overcome it, nature rewards us.
-Why don't you sell the foie gras to world class chefs?Great and inspirational stuff.
-They don't deserve my foie gras.
-What do you think of conventional foie gras?
-An insult to history.
Diabetic nephropathy and the lost Swede
Chris over at Conditioning Research forwarded me the link to the PLoS paper demonstrating partial reversal of diabetic nephropathy in a couple of mouse models. This isn't exactly a world shattering finding as anyone with diabetes who is not eating a mildly ketogenic diet probably has shares in dialysis machines or is being grossly mismanaged.
Anyway, the first thing to do with a paper like this is to check whether the authors cited Nielsen's 2006 case report of a human being having their diabetic renal failure halted and partially reversed. I mean, this might be relevant...
They didn't.
The Swedish group simply fixed a patient without a mouse model in sight. They got ignored for their temerity. Shocking to fix a human without the death of a single leptin deficient mouse, but there you go. And it's not so hard to do either............
As a complete aside:
It turned out to be interesting to go back and see where the mouse folks were coming from. They cited this paper.
Here is part of figure 6, the line to follow is the open triangles.
Up to day 84 a high fat diet was fed. As happens so often, the high fat diet is 31.7% sucrose/maltodextrin by weight and (gasp) 20.7% lard.
From day 84 onwards these lazy, greedy porkers of mice were switched to a diet which was 47.5% lard and, utter horror, 19.95% butter. Of course this is not really a high fat diet as it has no sucrose or maltodextrin...
Look at the weight drop to below (ns) that of the mice fed crapinabag throughout........
Obviously this must be the satiating effect of protein, so often cited by idiots as the reason for weight loss of LC diets. Except it's not, the ketogenic mice had the lowest protein intake, 9.5% by weight cf 24% in the crapinabag and HF diets. That is very low in protein.
Here are the actual diets in Table 1:
A far more plausible explanation is that ketosis induces dissatisfaction in these mice concerning their body image due to their obese state so they then started to cut calories and go to the gym every night. Duh.
Now please don't make me put up the fasting insulin levels. Aw, okay, you twisted my arm.
Edit: I noticed that these are the FED insulin levels, we don't get fasting levels in the paper...
No comment.
Peter
Anyway, the first thing to do with a paper like this is to check whether the authors cited Nielsen's 2006 case report of a human being having their diabetic renal failure halted and partially reversed. I mean, this might be relevant...
They didn't.
The Swedish group simply fixed a patient without a mouse model in sight. They got ignored for their temerity. Shocking to fix a human without the death of a single leptin deficient mouse, but there you go. And it's not so hard to do either............
As a complete aside:
It turned out to be interesting to go back and see where the mouse folks were coming from. They cited this paper.
Here is part of figure 6, the line to follow is the open triangles.
Up to day 84 a high fat diet was fed. As happens so often, the high fat diet is 31.7% sucrose/maltodextrin by weight and (gasp) 20.7% lard.
From day 84 onwards these lazy, greedy porkers of mice were switched to a diet which was 47.5% lard and, utter horror, 19.95% butter. Of course this is not really a high fat diet as it has no sucrose or maltodextrin...
Look at the weight drop to below (ns) that of the mice fed crapinabag throughout........
Obviously this must be the satiating effect of protein, so often cited by idiots as the reason for weight loss of LC diets. Except it's not, the ketogenic mice had the lowest protein intake, 9.5% by weight cf 24% in the crapinabag and HF diets. That is very low in protein.
Here are the actual diets in Table 1:
A far more plausible explanation is that ketosis induces dissatisfaction in these mice concerning their body image due to their obese state so they then started to cut calories and go to the gym every night. Duh.
Now please don't make me put up the fasting insulin levels. Aw, okay, you twisted my arm.
Edit: I noticed that these are the FED insulin levels, we don't get fasting levels in the paper...
No comment.
Peter
Women from a Male Perspective
I have a friend. Her name is Helene. She has four children and she is single. Two of them are now adults, and two around ten or so. Helene has been one of my heroes for a long time. Being a single mother of four is something almost unimaginable for a man. To succeed in bringing up four children alone is an admirable feat. Her children are great. Some parents can't even manage one child. And they are twice as many.
I know another mother. Her name is Heather. She has three children. Her life has been hell to say the least. But her children are fine and she has struggled like an beast to make ends meet and to raise her children well. She is another of my heroes.
