tag:blogger.com,1999:blog-87961278759155587292024-02-20T19:26:00.507-08:00trialblogThis is just a place to store text and pictures I don't want in Hyperlipid but need to be able to link to reliably. News reports tend to be unstable...Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comBlogger26125tag:blogger.com,1999:blog-8796127875915558729.post-53771256643096941082023-12-18T22:39:00.000-08:002023-12-18T22:39:47.339-08:00<p></p><div class="separator" style="clear: both; text-align: center;"><iframe allowfullscreen='allowfullscreen' webkitallowfullscreen='webkitallowfullscreen' mozallowfullscreen='mozallowfullscreen' width='320' height='266' src='https://www.blogger.com/video.g?token=AD6v5dx99xMSKhlMWIAoxrkuGsz3LXo3vnhCMQt7p-JHe0Em8JQ0DePKNiHUfatvvd5fQ5fMznULMKpwR0Uj0zb67w' class='b-hbp-video b-uploaded' frameborder='0'></iframe></div><br /> <p></p>Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-87937650468784851902014-01-21T14:11:00.000-08:002014-01-21T14:16:15.569-08:00<br />
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<a href="http://www.ncbi.nlm.nih.gov/pubmed/24336921" target="_blank">TEXT</a>Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-28044339970940557192013-09-06T12:18:00.000-07:002013-09-06T12:18:11.647-07:00Let's just summarise the role of omega 6 fats in Sauer's <a href="http://www.ncbi.nlm.nih.gov/pubmed/11016660" target="_blank">rat model</a> of cancer:<br />
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In the lab situation rapid hepatoma tumour growth needs either arachidonic or linoleic acids. The acids must be taken up in to the hepatoma cells, they must be acted on by lipoxygenase to produce 13-hydroxyoctadecadienoic acid, better known as 13-HODE. 13-HODE appears to be the mitogen which promotes rapid cancer growth. 13-HODE looks like a repair signal gone wrong in cancer cells. Omega 3 fatty acids block omega 6 fatty acid uptake in to hepatoma cells. That's all well and good but the reason I got in to this paper was omega 3 PUFA signalling, rather than those omega 6 issues...<br />
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OK, Sauer starts to give some pointers on the function of omega 3 fatty acids in health. That's interesting, as I'm no great lover of any sort of PUFA when I view them from the Protons perspective, yet omega 3s seem to come out pretty well, certainly at low doses. You know my fall back, omega 3 PUFA don't always behave like omega 6 PUFA because they get used as signalling molecules blah blah blah. My own inability to tie the molecular structure of omega 3s to their clinical effects is very frustrating! That they probably act are sites "above" the ETC suggest that they act as what I view as 'high level signals".<br />
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Well they do.<br />
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The signalling appears to be through a G-protein linked receptor with all of the usual cAMP cascade that follows binding of a ligand to such a receptor. What I found particularly interesting was the effect produced on fat pads of normal rats when EPA (other papers from Sauer suggest all omega 3s act on whichever receptor is involved) was added to the perfusate.<br />
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OK, here is a neat little graph taken from <a href="http://cancerres.aacrjournals.org/content/60/18/5289/F5.expansion.html" target="_blank">here</a>:<br />
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This is from fed rats. In the fed state the FFA uptake by the inguinal fat pad of a rat is about 6 mcg/min/gram, white open squares.<br />
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Adding EPA at 0.84mmol/l (a bit supraphysiological for EPA but let's let that ride) and FFA uptake by the fat pad drops to zero, or close to zero. Or, in fact, you could argue a suggestion of fatty acid relase, shown as a negative uptake value. Black circles. Fatty acids are not taken up, they end up in the venous effluent in the experiment, plus a little extra.<br />
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Whooooah, so do FFAs go through the roof when you take fish oil IRL??<br />
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Well no. That's because of this graph from <a href="http://cancerres.aacrjournals.org/content/60/18/5289/F4.expansion.html" target="_blank">here</a> in the same paper:<br />
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Here we have the free fatty acid release from the inguinal fat pad of a healthy rat who has been starved for 48 hours. Fatty acid release is trundling along at about 3mcg/min/gram until EPA is added, again at around 0.8mmol/l. The release of FFAs, in the fasted state, is eliminated. Table 1 in the same paper shows you can get this effect of halting lipolysis in starved rats with under 0.3mmol/l EPA.<br />
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Both effects are mediated through a G-protein coupled receptor, ie high level signalling compared to electrons and superoxide in the electron transport chain.<br />
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Obviously there are a number of serious problems with this paper but, as a proof of concept, I buy it. I doubt DHA or alpha linolenic acid would work as well (or the group would have used them for this proof of point exercise!) and I think the levels of EPA used produce a very artefactual "switch-like" effect which is probably a graded response. I doubt 0.8mmol/l or even 0.3mmol/l of EPA is exactly physiological but...<br />
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Let's suggest that there is a progressive removal of the influence of adipocytes from the FFA flux in/out of plasma as the level of omega 3s in arterial blood increases. Omega 3 fatty acids render adipocytes irrelevant to free fatty acid levels in the plasma.<br />
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That is one hell of an idea.<br />
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Next we need a brief look at hepatoma cells, again the graph is provided by Sauer and it shows that omega 3 fatty acids, in a G-protein coupled receptor manner, completely turn off the uptake of ALL fatty acids in to hepatoma cells.<br />
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If, and it's quite a big "if", the same effects apply to hepatocytes as well as hepatoma cells, we then have a very straightforward mechanism for the protective effects of omega 3 fish oils on hepatic lipidosis. From my point of view this is quite real as there are pretty convincing papers showing that cats, in real life, can be largely protected against the potentially fatal hepatic lipidosis of rapid weight loss by modest doses of omega 3 fatty acids.<br />
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Soooo while omega 3s stop the release of all FFAs from adipocytes, they simultaneously stop the uptake of all fatty acids in to the two primary storage organs for fatty acids, adipocytes and liver.<br />
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Do plasma FFAs go up or down?<br />
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They do, of course, go down. A paradox? <a href="http://www.ncbi.nlm.nih.gov/pubmed/22041134" target="_blank">Next paper</a>.<br />
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Health warning: This paper is so steeped in VLDL and ApoB lipophobia that it makes difficult reading. But there is so little published on FFAs and omega 3 supplementation that it's worth the ondansetron to read it. It's looking at how omega 3 supplements might lower fasting triglycerides, which are the devil incarnate for CVD risk. A huge chunk of VLDL comes from FFAs released from adipocytes and their subsequent repackaging by the liver. Apparently, and I quote from the abstract:<br />
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"FO [fish oil] counteracts intracellular lipolysis in adipocytes by suppressing adipose tissue inflammation"<br />
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A bit like insulin resistance is caused by "inflammation". Well, maybe it's that simple. They have taken the concept of high level signalling to its 2013 pedestal without looking for basic mechanisms. They have placed the G-protein coupled receptor on to macrophages in the fat pads, which subsequently control the adipocyte lipolysis using cytokines. I haven't checked how good this concept is. Sauer never looked that deeply. Looks a bit modern to me. <br />
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Personally I would guess that there are similar receptors on both adipocytes and hepatocytes, but the review does not seem to cover the ability of omega 3s to inhibit general fatty acid uptake by these two tissues. Ah well.<br />
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What they do argue is that omega 3 fatty acids upregulate lipoprotein lipase, pretty well whole body. Of course liver and adipocytes ignore this fatty acid bonanza, as above. LPL upregulation is what I needed to know from this paper.<br />
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So where do "spare" fatty acids go to? They go to muscles. Upregulated lipoprotein lipase (heralded as the saviour from elevated fasting triglycerides) allows increased lipid release from VLDL to lower those fasting triglycerides. But it's worth bearing in mind that cells do not "see" VLDL, the LPL is on the vascular endothelium and the cells behind the vessel wall only ever receive "free" fatty acids. These are not labelled as from albumin, VLDL or chylomicrons.<br />
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Slight aside for later: It seems likely that chylomicrons are going spill their lipids via that same LPL, worth remembering.<br />