I listened to a radio show a while ago. Four mothers were talking. One said:
"The mother is always the dumpster. She always stays. The children know a mother never abandons. Fathers are away so much the children are grateful for what little they get from him. The father must not be pressured, questioned or intimidated. If he is, he might leave for goodThen maybe he abandons the kids forever. The mother's reward for her loyalty, kindness and love is - she gets to be the garbage can. "We live in a so-called equal country. An equal country where women still face discrimination daily. Equal pay for equal work is probably not even worth mentioning. Nor that typical "female professions" are lower paid than typical "male professions".
When you go shopping together, it does not matter if it's the woman who starts off the negotiations with the salesman. The salesman sooner or later turns to the man to conclude the sale. I have personally experienced this multiple times and every time I shake my head: Don't look at me, talk to her.
Women give birth. They have their period. When they give birth, they get stretch marks. They go through menopause. Men shave. Poor men.
In the United States, a single mother over thirty is as attractive on the relation market, as that moldy thing in the back of the fridge you know you should throw away, but you think is too disgusting to touch, so you wait a little longer to toss it.
On the coast of West Africa, there is an indigenous tribe ruled by women. Their language has no word for war. That says everything needing to be said about women. And men.
Men are not really worthy of women's love. Men rape, murder and pillage. Women love, educate and nurture.
Women deserve all our respect. I love women. Because they exist and because they tolerate us men. Thank you.
Interview with an ex-vegan
I discovered I was deficient in a multitude of different nutrients that are readily available in animal products. (b12, zinc, iron, magnesium, vit D, Retinol Vit A). I also found out I had hypothyroidism, and when I did some research I found the link between raw cruciferous vegetables and soy blocking thyroid function. Protein and pre-formed Vitamin A from animal products are critical for thyroid health. When you have a slow thyroid you cannot convert beta carotene into Retinol Vitamin A, the form you need for healthy thyroid function.Entire interview.
Oh, and one more thing: Why do vegans eat fake meat? You don't see carnivores eat fake vegetables. Honest question.
Making ends meet
Not the kind of foods I would recommend, but still an amazing mother. She feeds a family of 6 with 4 dollars a week.
Please stop GMO in Europe
We say no to Monsanto, and change our mind 12 years later?
New York Times: E.U. Approves First Modified Crop for Planting in 12 Years
***
Monsanto's GMO Corn Linked To Organ Failure, Study Reveals
A Comparison of the Effects of Three GM Corn Varieties on Mammalian Health
***
Please sign the petition to STOP GMO in Europe once and for all.
GM Food: get the facts first
The EC has just allowed GM crops into Europe, ignoring the concerns of the public. I've signed a petition for independent research and a moratorium on GM crop development. With 1 million citizens' signatures, we can make an official legal request to the European Commission. Sign below and let's get to 1 million:
http://www.avaaz.org/en/eu_health_and_biodiversity/98.php?CLICK_TF_TRACK
Thanks!
------
Dear friends,
The European Commission has just approved growing genetically modified crops in the European Union for the first time in 12 years!
Caving to the GM lobby, the commission has ignored 60% of Europeans who feel we have to get the facts first before growing foods that could pose a threat to our health and environment.
A new initiative allows 1 million EU citizens to make official legal requests of the European Commission. Let's build a million voices for a ban on GM foods until the research is done; they will be delivered to the President Barroso of the European Commission. Sign the petition and forward this email to friends and family:
http://www.avaaz.org/en/eu_health_and_biodiversity/98.php?CLICK_TF_TRACK
Consumers, public health, environmental and farmers groups have long rallied against a few international GM companies having such significant influence over European agriculture. Concerns about growing GM crops include: contamination of organic crops and the environment; their impact on climate due to the excessive need for pesticides; the destruction of biodiversity and local agriculture; and the effects of GM food on public health.
EU member states have voiced strong opposition to last week's decision to authorise BASF's potato and Monsanto's maize -- Italy and Austria are opposed, and France said it would ask for further scientific research.
There is still no consensus on the long-term effects of GM crops. And it is the GM industry, pursuing profits not public well being, that is funding the science and driving the regulatory environment. That is why European citizens are calling for more independent research, testing and precaution before crops are unleashed onto our land.