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The story in the review can be sumarised as omega 3 fatty acids block the release of FFAs from adipocytes and increase the activity of lipoprotein lipase pretty well whole body. VLDL drops, FFAs drop. All is happy in the cardiovascular system. If you believe.<br />
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Various "bits" of omega 3s, especially the lipid peroxides of DHA, are signals for mitochondrial biogenesis. I had a paper which specified which lipoxide was most effective but must have missed the "save" button. Mea culpa yet again. There are hints <a href="http://www.ncbi.nlm.nih.gov/pubmed/16205884" target="_blank">here</a>.<br />
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That's a very neat story, which has more than a grain of truth to it.<br />
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Why is it like this? What does it mean, physiologcally? Speculation time:<br />
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Omega 3 fats come from plants. Mostly from chloroplasts. Where do humans get their omega 3s from? Certainly not from plants. If we did then the rabid Dr Furhman would not be (correctly) recommending DHA supplementation (along with B12) to avoid brain collapse on veg*n diets. Actually, <a href="http://www.ncbi.nlm.nih.gov/pubmed/19500961" target="_blank">this link</a> is quite funny when cited by Mc-Starch-Dougall:<br />
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"There is no evidence of adverse effects on health or cognitive function with lower DHA intake in vegetarians"<br />
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Well, I found it amusing. It's almost the converse of the neurological truism which states that being concerned about having a neurodegenerative disease probably means you don't actually have one.<br />
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Anyhoo. Away from the coast we have to get our DHA from animals (or buy algae derived supplements). They get it from grass. There is DHA present in adipose tissue of herbivores just as much as it is present in lipid membranes of their cells. My suspicion is that DHA is a signal to your metabolism that you have just eaten animal fat, from an animal who's food chain starts with grass [or algae]. The more fat you eat, the stronger the signal. We do not need much DHA overall for our brains as it is well protected in this site, but we might well be using it at low levels as a [G-protein coupled receptor sensed] signal to target metabolic adaptation to process fat. So is McDougall correct that veg*n "brain" tissue is OK, despite their periphery being depleted? Shrug.<br />
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Fish oil supplements? Well, using our "dietary fat is here" marker to pharmacologically modify some perceived CVD risk factor, without the appropriate change in source of metabolic fuel supply, looks to me to be of very limited value. Large intervention trials do show some benefit from omega 3s provided you do your stats well enough, you have a large enough population to pick up a very small effect and you give a high enough dose. But they do not seem to be any sort of panacea. Especially of you are avoiding dietary fat while "faking" the signal that you have eaten dietary fat...<br />
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This is not exactly surprising when you try to pick the likely physiology apart. I like the concept of DHA as an animal fat signal.<br />
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Peter<br />
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Final thought: Do we need omega 3 PUFA at anything above the most minimal levels if we are in saturated fat based ketosis? Of course I don't know. But the signal to cope with starvation is palmitic acid (physiological insulin resistance), not DHA. I live in starvation mode, not on a mixed diet with only intermittent access to healthy ruminant fat. I have long wanted to look at the selective release of FFAs from adipocytes in extended starvation. My suspicion is that in the early days after glycogen depletion palmitic acid is preferentially released over other lipids, PUFA are not needed/wanted. By a few weeks all the palmitate is gone and whatever is left then gets released. People like David Blaine suddenly start to feel weak, wobbly and are probably hypoglycaemic once they run out of palmitate and have to release less saturated fats. Two to four weeks if you carry some spare weight. Sauer's rats had only ever been fed a low fat omega 6 based diet and had no serious palmitate reserves, PUFA release came early for these.Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-29894342864389024592013-03-20T13:10:00.002-07:002013-03-20T13:10:38.669-07:00Let them eat fat: Ron RosenbaumTHE SATURDAY ESSAY March 15, 2013, 9:05 p.m. ET<br />
<br />Let Them Eat Fat<br />
<br />Listening to the doctors on cable TV, you might think that it's better to cook up a batch of meth than to cook with butter. But eating basic, earthy, fatty foods isn't just a supreme experience of the senses—it can actually be good for you.<br />
<br />By RON ROSENBAUM<br />
<br />The hysterical crusade against fat has become a veritable witch hunt. With New York City Mayor Michael Bloomberg's ban on supersize sodas (now temporarily thwarted) and the first lady's campaign to push leaves and twigs (i.e., salad) on reluctant school children—all in the name of stamping out obesity—it is fat-shaming time in America. Yes, there are countertrends, like the pro-fat TV shows of Paula Deen and Guy Fieri. But in the culture at large, eating that kind of fat has become a class-based badge of shame: redneck food (which I say as someone who likes rednecks and redneck food). It isn't food for someone who drives a Prius to Pilates class.<br />
<br />But there's another world of fatty foods, a world beyond bacon and barbecue—not the froufrou fatty foods of foodies either, but basic, earthy, luxuriant fatty foods like roast goose, split-shank beef marrow and clotted cream. In the escalating culture war over fat, which has clothed itself in sanctity as an obesity-prevention crusade, most of these foods have somehow been left out. This makes it too easy to conflate eating fatty food with eating industrial, oil-fried junk food or even with being or becoming a fat person.<br />
<br />Preventing obesity is a laudable goal, but it has become the rationale for indiscriminate fat hunters. It can shade into a kind of bullying of the overweight, a badgering of anyone who likes butter or heavy cream. To the antifat crusaders, I say: Attack fatty junk food all you want. I'm with you. But you can deny me my roasted marrow bones when you pry them from my cold, dead hands.<br />
<br />I'm not suggesting that we embrace these life-changing food experiences just on grounds of pure pleasure (though there's much to be said for pure pleasure). As it turns out, the science on the matter is changing as well. We are discovering that fatty delights can actually be good for you: They allow Spaniards, Italians and Greeks to live longer, and they make us satisfied with eating less. I'm speaking up not for obesity-generating fat, then, but for the kind of fatty food that leads to swooning sensual satiety.<br />
<br />Roast goose, for instance, is a supremely succulent, mind-alteringly flavorful fatty food. In most of America, roast goose would be viewed as the raven of cardiac mortality, hoarsely honking "never more." And listening to the doctors on cable TV, you might think that it's better to cook up a batch of meth than to cook with butter.<br />
<br />Eating fatty foods has become the culinary version of "Breaking Bad": a dangerous walk on the wild side for the otherwise timid consumers of tasteless butter substitutes and Lean Cuisine. Soon the fear-of-food crowd will leave us with nothing but watery prison gruel (whole grain, of course) and the nine daily servings of kale, collards, spinach and other pesticide-laced and e-coli-menaced greens and fruits on the agribusiness-promoted "food pyramid."Still worse is the ninth circle of food hell to which the fat-phobic ninnies have consigned us: egg-white omelets. Is life worth prolonging for a few (alleged) extra months if said life has been spent enduring the repellent slabs of gluey, pasty albumen that so many self-congratulatory "health conscious" types consider to be a sign of their sanity? They want to purge themselves of dietary sin. I just want to purge.<br />
<br />Fear of fat has become a national sickness, an all-American eating disorder: Call it fatnorexia. Where is Uncle Toby from Shakespeare's "Twelfth Night" lamenting that, under the oncoming reign of Puritan strictures, "there shall be no cakes and ale"?<br />
<br />Something deeper than concern for nutrition and cholesterol is going on here. You don't have to be a Freudian (I'm not) to see in the antifat crusade a cowering fear of sexuality. The evil of oral pleasure as Satan's tool of seduction, dating back to Eve, is deeply embedded in American culture. Recall Cotton Mather's denunciation of the hell-bound wickedness of the pleasures of the flesh and his call for self-mortification (anticipating today's egg-white omelets).<br />
<br />We live in a culture where food has become a symbol of imminent mortality, where Zagat reviews of high-end steakhouses tediously joke about the need to have "your cardiologist approve in writing," variations of which are repeated practically every time a piece of meat is mentioned anywhere ("a heart attack on a plate," "adding insult to arteries" and other super-clever jests).<br />
<br />In fact, some new developments have undermined antifat absolutism. Consider the recent New England Journal of Medicine report on a study of the olive-oil-heavy "Mediterranean diet," a study that included this fairly sensational revelation (as summarized by the Atlantic Online): "After five years of watching trends in heart disease and strokes among people at high risk, the researchers could not in good conscience continue to recommend a 'low-fat diet' to anyone."<br />
<br />Hear that, you fat-shamers? You're killing your credulous low-fat followers. Condemning high-risk people to a life that is not only dangerous but terminally boring—a terrifyingly tedious life of austere cuisine. Doctors had to intervene to save lives from your low-fat junk science!<br />
<br />Paradoxically, the most conclusive argument for eating sumptuously delicious fatty foods can be found in Michael Moss's well-intentioned but scarifying new book, "Salt, Sugar, Fat: How the Food Giants Hooked Us," where he uses the telling phrase "sensory-specific satiety point." As Mr. Moss defines it, this is "the tendency for big, distinct flavors to overwhelm the brain, which responds by depressing your desire to have more."<br />
<br />Whoa! This is big. The author, however, misses the far-reaching implications. He focuses on bashing the use of the "sensory-specific satiety" concept by the evil processed-food industry, which goes to great lengths to get you to overeat fatty fried junk by purposely avoiding the "sensory-specific satiety" point that stops the craving.<br />
<br />In other words, sensory satiety is our friend. Voilà! The foods that best hit that sweet spot and "overwhelm the brain" with pleasure are high-quality fatty foods. They discourage us from overeating. A modest serving of short ribs or Peking duck will be both deeply pleasurable and self-limiting. As the brain swoons into insensate delight, you won't have to gorge a still-craving cortex with mediocre sensations. "Sensory-specific satiety" makes a slam-dunk case (it's science!) for eating reasonable servings of superbly satisfying fatty foods.<br />
<br />So, as part of my unceasing desire to serve humanity, I will offer you a few of my fattiest things—signature experiences of "sensory-specific satiety" that I've had with fat.<br />
<br />For me, the transformative Ur-experience of the beauty and power of fat was my late Aunt Hortense's cheesecake. Don't laugh. This was heavy duty. When I first had this as a child at a maternal family gathering, I felt transported into a realm of pleasure I had never imagined. It rearranged my brain circuits forever. She made it by supersaturating heavy, heavy cream, with heavy sour cream, creating a creamy near-thermonuclear critical mass of density and intensity.<br />
<br />Next: roast goose. It's astonishing to me that so many people I know have never had the roast-goose experience. No wonder they're in a bad mood all the time. I'd always preferred duck to chicken and turkey (and still do by a miracle mile). But roast goose! The crispy, golden-hued skin, the dark meat seething with juicy, fatty, flavorsome goodness. (Don't overcook!)<br />
<br />Forget foie gras. (Something evil about it.) Substitute a big old goose for the dry, overcooked slabs of fibrous white meat that you get from your Thanksgiving "Butterball" turkey, with its injection of "basting material," which the Butterball people hasten to assure the fat-phobic public has nothing, but nothing, to do with butter. Too bad!<br />
<br />As long as we're on the subject of fowl, let us not forget Peking duck, although be sure you go to a place that doesn't serve yesterday's holdovers, as some do. Go to a place where you order it in advance. It's all about the skin, each gleaming, crisp scallop of which bears a slender, super-tender cargo of meat and fat (which shouldn't need the hyped-up hoisin sauce it's often served with).<br />
<br />From the fancy to the humble: lard. An ex-girlfriend from the Midwest introduced me to cookies baked with lard instead of those plastic shortenings. Though I still prefer heavy lacings of butter in my pastries, lard-infused cookies have some kind of smoky peasant savoriness. And lard is great for frying hash browns, although I prefer rendered duck or goose fat. (Ever had hash browns in cream? The old Gage & Tollner place in Brooklyn used to serve this specialty. That was living.)<br />
<br />And then there are steaks. I'm down with Jeffrey Steingarten, Vogue's food writer, who says that the carapace of super-fatty beef that curves around the top of most rib-eye cuts is the best there is (though a case can be made for the tender smaller side of a Porterhouse or T-bone). Still, for true beefy fattiness, slow-simmered short ribs may capture the meaty soul of beef better than most steak cuts: molten spoon-tender beef with melting fat and savory juices.<br />
<br />On second thought, speaking of the soul of beef, roasted marrow is its meaty essence. It looks like pure fat, but it isn't, really, just mainly, and when served in the split shank bone (as at places like the Knickerbocker or Prune in New York City), one portion will keep you in a state of sensory-specific satiety for a week.<br />
<br />Nut butters: One of the great scandals in American food is that when you try to talk about nut butters—some of the supreme fatty food experiences available—all that most people can say is, "Is it like peanut butter?"<br />
<br />This is ignorant blasphemy! Almond butter, cashew butter, pecan butter, pistachio butter, macadamia butter (!)—here is a multiflavored fat heaven that even fat-deprived vegetarians can enjoy. They are so good that you reach sensory-specific satiety after about two tablespoons. They leave peanut butter, even the unhomogenized, non-Jif-like pastes, in the dust. If you haven't had these nut butters, you truly you have not lived a full life.<br />
<br />I could go on about burgers, but that terrain is so well-trodden that it's pointless. When you get a chance, though, you must try lamb burgers—just plain with raw onions and spicy North African harissa sauce. You'll never go back to mere hamburgers again.<br />
<br />Finally, clotted cream. I've provided a good start for your fatty-food future, but clotted cream owns the scones, so to speak. I first had it in pastoral Devonshire itself, and I've never had it so good. It's cream that's thickening—on the verge of turning into sweet butter or souring into sour cream—but it has instead decided to clump together its richest essences into buttery solids in the thick, silky, creamy liquid. You can get it by mail order, but a recent trip to various expat Brit outlets in New York yielded what was to me more like a somewhat velvety cream cheese spread than the soupier, clottier Double Devonshire clotted cream of memory.<br />
<br />These are just a few of my favorite fattiest things. So much fat, so little time.<br />You watch: Once my style of luxe fatty eating catches on and people start to see that moderate portions of extreme pleasure don't make them obese, fat will become the new health food. My dream diet book: "Eat Fat, Stay Slim." I'll have my cakes and ale with a helping of roast goose, if you please.<br />
<br />—Mr. Rosenbaum's books include "Explaining Hitler" and "The Shakespeare Wars." He is a columnist for Slate and national correspondent for Smithsonian.<br />Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-7910033361771690432012-12-13T13:30:00.001-08:002012-12-13T13:30:07.519-08:00<div class="separator" style="clear: both; text-align: center;">
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<br />Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-42396742872016153602012-08-26T02:05:00.003-07:002012-08-26T02:12:25.315-07:00Toffee Fudge Cheesecake"The high-fat diet contains 195 g/kg casein, 3 g/kg DL-methionine, 377 g/kg sucrose, 150 g/kg corn starch, 153 g/kg anhydrous milkfat, 10 g/kg corn oil, 1.5 g/kg cholesterol, 60.067 g/kg cellulose, 35 g/kg mineral mix AIN-76 (170915), 4 g/kg calcium carbonate, 10 g/kg vitamin mix Teklad (40060), 1.2 g/kg choline bitartrate, and 0.033 g/kg ethoxyquin (antioxidant)"<br /><br />Please don't try this at home!<br /><br />PeterPeterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-9379613089330411292012-01-28T03:21:00.000-08:002012-01-28T03:25:35.984-08:00FIRKO thermogenesis and movement<a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjo_BxGlU6NJiGsRdEO2l4YG-Jp6JXuJH8-8Gf5-deAkGm3jpBfcxM9vNkzqW_cq4cvEQ-riu83iwKGDYA3tqBGRl8IL5nu2th77OCJoIiSmcL04MQ4FQqZFeelcjc-wYzDJ90lQsSadBtq/s1600/FIRKO+heat.jpg"><img style="cursor:pointer; cursor:hand;width: 400px; height: 343px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjo_BxGlU6NJiGsRdEO2l4YG-Jp6JXuJH8-8Gf5-deAkGm3jpBfcxM9vNkzqW_cq4cvEQ-riu83iwKGDYA3tqBGRl8IL5nu2th77OCJoIiSmcL04MQ4FQqZFeelcjc-wYzDJ90lQsSadBtq/s400/FIRKO+heat.jpg" border="0" alt=""id="BLOGGER_PHOTO_ID_5702641563213180546" /></a>Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-29617941746826241272011-09-08T21:48:00.000-07:002011-09-08T21:50:02.439-07:00Weight loss Shai et al<a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgcUO1X5i9hl-DzDGEi11Ldmi6hzwJ4hwUmzH4HN2x-ZAfVNyBu8Q5hBX0J9ar7hXX0qKE2jHs8SAZB2995oPoSRrQncNExVWZXNIGe60t3fTKL2PuW-0h2_1_t7sTA2q4KxsXtJHmYCwQW/s1600/weight+loss+israel.jpg"><img style="cursor:pointer; cursor:hand;width: 385px; height: 400px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgcUO1X5i9hl-DzDGEi11Ldmi6hzwJ4hwUmzH4HN2x-ZAfVNyBu8Q5hBX0J9ar7hXX0qKE2jHs8SAZB2995oPoSRrQncNExVWZXNIGe60t3fTKL2PuW-0h2_1_t7sTA2q4KxsXtJHmYCwQW/s400/weight+loss+israel.jpg" border="0" alt=""id="BLOGGER_PHOTO_ID_5650217344787694994" /></a>Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-37855886344105771382011-06-17T13:06:00.000-07:002011-06-17T13:07:59.835-07:00high protein