Now, the "European Citizens' Initiative" gives 1 million EU citizens the opportunity to submit policy proposals to the European Commission and offers us a unique chance to drown out lobbyists' influence.
Let's raise 1 million voices to put a moratorium on the introduction of GM crops into Europe and set up an independent, ethical and scientific body to research and determine the strong regulation of GM crops. Sign the petition now and then forward it widely:
http://www.avaaz.org/en/eu_health_and_biodiversity/98.php?CLICK_TF_TRACK
With determination,
Alice, Benjamin, Ricken, Luis, Graziela and the entire Avaaz team.
More information:
Last Eurobameter Survey 2008 'Attitudes of European citizens towards the environment', page 66:
http://bit.ly/aMkeVJ
The Independent, Fury as Brussels authorises GM potatoes:
http://www.independent.co.uk/environment/green-living/fury-as-eu-approves-gm-potato-1915833.html
Reuters, France blasts GM crop approvals by EU agency:
http://uk.reuters.com/article/idUKTRE6241ZQ20100305
New Report: GMOs Causing Massive Pesticide Pollution:
http://www.huffingtonpost.com/andrew-kimbrell/new-report-gmos-causing-m_b_362888.html
Summary of the International Assessment on Agricultural Science and Technology for Development, including critics of GMOs use in agriculture:
http://globalpolicy.org/social-and-economic-policy/international-trade-and-development-1-57/genetically-modified-organisms.html#key
Please sign petition here: http://bit.ly/c55DIq
Signed when posting this: 269,356
Update 2010 March 25th: Total signatures 300,925
Update 2010 March 26th: Total signatures 315,553
Update 2010 March 30th: Total signatures 342,852
Help us get to 1,000,000
New York Times: E.U. Approves First Modified Crop for Planting in 12 Years
The European Union today approved the first new genetically modified (GM) crop for domestic growing in more than a decade, ending what has been a long stalemate over a backlog of GM crops awaiting cultivation approval.
The decision by the European Commission, the E.U.'s executive arm, will allow farmers to grow Amflora potatoes, a controversial GM crop developed by the German chemical giant BASF. The potatoes can be used solely for industrial or animal feed purposes, the bloc said.
The potatoes, engineered to produce high levels of starch for use in paper production or textiles, are the first crop to be approved for farming since a strain of Monsanto's insect-resistant corn 12 years ago. That decision set off a storm of protest from European countries, some of which, like Austria and Germany, have invoked science-based protection clauses to prevent the corn's growth (Greenwire, Oct. 21, 2009).http://nyti.ms/9RXvxG
***
Monsanto's GMO Corn Linked To Organ Failure, Study Reveals
In a study released by the International Journal of Biological Sciences, analyzing the effects of genetically modified foods on mammalian health, researchers found that agricultural giant Monsanto's GM corn is linked to organ damage in rats.http://huff.to/bYojbQ
A Comparison of the Effects of Three GM Corn Varieties on Mammalian Health
Effects were mostly concentrated in kidney and liver function, the two major diet detoxification organs, but in detail differed with each GM type. In addition, some effects on heart, adrenal, spleen and blood cells were also frequently noted. As there normally exists sex differences in liver and kidney metabolism, the highly statistically significant disturbances in the function of these organs, seen between male and female rats, cannot be dismissed as biologically insignificant as has been proposed by others [4]. We therefore conclude that our data strongly suggests that these GM maize varieties induce a state of hepatorenal toxicity.http://bit.ly/cZeQ94
***
Please sign the petition to STOP GMO in Europe once and for all.
GM Food: get the facts first
The EC has just allowed GM crops into Europe, ignoring the concerns of the public. I've signed a petition for independent research and a moratorium on GM crop development. With 1 million citizens' signatures, we can make an official legal request to the European Commission. Sign below and let's get to 1 million:
http://www.avaaz.org/en/eu_health_and_biodiversity/98.php?CLICK_TF_TRACK
Thanks!
------
Dear friends,
The European Commission has just approved growing genetically modified crops in the European Union for the first time in 12 years!
Caving to the GM lobby, the commission has ignored 60% of Europeans who feel we have to get the facts first before growing foods that could pose a threat to our health and environment.