diets<a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgfW1Cs7scqbS69RDhBXyHdkC2_c_FILoJylEkioUyKBHbaJT6i2697LO_Hlw7ZthNdzhSbtNpI4s1ArVRprA9zMVz_Hi3tP0nTnwkrMEerJH3UDJeyR-L6rVrD6la5vYKakxIlpJ47J2s0/s1600/diets.jpg"><img style="cursor:pointer; cursor:hand;width: 400px; height: 248px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgfW1Cs7scqbS69RDhBXyHdkC2_c_FILoJylEkioUyKBHbaJT6i2697LO_Hlw7ZthNdzhSbtNpI4s1ArVRprA9zMVz_Hi3tP0nTnwkrMEerJH3UDJeyR-L6rVrD6la5vYKakxIlpJ47J2s0/s400/diets.jpg" border="0" alt=""id="BLOGGER_PHOTO_ID_5619282757699406498" /></a>Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-32072854394837577662011-05-29T12:39:00.000-07:002011-05-30T00:38:11.676-07:00<a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgJ8hX4XZhAaNg0TXVT57x5H8fpVeuuCOnW3u1gVuPrOeaBf367WFNAJOwOQ8GyDtmOiKw4H782bnmX8cCak4ZukE20xW_nPC7fpwJrYE-7WcqF9D7_HO4MjGvFzXaKULHjcRUOq4js5Yp2/s1600/altered+thumb+tack.jpg"><img style="cursor:pointer; cursor:hand;width: 400px; height: 300px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgJ8hX4XZhAaNg0TXVT57x5H8fpVeuuCOnW3u1gVuPrOeaBf367WFNAJOwOQ8GyDtmOiKw4H782bnmX8cCak4ZukE20xW_nPC7fpwJrYE-7WcqF9D7_HO4MjGvFzXaKULHjcRUOq4js5Yp2/s400/altered+thumb+tack.jpg" border="0" alt=""id="BLOGGER_PHOTO_ID_5612410210701559138" /></a><br /><br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEirgv-w_Pr-y_Q34BMaZqhT1SpId7EkrHlzoMJyU275nSsPFgOc5Lr8Qy6lvAgZhARk-0gfBQSRuINkc_b0w9w2UY3Jt8HkFt7mCApwEASje7PCO6S5HqUL1Wy6Xd6uDKubdzZDMDyfiV3K/s1600/obese+calories+out.jpg"><img style="cursor:pointer; cursor:hand;width: 400px; height: 300px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEirgv-w_Pr-y_Q34BMaZqhT1SpId7EkrHlzoMJyU275nSsPFgOc5Lr8Qy6lvAgZhARk-0gfBQSRuINkc_b0w9w2UY3Jt8HkFt7mCApwEASje7PCO6S5HqUL1Wy6Xd6uDKubdzZDMDyfiV3K/s400/obese+calories+out.jpg" border="0" alt=""id="BLOGGER_PHOTO_ID_5612225103751873042" /></a>Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-73824302146429865402011-03-19T13:45:00.001-07:002011-03-19T13:53:49.752-07:00<iframe title="YouTube video player" width="400" height="390" src="http://www.youtube.com/embed/nYUjNQrokeg" frameborder="0" allowfullscreen></iframe>Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-47281276742721785462011-01-04T12:04:00.000-08:002011-01-04T12:45:00.363-08:00Sea Palling Jan 2nd 2011<object height="344" width="425"><param name="movie" value="http://www.youtube.com/v/vVngDqR6Zt0?hl=en&fs=1"><param name="allowFullScreen" value="true"><param name="allowscriptaccess" value="always"><embed src="http://www.youtube.com/v/vVngDqR6Zt0?hl=en&fs=1" type="application/x-shockwave-flash" allowscriptaccess="always" allowfullscreen="true" height="344" width="425"></object><br /><br /><object width="425" height="344"><param name="movie" value="http://www.youtube.com/v/j4gbyjfmEN4?hl=en&fs=1"></param><param name="allowFullScreen" value="true"></param><param name="allowscriptaccess" value="always"></param><embed src="http://www.youtube.com/v/j4gbyjfmEN4?hl=en&fs=1" type="application/x-shockwave-flash" allowscriptaccess="always" allowfullscreen="true" width="425" height="344"></embed></object>Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-65729137389836080852010-10-28T14:19:00.000-07:002010-10-28T14:22:14.623-07:00Hepatic metabolism<a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhg559bltjtawi4ak4ZmBGOv7IZjflC6Hy7tYvvlXkQIk7qIUY0K3yHGAFeFG0wLs9uD1103ongNS3VhqHNiDwQuC8ZcIrZzvxqxf0MjBwX026RLfVC66F6ofMWgLv3Z41mqWNmv8_f8LyA/s1600/liver+metabolism.jpg"><img style="cursor:pointer; cursor:hand;width: 338px; height: 400px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhg559bltjtawi4ak4ZmBGOv7IZjflC6Hy7tYvvlXkQIk7qIUY0K3yHGAFeFG0wLs9uD1103ongNS3VhqHNiDwQuC8ZcIrZzvxqxf0MjBwX026RLfVC66F6ofMWgLv3Z41mqWNmv8_f8LyA/s400/liver+metabolism.jpg" border="0" alt=""id="BLOGGER_PHOTO_ID_5533209910018664722" /></a>Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-54525393417940996272010-09-14T11:41:00.000-07:002010-09-14T11:42:45.394-07:00Fructose trans scarring(Best Syndication News) - High amounts of fructose, sucrose, and trans fats increases the risk for fatty liver disease with scar tissue reported researchers from the Cincinnati Children's Hospital Medical Center in a new study. Fructose and Trans Fats in excess can also contribute to obesity.<br /><br />The researchers point out that 10.2 percent of calories in the average American diet comes from Fructose, which eaten in excess has been associated with obesity, cardiovascular disease and liver disease. The researchers used a mouse model to investigate how obesity-related fatty liver disease develops from over consumption of fructose, sucrose, and trans fats.<br /><br />The researchers sampled the blood of the mice before and during the 16 week study. They divided the mice into one group being fed a normal diet of rodent chow and another group of mice being fed fructose and sucrose enriched drinking water along with trans-fat solids. The researchers studied the liver tissue for fat content as well as scar tissue fibrosis. They measured the reactive oxygen stress markers in the blood to determine the extent of liver damage.<br /><br />The normal fed mice stayed thin and didn't develop fatty liver disease while the mice that were fed a high calorie diet with the fructose, sucrose, and trans fats became obese and developed fatty liver disease.<br /><br />Only the group that received the combination of trans-fat along with the high fructose diet developed the advanced fatty liver disease with scar tissue.<br /><br />The researchers want to investigate how antioxidants might help to reduce liver damage in future studies. The researchers also want to further their studies with human diets on fatty liver disease and prevention.Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-67563137184362689542010-07-19T22:23:00.000-07:002010-07-20T13:32:44.344-07:00Eating healthy fruit and vegetables won't stop cancerEating healthy fruit and vegetables won't stop cancer<br /><br /> * By Clair Weaver<br /> * From: The Sunday Telegraph<br /> * August 26, 2007 12:00AM<br /><br />FRUIT and vegetables provide no protection against cancer, according to latest Australian research that has shocked nutritionists.<br /><br />In a discovery that turns conventional advice on its head, experts have admitted there is "zero evidence" that eating fruit and vegetables can help people avoid a disease that kills nearly 40,000 Australians every year.<br /><br /><br />Research presented for the first time at last week's CSIRO Prospects for Cancer Prevention Symposium shows that what people eat is far less important in cancer prevention than previously believed.<br /><br /><br />Instead, the three prime risk factors driving up Australian cancer rates have been identified as obesity, drinking too much alcohol and smoking.<br /><br /><br />Staying within a healthy body weight range was found to be more important than following particular nutritional guidelines.<br /><br />This means a slim person who doesn't eat enough fruit and vegetables would probably have a lower risk of developing cancer than someone who is overweight but eats the recommended daily amount of fruit and vegetables.<br /><br /><br />The findings emerged from the Cancer Council's Melbourne Collaborative Cohort Study, an ongoing research project involving 42,000 Australians who have been monitored since 1990.<br /><br /><br />Revealed exclusively to The Sunday Telegraph, they challenge widespread belief in the power of juices and vegetable-based "anti-cancer" diets to avoid or fight various types of the disease.<br /><br />Dr Peter Clifton, director of the CSIRO's Nutrition Clinic, told The Sunday Telegraph there was "zero evidence" that eating fruit and vegetables could protect against cancer.<br /><br /><br />Heart disease is Australia's biggest killer, so fruit and vegetables are still regarded as important in maintaining health.<br /><br /><br />Professor Dallas English, of the Cancer Council of Victoria, told the symposium that despite decades of research, there was no convincing evidence on how Australians could modify their diet to reduce the risk of cancer.<br /><br /><br />"The most important thing about diet is limiting energy (kilojoule) intake so people don't become overweight or obese, because this has emerged as a risk factor for a number of cancers, including breast, prostate, bowel and endometrial (uterus)," he said.<br /><br /><br />The link between eating red meat and bowel cancer was "weak" and the Cancer Council supported guidelines advising people to eat red meat three or four times a week, Professor English said.<br /><br /><br />His advice comes after Health Minister Tony Abbott last week backed a report, funded by Meat & Livestock Australia, on the dietary role of red meat.<br /><br /><br />Surprisingly, fibre was deemed to have no significant benefit in avoiding bowel cancer _ although calcium was associated with a 20 per cent reduced risk.<br /><br /><br />Likewise, a high intake of fat, considered a prime culprit since the 1970s, was found to have only a "modest" link to breast cancer.<br /><br /><br />Smoking caused one in five cancer deaths, while regularly drinking too much alcohol boosted the risk of several cancers including breast and bowel, Professor English said.<br /><br /><br />He and Dr Clifton acknowledged that eating fruit and vegetables might help people avoid obesity, as they were lower in kilojoules than other foods.<br /><br /><br />"The risk of every type of cancer is increased by obesity," Dr Clifton added.<br /><br /><br />Both experts predict a surge in cancer as a result of Australia's obesity epidemic, but say exercise can play a vital role in cutting cancer rates, potentially halving the risk of some cancers.<br /><br /><br />Sydney mother Tauri Smart, 29, said the findings "take the pressure off" meal preparation.