A new initiative allows 1 million EU citizens to make official legal requests of the European Commission. Let's build a million voices for a ban on GM foods until the research is done; they will be delivered to the President Barroso of the European Commission. Sign the petition and forward this email to friends and family:
http://www.avaaz.org/en/eu_health_and_biodiversity/98.php?CLICK_TF_TRACK
Consumers, public health, environmental and farmers groups have long rallied against a few international GM companies having such significant influence over European agriculture. Concerns about growing GM crops include: contamination of organic crops and the environment; their impact on climate due to the excessive need for pesticides; the destruction of biodiversity and local agriculture; and the effects of GM food on public health.
EU member states have voiced strong opposition to last week's decision to authorise BASF's potato and Monsanto's maize -- Italy and Austria are opposed, and France said it would ask for further scientific research.
There is still no consensus on the long-term effects of GM crops. And it is the GM industry, pursuing profits not public well being, that is funding the science and driving the regulatory environment. That is why European citizens are calling for more independent research, testing and precaution before crops are unleashed onto our land.
Now, the "European Citizens' Initiative" gives 1 million EU citizens the opportunity to submit policy proposals to the European Commission and offers us a unique chance to drown out lobbyists' influence.
Let's raise 1 million voices to put a moratorium on the introduction of GM crops into Europe and set up an independent, ethical and scientific body to research and determine the strong regulation of GM crops. Sign the petition now and then forward it widely:
http://www.avaaz.org/en/eu_health_and_biodiversity/98.php?CLICK_TF_TRACK
With determination,
Alice, Benjamin, Ricken, Luis, Graziela and the entire Avaaz team.
More information:
Last Eurobameter Survey 2008 'Attitudes of European citizens towards the environment', page 66:
http://bit.ly/aMkeVJ
The Independent, Fury as Brussels authorises GM potatoes:
http://www.independent.co.uk/environment/green-living/fury-as-eu-approves-gm-potato-1915833.html
Reuters, France blasts GM crop approvals by EU agency:
http://uk.reuters.com/article/idUKTRE6241ZQ20100305
New Report: GMOs Causing Massive Pesticide Pollution:
http://www.huffingtonpost.com/andrew-kimbrell/new-report-gmos-causing-m_b_362888.html
Summary of the International Assessment on Agricultural Science and Technology for Development, including critics of GMOs use in agriculture:
http://globalpolicy.org/social-and-economic-policy/international-trade-and-development-1-57/genetically-modified-organisms.html#key
--------------If there ever was a time when you could make a difference, this is it.
Please sign petition here: http://bit.ly/c55DIq
Signed when posting this: 269,356
Update 2010 March 25th: Total signatures 300,925
Update 2010 March 26th: Total signatures 315,553
Update 2010 March 30th: Total signatures 342,852
Help us get to 1,000,000
Prostate cancer paradox
Many observational studies associate prostate cancer with markers of metabolic syndrome. Which gives us the omega3/trans fat paradox, well discussed in several places around the net.
Here's a similar prostate paradox.
How come these two exceptions buck the trend? Here's a random thought:
Let's assume prostate cancer is related to chronic hyperinsulinaemia, a reasonable idea, ie it is "metabolic syndrome of the prostate".
Conversely, castration is a component of conventional prostate cancer treatment.
Getting to the chemical-castration stage of metabolic syndrome might well be prostate cancer protective.
Omega 3 fats probably slow progression of metabolic syndrome, trans fats probably accelerate it.
If you want to get to the castration level of metabolic syndrome as fast as possible, to maximise this prostate benefit, never forget to ask for your favourite lipotoxin by name.
For metabolic castration you should always ask for Crisco.
Peter
Alternatively I have a couple of bricks available. It's an old anaesthetist's joke:
Surgeon: "I don't need to use anaesthesia for castration."
Anaesthetist: "Really, what's your technique?"
Surgeon: "I have these two bricks and I smash them together on the testicles."
Anaesthetist (aghast): "Doesn't that hurt?"
Surgeon: "Only if you get your thumbs in the way."
Here's a similar prostate paradox.
How come these two exceptions buck the trend? Here's a random thought:
Let's assume prostate cancer is related to chronic hyperinsulinaemia, a reasonable idea, ie it is "metabolic syndrome of the prostate".
Conversely, castration is a component of conventional prostate cancer treatment.
Getting to the chemical-castration stage of metabolic syndrome might well be prostate cancer protective.
Omega 3 fats probably slow progression of metabolic syndrome, trans fats probably accelerate it.
If you want to get to the castration level of metabolic syndrome as fast as possible, to maximise this prostate benefit, never forget to ask for your favourite lipotoxin by name.
For metabolic castration you should always ask for Crisco.
Peter
Alternatively I have a couple of bricks available. It's an old anaesthetist's joke:
Surgeon: "I don't need to use anaesthesia for castration."
Anaesthetist: "Really, what's your technique?"
Surgeon: "I have these two bricks and I smash them together on the testicles."
Anaesthetist (aghast): "Doesn't that hurt?"
Surgeon: "Only if you get your thumbs in the way."
Proven: Vitamin D Prevents the Flu -- Throw Out Your Tamiflu
"Well, technically we only "prove" things in math and logic, when we assume our premises. But the most recent study on vitamin D and the flu, published in the American Journal of Clinical Nutrition, gets as close to proving anything as we can get in nutritional and medical science."
The Daily Lipid: http://bit.ly/autPy3
A novel idea
Here is a novel idea for all foodies out there. There is veganism, vegetarianism, fruiterianism, low carb, paleo, Atkins, Ornish, South Beach, Zone, LEARN, Mediterranean and God knows what. Despite having different ideas on what to eat and how to eat it, we all have one thing in common:
Food lovers, also known as humans, are under attack. You might not know it, but we are. The common foe is Genetically Modified Organisms (GMO).
The effects of GMO are devastating.
We all care about what we put in our body.
We all want to eat fresh, natural, high quality food.
When a nation is attacked by a common foe, the people of that nation join ranks to survive. Survival of the whole becomes more important than the individual beliefs.Food lovers, also known as humans, are under attack. You might not know it, but we are. The common foe is Genetically Modified Organisms (GMO).
The effects of GMO are devastating.
- Brazil are deforesting Earth's lungs; the rain forest, to plant GMO soy.
- Monsanto, the worlds biggest biotech company, owns around 90% of all the soybean seeds in the USA, their goal being monopoly. All of that seed is Roundup resistant, a toxic pesticide, which kills everything living when applied. Roundup is a Monsanto product.
- They also own the larger part of the US corn production.
- In India Monsanto's products and business methods have led to thousands of Indian farmers committing suicide.
- There are studies showing kidney and liver failure in rat populations fed Monsanto's GMO corn. In experiments animals are fed large quantities of the corn. So the effects are visible much faster than among humans. Does the Monsanto corn have the same effect on humans? We don't know. Yet the same governments put in office by the people, approve these products for human consumption. Despite not knowing the effects.
- Monsanto has offices in the following countries: Argentina, Australia, Austria, Bangladesh, Belgium, Brazil, Bulgaria, Canada, Chile, China, Colombia, Croatia, Czech , Denmark, Ecuador, France, Germany, Greece, Guatemala, Honduras, Hungary, India, Indonesia, Ireland, Italy, Japan, Jordan, Kenya, Korea, Malawi, Malaysia, Mexico, Netherlands, New Zealand,, Pakistan, Paraguay, Peru, Philippines, Poland, Portugal, Romania, Russian Federation, Singapore, Slovakia, South , Spain, Sri Lanka, Switzerland, Taiwan, Thailand, Turkey, Uganda, Ukraine, United , United , Venezuela, Vietnam and Zimbabwe. So far...
- BASF is the European equivalent of Monsanto. The recently had their GMO potato Amflora approved for production in the EC. The potato is not to be used for food production nor fodder, but it is a starting point for giants like Monsanto and BASF to gain acceptance for their products.
- BASF writes the following on their website: "Seed treatment is a business area with growth potential: Genetically modified crops are playing an increasingly important role worldwide."
- When a company like BASF or Monsanto develop a GMO they patent the product. If i.e. a Monsanto soybean spreads, intentionally or unintentionally, to a neighboring farmer, Monsanto can sue the farmer for patent infringement.
- Farmers buying Monsanto product are not allowed to save seed for next years production. They have to buy new seed. If they save seed they can be sued for breach of contract. In effect the farmers are made dependent on Monsanto's product.
- Monsanto's latest venture is to patent pigs.
- Their agenda? Control food, control everything.
Is this a common enemy, food lovers can join ranks against? You tell me.
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