<br /><br /><br />She and her husband try to eat healthily and want to set a good example for their daughters Poppy, 3, and Sadie, six weeks.<br /><br /><br />"I've always tried to push fruit and vegetables, and have a vegetarian meal at least once a week," Ms Smart said. "Being able to have meat makes it easier."<br /><br /><br />Nutritionist Dr Rosemary Stanton cast doubt on the findings and suggested the study could be flawed.Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-56460796414855890522010-05-14T14:04:00.000-07:002010-05-14T14:05:38.148-07:00Chicken and insulin<a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj0lsTFgzi4uB32SXSdDakgdjM99kN4vhsdoY9vlAHe9ohZKHcdUxYs7NFl1FLcSm6wVsGVbWDssnL9xTcbH9PLeIXZmLdEpfapXNSo4dHttPf_-Y023_pE-1uC6WVyZor5Wpb_aH7og8Sj/s1600/chicken+insulin.jpg"><img style="cursor:pointer; cursor:hand;width: 345px; height: 347px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj0lsTFgzi4uB32SXSdDakgdjM99kN4vhsdoY9vlAHe9ohZKHcdUxYs7NFl1FLcSm6wVsGVbWDssnL9xTcbH9PLeIXZmLdEpfapXNSo4dHttPf_-Y023_pE-1uC6WVyZor5Wpb_aH7og8Sj/s400/chicken+insulin.jpg" border="0" alt=""id="BLOGGER_PHOTO_ID_5471234611749522642" /></a>Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-40026720211853438112010-03-17T04:20:00.001-07:002010-03-17T04:21:00.002-07:00Obesity and pacemakersObesity Reduces Risk Of Cardiac Death?<br /><br /><br />Being skinny confers no advantage when it comes to the risk of dying suddenly from cardiac causes, a study presented today at the American College of Cardiology Annual Scientific Session has found.<br /><br />According to the authors, non-obese heart failure patients – including overweight, normal and underweight patients – had a 76 percent increase in risk of sudden cardiac death compared to obese heart failure patients. Normal and underweight patients showed a startling 99 percent increase in risk for sudden cardiac death compared to obese patients.<br /><br />Risk of sudden cardiac death was studied in 1,231 patients who had suffered at least one prior heart attack and had been diagnosed with a low ejection fraction, a measurement of how much blood is pumped from the heart with each beat. The analysis found that decreased BMI or body mass index was associated with a large increase in the risk of sudden cardiac death. <br /><br />Compared to the overweight, normal and underweight patients, obese patients were younger, had a higher ejection fraction, higher blood pressure, diabetes and were more likely to be smokers. BMI was calculated as weight in kilograms divided by the square of height in meters for all study participants. The clinical definition of obesity – BMI ≥30 kg/m2 – was used. Overweight patients fell into the 25 to 29 kg/m2 range of BMI values and normal/underweight patients fell into the < 25 kg/m2 range of values.<br /><br />The findings highlight the "obesity paradox," a phenomenon long recognized by cardiologists that, once afflicted, obese heart failure patients fare better than their slimmer counterparts. This study adds to a growing body of conflicting data regarding the relation of BMI to outcome in patients with heart failure.<br /><br />"When we started this study we were hoping the data would disprove the 'obesity paradox,'" said Bonnie Choy, co-lead author and a second year medical student at the University's School of Medicine and Dentistry. "Our study is the first to create and analyze subcategories within non-obese patients, looking at overweight, normal and underweight patients, but even with this advanced analysis we still the saw an inverse relationship between BMI and sudden cardiac death."<br /><br />The science behind the obesity paradox in the heart failure population is unresolved, but some researchers believe timing may have something to do with it. One possible explanation is that the long-term negative effects of conventional risk factors, such as increased BMI, may be overwhelmed by the short-term effects of other factors on heart failure mortality. In addition, survival advantages that exist in obese patients with heart failure may, in the short term, outweigh the harmful effects of increased BMI.<br /><br />"Obese patients are hard on their bodies; many don't eat right, don't exercise, and many smoke," explained Eric Hansen, co-lead author and also a second year medical student at the University of Rochester. "If their bodies are surviving this bad treatment then perhaps they are better equipped, from a genetic standpoint, to live with heart failure."<br /><br />Researchers also assessed the effect of BMI on the benefit of implantable cardioverter defibrillator (ICD) therapy. An implantable cardioverter defibrillator is a medical device about the size of a pager that is surgically implanted in the chest under local anesthesia. The device detects irregular and potentially fatal heart rhythms (arrhythmias), which often lead to sudden cardiac death, and shocks the heart back into a normal rhythm. <br /><br />Results indicated that implantable cardioverter defibrillator therapy was more effective in the non-obese patients with lower BMI values who were at higher risk for sudden cardiac death. These findings may help identify patients who would get the most benefit from an ICD – patients with a lower BMI.<br /><br />Citation: Hansen et al., 'Relation of Body Mass Index to Sudden Cardiac Mortality and Defibrillator Efficacy in Patients With Left Ventricular Dysfunction,' March 2010, American College of Cardiology Annual Scientific SessionPeterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-70231884807436018772010-01-17T14:04:00.000-08:002010-01-17T14:05:50.861-08:00liver and bacon after keep fit at 100Diet the key for keep fit fan, 100<br /><br />Friday, January 15 12:02 pm<br />Press Assoc.<br /><br /> *<br /> Buzz Up!<br /> * Print Story<br /><br />A refusal to eat junk food, that is the secret of Georgina Easter, who at the age of 100 has emerged as possibly Britain's oldest keep-fit fanatic. Skip related content<br />Related photos / videos<br />Diet the key for keep fit fan, 100<br /><br />Whether she's limbering up to the latest chart hits or stretching her legs on a wooden chair, Ms Easter rarely fails to miss one of her Keep-Fit For Mature Movers lessons in Derby.<br /><br />Her secret to her youthful exuberance is a healthy diet, but even her fellow classmates, some 30 years her junior, are astounded how she keeps going despite reaching her century last month.<br /><br />Derby Adult Learning Service, part of the city's council, organises the sessions at a church hall in the suburb of Chaddesden.<br /><br />Officials at the service now want to know whether she is the oldest member of a keep-fit class in the country.<br /><br />But for Miss Easter, who was born when Edward VII was still king and the Titanic was only being built, the keep-fit classes are just a bit of fun. She said: "What's my secret? Keep away from junk food. I also do a bit of gardening, I cook every day and I am going to have liver and onions ... when I get home.<br /><br />"I enjoy the friendship of the classes. All the people who take part, we are all good friends. At the end of term we have a big get together and a meal. It's very enjoyable."<br /><br />The council says the classes, which run in ten-week blocks, three times a year, are part of an effort to ensure the elderly in the area stay as independent as possible.<br /><br />Ruth Skelton, in charge of adult services at the Council, said: "She's a brilliant example to all people her age and younger.<br /><br />"It may well be that Georgina is the oldest keep-fit member in the county and we would be very interested to know whether she's the oldest person to go to keep-fit classes in the country."Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-71505797529268327482009-12-19T21:27:00.000-08:002009-12-19T21:29:00.874-08:00cross clamped mice<a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgU4C7X4pjuWLz4T_FXlQFT0SXsTg6VXMuLepJNGQzY26JBTuJH4uGC8ovQf6bOLwl1X-Qepp9Id78BJ4s7MLjZ6_xQXhl-RoQQf13zSOz2QGDX3_rZN06YFnMoOintRdX29gaHIbrJPsUV/s1600-h/mice.jpg"><img style="cursor:pointer; cursor:hand;width: 400px; height: 166px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgU4C7X4pjuWLz4T_FXlQFT0SXsTg6VXMuLepJNGQzY26JBTuJH4uGC8ovQf6bOLwl1X-Qepp9Id78BJ4s7MLjZ6_xQXhl-RoQQf13zSOz2QGDX3_rZN06YFnMoOintRdX29gaHIbrJPsUV/s400/mice.jpg" border="0" alt=""id="BLOGGER_PHOTO_ID_5417186071126377586" /></a>Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-59475507663861241752009-11-05T03:55:00.000-08:002009-11-24T01:12:38.416-08:00Interview with Dr Uffe Ravnskov MD PhDIs High Cholesterol The Cause of Heart Disease? An Interview with Uffe Ravnskov M.D. PhD. <br /><br />(not with me, the interviewer does not wish to be associated!)<br /><br /><br />When did you begin to suspect that the cholesterol theory of atherosclerosis might be wrong? What led you to this conclusion? Before then, had you believed in the cholesterol theory? Was this part of your training?<br /><br />I have never thought that it was true. I heard about it for the first time in 1962 shortly after having got my MD. My biochemical knowledge was still intact at that time and I knew that cholesterol was one of the most important molecules in our body, indispensable for the building of our cells and for producing stress and sex hormones as well as vitamin D. The idea that cholesterol in the blood should kill us if its concentration is a little higher than normal, as they wrote in the Framingham paper, seemed to me just as silly as to claim that yellow fingers cause lung cancer.<br /><br /><br /><br />Would you tell my readers about your training, publications, university appointments, other professional activities?<br /><br />The first seven years as a doctor I worked on different medical departments in Denmark and Sweden. In 1968 I started my academic career at the Department of Nephrology, University Hospital in Lund where I got my PhD. After a few years I organized a research team investigating the association between hydrocarbon exposure and glomerulonephritis. Unfortunately I caught one of my coworkers in producing a fraudulent paper. It was unfortunate, because it is risky to be a whistleblower in the academic world. Instead of excluding the fraudulent researcher it was my research that was questioned. The resistance against my research from my superiors became intolerable and I therefore decided to go into private practice. Nevertheless I succeeded in publishing the main part of my research in major medical journals after having left the department. I have summarized my findings and conclusions on the web as well.<br /><br />In the late eighties the cholesterol campaign was started in Sweden. I was much surprised because I couldn’t recall anything in the scientific literature in support. I started reading it systematically and I soon realized that I was right. Since then I have published about eighty papers and letter and also books, translated into five languages, where I have presenting my arguments and criticism.<br /><br /><br /><br />How has your work believe received by your colleagues? By healthcare professionals and consumers around the world?<br /><br />In the beginning nobody took notice. To ignore criticism is the most effective way to maintain a false idea. My first book was published in Sweden in 1991 and a Finnish edition shortly afterwards. The Swedish one made no impact whatsoever and the Finnish one was put on fire in a television show. Ridicule and slander have been used as well as a means to muffle me. After I had aired my warnings against statin treatment in Dutch television for instance, Dutch researchers described me in a following show as a crackpot who had been kicked from the universities of Copenhagen and Lund. The directors of the show offered my critics a possibility to discuss the issue with me on television, but all of them declined. On his blog Michael Eades has described how one of them later on belittled me in a scientific paper.<br /><br />But I have also realized that I am not alone. Seven years ago I started THINCS, The International Network of Cholesterol Skeptics (www.thincs.org), which by now includes about eighty doctors, professors and other researchers from all over the world, who share my scepticism, and I have received two international awards for my contributions. Also encouraging is the hundreds of emails that I receive every year from patients, who have regained their health after having stopped their cholesterol-lowering treatment...<br /><br /><br /><br />Your work seems to validate what many integrative health care professionals have been saying for decades. How does the alternative community respond to you?<br /><br />There is a much more open attitude from these people.<br /><br /><br /><br />If the cholesterol hypothesis is in error, does this mean that all of its therapies – low cholesterol diet, cholesterol lowering natural therapies and medications -- are wrong?<br /><br />Absolutely. This kind of treatment is meaningless, costly and has transformed millions of healthy people into patients. <br /><br /><br /><br />Specifically, what are your views on statins?<br /><br />Their benefit is trivial and has been seen only in male patients who already have heart disease. Worse is that their many adverse effects are ignored or cleverly belittled by the trial directors. Independent researchers have found many more and in much higher numbers. If they are true it means that today millions of previously healthy people probably consider their weak and painful muscles, their bad memory, their sexual failure and their cancer to be a consequence of increasing age and so do their doctors. The risk of cancer is most alarming. Both animal experiments, epidemiological studies and several of the statin trials have shown that low cholesterol predisposes to cancer. The widespread use of statin treatment probably explains why the decrease of the smoking habit that has been going on in many countries hasn’t been followed by a decrease of cancer mortality. We should have seen a decrease because smoking predispose not only to bronchial cancer, but to all kinds of cancer.<br /><br /><br /><br />Drug companies market vigorously the highest, strongest doses of statins. Lipitor is pushed at the highest dosage, 80 mg. This dosage is the most powerful for lowering cholesterol and LDL, but it also causes more adverse effects and costs more than lower doses. What are your thoughts about this?<br /><br />The outcome from these trials is a further demonstration that the small benefit from statin treatment has nothing to do with cholesterol. For instance, although cholesterol plummeted and remained at about fifty percent below the initial value during the whole SEAS trial, it did not change mortality, but it increased the number of cancer with statistical significance. Even worse was the result of the ENHANCE trial, where atherosclerosis in patients with familial hypercholesterolemia progressed the most among those whose cholesterol was lowered the most. <br /><br /><br /><br />If statins can be helpful in reducing the incidence of heart attacks, who should take them?<br /><br />In my view nobody. When I was practicing I used to describe the benefit in this way: Considering your age and your previous heart attack your chance to be alive in five years is about 90%. You can increase that chance to 92% if you take a statin pill every day, but then you may also expose yourself to its many adverse effects.<br /><br /> <br /><br />From the data I have seen, statins have not produced a reduction in overall cardiac deaths. Do you have any idea of why this is?<br /><br />You are right. Heart mortality in Sweden is going downwards, but the reduction started already in the sixties. The cause is most probably that treatment of acute myocardial infarction has improved because the mortality curve has not changed after the introduction of the statins. The reason may be that their small benefit is counteracted by an increasing frequency of heart failure. As you know the statins block not only the synthesis of cholesterol, but also of other vital molecules, for instance coenzyme Q10, and muscle cells, including those of the heart, can’t function properly without Q10.<br /><br /><br /><br />Do you think mainstream medicine will ever relinquish its view that elevated cholesterol causes heart disease and that statins are the magic bullet?<br /><br />I hope so. The failures of the most recent statin trials has been commented by several journalists in the major US newspapers. In Sweden a revolution is going on. Here, a general practitioner treated her own obesity successfully by eating a low-carbohydrate diet with a high content of animal fat. When she advised her obese and diabetic patients to do the same, she was reported to the National Board of Health and Welfare for malpractice. After a two-year-long investigation she was acquitted, as her treatment was considered to be in accord with scientific evidence. At the same time, the Board dismissed two experts, who had been appointed for updating the dietary recommendations for diabetics, because it came up that they were sponsored by the food industry. Instead the Board has asked independent researchers to review the scientific literature.<br /><br />The subject has gained general attention due to a number of radio and television shows, where critical experts including myself have discussed the issue with representatives of the official view. Most important, thousands of patients have experienced themselves that by doing the opposite as recommended by the current guidelines they have regained their health. The effect has been that the sales of butter, cream and fat milk are increasing in Sweden after many years of decline, and a recent poll showed that a majority of Swedish people today think that the best way of losing weight is by a low-carbohydrate, fat-rich diet.<br /><br />Further progress was achieved this spring. Several times colleagues of mine and also myself have asked the Swedish Food Administration for the scientific basis of their warnings against saturated fat. We have been met with the argument that there are thousands of such studies, or by referrals to the WHO guidelines or the Nordic Nutrition Recommendations. As the main argument in the latter two is that saturated fat raises cholesterol we were not satisfied with their answer and finally the Food Administration published a list with 72 studies that they claimed were in support of their view on saturated fat and twelve that were not.<br /><br />We scrutinized the lists and found that only two of the 72 studies supported their standpoint; eleven studies did not concern saturated fat at all, and the unsupportive list was incomplete, to put it mildly. We published a short report with our comments to these lists in the Swedish medical journal Dagens Medicin. A response from the Food Administration appeared seven weeks later in which they pointed out that their recommendations were directed to healthy people, not to patients. They maintained that they were based on solid scientific evidence without mentioning anything about saturated fat and without answering our critical comments.<br /><br />But this is not all. Earlier this year Sachdeva et al reported that the mean cholesterol in 137,000 patients with acute myocardial infarction was lower than normal. As usual, the authors didn’t understand their own findings, but concluded that cholesterol should be lowered even more. A few months later Al-Mallah et al. came up with the same result and conclusion, although they also reported that three years later, mortality was twice as high among those who had been admitted with the lowest cholesterol.<br /><br />These results created a fierce debate in one of the major Swedish newspapers. It was opened by ninety-one-year old Lars Werkö, the ‘Grand Old Man’ in Swedish medical science, retired professor in internal medicine and former head of The Swedish Council on Technology Assessment in Health Care, together with Tore Scherstén, retired professor in surgery and former secretary of the Swedish Medical Research Council. “Now it is time to sack the cholesterol hypothesis and to investigate the reason of this scientific breakdown” they wrote. They also criticized American researchers in AHA and NHLBI and their followers for sloppy and fraudulent science.<br /><br />They were of course attacked by two professors and representatives of the current view, but none of them came up with any substantial evidence, only by personalities. <br /><br /><br /><br />Are there other risk factors that should be followed? Such as: C-reactive protein, fibrinogen, homocysteine, lipoprotein A. Any other factors?<br /><br />Such analyses may be helpful for doctors to put the right diagnosis in patients with a disease of unknown origin. But to check healthy people’s blood to find deviations from normal is the freeway to unnecessary medication.<br /><br /><br /><br />Are there other alternative therapies besides statins that people might consider?<br /><br />There is no reason for healthy people to take drugs or anything else to prevent heart disease as long as we do not know the very cause. Don’t forget that people who die from a myocardial infarction have on average lived just s long as other people. On my talks I use to ask people, who put the same question to me, if they know a better way of dying. <br /><br /><br /><br />What diet do you recommend people follow?<br /><br />I do not give medical advice to people I haven’t seen and examined myself and as I am retired it means that I give no advice at all except to my family and nearest friends. I inform people by writing and lecturing. Then they have to decide themselves what to do. <br /><br /><br /><br />In 20 years, do you expect changes in how we view heart disease, its causes and treatments?<br /><br />I am confident that we will see a change in the next few years. There is a growing skepticism among medical scientists. What is happening in Sweden these days may hopefully inspire researchers in other countries to air their skepticism openly. Recently experts selected by WHO and FAO published a new report. Here the authors concluded that there was no satisfactory or reliable evidence to support the idea that saturated fat causes heart disease, or diabetes or obesity. A revolutionary change of direction, you may say. However, they did not change their recommendations.<br /><br />Together with Kilmer McCully, the discoverer of the association between homocysteine and atherosclerosis, I have presented another hypothesis. We think it is much more likely because we are able to explain the many observations that do not fit with the present one. If anyone wants to read the full paper I shall send it on request.<br /><br />EDIT Ted has a link to the full pdf in the comments section of <a href="http://high-fat-nutrition.blogspot.com/2009/11/uffe-ravnskov-interview.html" target="_blank">the original post</a>.<br /><br /><br />Finally, I assume that much of what I have mentioned here may seem incredible, but all the facts including references to the scientific literature are available in my new book Fat And Cholesterol Are GOOD For You!Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-27999795061861822492009-10-31T07:29:00.001-07:002009-10-31T07:34:11.104-07:00Drug Decriminalization in PortugalWith apologies to Salon for stealing their text. I'll take it down if anyone objects, but the original article does seem to have disappeared already. Here it is.<br /><br /><br />Glenn Greenwald is a civil rights attorney, a blogger for Salon, and the author of a new Cato Institute policy study called “Drug Decriminalization in Portugal: Lessons for Creating Fair and Successful Policies.” The paper examines Portugal’s experiment with decriminalizing possession of drugs for personal use, which began in 2001. Nick Gillespie, editor of reason.com and reason.tv, sat down with Greenwald in April.<br /><br />Q: What is the difference between decriminalization and legalization?<br /><br />A: In a decriminalized framework, the law continues to prohibit drug usage, but it’s completely removed from the criminal sphere, so that if you violate that prohibition or do the activity that the law says you cannot do you’re no longer committing a crime. You cannot be turned into a criminal by the state. Instead, it’s deemed to be an administrative offense only, and you’re put into an administrative proceeding rather than a criminal proceeding.<br /><br />Q: What happened in Portugal?<br /><br />A: The impetus behind decriminalization was not that there was some drive to have a libertarian ideology based on the idea that adults should be able to use whatever substances they want. Nor was it because there’s some idyllic upper-middle-class setting. Portugal is a very poor country. It’s not Luxembourg or Monaco or something like that.<br /><br />In the 1990s they had a spiraling, out-of-control drug problem. Addiction was skyrocketing. Drug-related pathologies were increasing rapidly. They were taking this step out of desperation. They convened a council of apolitical policy experts and gave them the mandate to determine which optimal policy approach would enable them to best deal with these drug problems. The council convened and studied all the various options. Decriminalization was the answer to the question, “How can we best limit drug usage and drug addiction?” It was a policy designed to do that.<br /><br />Q: One of the things you found is that decriminalization actually correlates with less drug use. A basic theory would say that if you lower the cost of doing drugs by making it less criminally offensive, you would have more of it.<br /><br />A: The concern that policy makers had, the frustration in the 1990s when they were criminalizing, is the more they criminalized, the more the usage rates went up. One of the reasons was because when you tell the population that you will imprison them or treat them as criminals if they identify themselves as drug users or you learn that they’re using drugs, what you do is you create a barrier between the government and the citizenry, such that the citizenry fears the government. Which means that government officials can’t offer treatment programs. They can’t communicate with the population effectively. They can’t offer them services.<br /><br />Once Portugal decriminalized, a huge amount of money that had gone into putting its citizens in cages was freed up. It enabled the government to provide meaningful treatment to people who wanted it, and so addicts were able to turn into non–drug users and usage rates went down.<br /><br />Q: What’s the relevance for the United States?<br /><br />A: We have debates all the time now about things like drug policy reform and decriminalization, and it’s based purely in speculation and fear mongering of all the horrible things that are supposedly going to happen if we loosen our drug laws. We can remove ourselves from the realm of the speculative by looking at Portugal, which actually decriminalized seven years ago, in full, [use and possession of] every drug. And see that none of that parade of horribles that’s constantly warned of by decriminalization opponents actually came to fruition. Lisbon didn’t turn into a drug haven for drug tourists. The explosion in drug usage rates that was predicted never materialized. In fact, the opposite happened.Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-5318925130750299322009-10-30T15:23:00.000-07:002009-10-30T15:25:04.810-07:00Jebb vs NuttDrugs tsar 'sacked over comments'<br /><br />Friday, October 30 07:10 pm<br />The Government's chief drugs adviser has been forced to resign in the wake of the row over the dangers of class A drugs. Skip related content<br />Related content<br /><br />Home Secretary Alan Johnson asked Professor David Nutt to resign as chairman of the Advisory Council on the Misuse of Drugs (ACMD), saying he had "lost confidence" in his ability to give impartial advice.<br /><br />He accused Prof Nutt of going beyond his remit as an evidence-based scientist and accused him of "lobbying for a change in government policy".<br /><br />But Prof Nutt hit back, accusing the Government of "misleading" the public in their messages about drugs and of "Luddite" tendencies. He linked his sacking to "political" considerations, citing the forthcoming election.<br /><br />Professor Nutt sparked controversy this week when he said ecstasy and LSD were less harmful than alcohol and cigarettes, and criticised the decision to upgrade cannabis to class B.<br /><br />Speaking after he agreed to step down he said: "It's unusual political times, I suppose, elections and all that. It's disappointing. But politics is politics and science is science and there's a bit of a tension between them sometimes."<br /><br />He attacked Prime Minister Gordon Brown for making what he said were "completely irrational" statements about cannabis.<br /><br />Confessing himself "extremely surprised" by the decision he said: "The danger is they (politicians) are misleading us. The scientific evidence is there, it's in all the reports we published."<br /><br />In his letter demanding Prof Nutt's resignation, Mr Johnson wrote: "It is important that the Government's messages on drugs are clear and as an adviser you do nothing to undermine the public understanding of them. As my lead adviser on drugs harms I am afraid the manner in which you have acted runs contrary to your responsibilities.<br /><br />"I cannot have public confusion between scientific advice and policy and have therefore lost confidence in your ability to advise me as chair of the ACMD. I would therefore ask you to step down from the council with immediate effect."Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-63630743359396020332009-09-27T09:22:00.001-07:002009-09-27T09:22:47.716-07:00Jebb on AtkinsAtkins Diet 'Dangerous'<br /> <br />August 13, 2003<br />Daily Mail (London)<br />by Jenny Hope<br /><br />THE hugely-popular Atkins Diet is medically unsound and a major health risk, nutrition experts warned yesterday.<br /><br />They said the high-protein high-fat diet, followed by stars such as Catherine Zeta-Jones and Geri Halliwell, was a giant experiment which could have disastrous effects for millions.<br /><br />Dr Susan Jebb of the Government-funded Medical Research Council said it would be 'negligent' to recommend it for long-term use and called for research into its safety.<br /><br />She dismissed the theory behind the diet, that it changes the body's chemistry to burn off fat, as 'pseudo-science'. Adverse effects could include kidney damage and bone loss.<br /><br />The alert comes from one of the country's leading experts on obesity. Dr Jebb is head of nutrition and health research at the MRC's Human Nutrition Research Centre in Cambridge.<br /><br />She was speaking at a special summit held in London to warn of the dangers that crash dieting poses to the nation's health.<br /><br />Dr Jebb said the Atkins Diet was the least healthy of a number of trendy 'faddy diets' followed by people desperate to lose pounds in a hurry. She said: 'Fad diets prey on the overweight, offering quick fixes and psychological tricks. I see no medical benefit at all in them, and in particular the Atkins Diet.<br /><br />'It is nutritionally incomplete. It works in the short term but so does any diet that reduces the amount of calories eaten.<br /><br />'The diet is a massive health risk, it's medically unsound. We have no idea what will happen in the long term because no one is evaluating the results of the experiment.<br /><br />'Obesity is a massive problem in the UK but this is not the way to solve it.' The warning is the latest in a series from health professionals over 'gimmicky' diet regimes, endorsed by celebrities.<br /><br />A multimillion-pound book industry has grown on the back of claims that extreme eating patterns work.<br /><br />The Atkins Diet is even challenging Harry Potter for world sales figures books about it are currently in first and third place on the British Hot 100 of online retailer Amazon.<br /><br />Invented 30 years ago by American Dr Robert Atkins, who died earlier this year, it tells followers to eat vast amounts of meat but severely restrict carbohydrates such as bread, pasta, rice and starchy vegetables.<br /><br />The theory is that carbohydrates increase the body's production of the hormone insulin, which encourages cells to store fat. This leads to both hunger and weight gain.<br /><br />Cutting carbohydrates right down, Dr Atkins asserted, turns the body from a carbohydrate-burning machine to one that burns fat.<br /><br />But Dr Jebb dismissed the claim as 'pseudo-science'.<br /><br />She said following the diet long-term would mean a dramatic change in eating habits for most people, protein accounts for only around 15 per cent of total calorie intake.<br /><br />Dr Jebb said: 'It's a profound change and we simply do not know the long-term health implications.<br /><br />'I certainly think we should be adopting a precautionary principle in terms of public health.' The diet is known to put extra stress on the kidneys, which can lead to kidney stones and more serious damage particularly for those with pre-existing problems they might be unaware of.<br /><br />There is also a fear of bone problems because the diet encourages the excretion of calcium which would otherwise go to build them.<br /><br />Although two U.S. studies found the Atkins Diet was safe and effective, Dr Jebb said the dieters involved had been on it for only six months and a year.<br /><br />She also pointed out that, longer-term, it had proved to be no better at permanent weight loss than a conventional low-fat diet.<br /><br />Dr Jebb said people had to lose weight sensibly and slowly because 'there is no way to lose a stone in a few weeks without putting your health at risk'.<br /><br />Among other experts warning about the Atkins Diet is Amanda Wynne of the British Dietetic Association. She says the process of ketosis it triggers where the body burns up stored fat can result in nausea and tiredness, while drastic reduction in carbohydrates can lead to constipation and digestive problems.<br /><br />Dr Jebb's colleague Toni Steer says: 'If you don't eat fruit and veg, you are excluding a lot of essential minerals and vitamins.<br /><br />'And we know that consuming these foods reduces your risk of cancer and cardiovascular disease.' Professor David Barker, a specialist in foetal health at Southampton University, has warned that mothers-to-be who follow such diet regimes are putting their baby's health at risk.<br /><br />The diet would deprive an unborn child of essential nutrients and raise the risk of heart disease, diabetes and strokes in adulthood.<br /><br />Dr Jane Ogden, a reader in health psychology at King ' s College, London, told yesterday's meeting the Atkins Diet was popular because weight watchers could follow the instructions to the letter.<br /><br />She said: 'What fad diets do is tell people in black and white what they can and can't do, and they identify with that.'Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-30223806812286601432009-09-18T06:50:00.000-07:002009-09-18T06:55:02.657-07:00Kebab text (news report link is down)Post-Pub Kebabs Add 1000 Calories<br /><br />4:33pm UK, Tuesday January 27, 2009<br /><br />Doner kebabs in the UK have been found to contain the equivalent fat to drinking more than one and a half wine glasses of cooking oil.<br /><br />A nationwide sample of the nutritional content of the takeaway meal found the average doner also contained close to an adult's entire daily recommended intake of salt.<br />Before adding salad and sauce the average kebab contained 1,000 calories but researchers found some with 1,990.<br /><br />Last year food scientists tested a doner kebab containing 140g of fat - twice the amount a woman should eat in a day.<br /><br />This was said to be the calorific equivalent to drinking a wine glass full of cooking oil.<br /><br />The most gut busting kebabs in this latest study provide 346% of a woman's saturated fat intake, close to drinking two wine glasses of cooking oil.Given that 60% of kebabs have been found to contain cholesterol raising trans fats, fans of the takeaway could be risking their health.<br /><br />Another big finding was that 35% of the meat sent to kebab shops listed a different meat species than was actually contained.<br /><br />Six kebabs were found to include pork when it was not listed as an ingredient, two of which were described as Halal - which Muslims are permitted to eat.<br /><br />Christopher Baylis told Sky News that Lacors want to make sure everyone is given the right information.<br /><br />We had never assumed that kebabs were a health food option - but it was certainly surprising.<br /><br />Christopher Baylis, Lacors spokesperson<br /><br />"The labelling is on the kebabs when they come from the manufacturers. It is bad not to convey exactly what is in the kebab," he said.<br /><br />The minute weight difference between a small and large kebab is also a problem, said chairman of Lacors, councillor Geoffrey Theobald.<br /><br />"With obesity rates rising so rapidly in the UK, portion size is as important as what is being consumed," he said.<br /><br />"Reducing portion size is an easy and cost-effective way for small businesses to help people eat sensibly."<br /><br />The study sampled 494 kebabs from 76 councils and found that the calorie count varied up and down the country.<br /><br />The average kebab in the North West of England contained 1,101 calories while in Scotland it was 1,084, in Wales 1,055 and 1,066 in south-west England.<br /><br />The lowest calorie kebabs can be found in Northern Ireland where the snack weighed in at an average of 843.Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-8796127875915558729.post-24418965321331410102009-08-25T13:10:00.001-07:002009-08-25T13:11:02.970-07:00High fat apoE-/-Even as low-carbohydrate/high-protein diets have proven successful at helping individuals rapidly lose weight, little is known about the diets' long-term effects on vascular health.<br />Now, a study led by a scientific team at Beth Israel Deaconess Medical Center (BIDMC) provides some of the first data on this subject, demonstrating that mice placed on a 12-week low carbohydrate/high-protein diet showed a significant increase in atherosclerosis, a buildup of plaque in the heart's arteries and a leading cause of heart attack and stroke. The findings also showed that the diet led to an impaired ability to form new blood vessels in tissues deprived of blood flow, as might occur during a heart attack.<br />Described in today's Online Version of the Proceedings of the National Academy of Sciences (PNAS), the study also found that standard markers of cardiovascular risk, including cholesterol, were not changed in the animals fed the low-carb diet, despite the clear evidence of increased vascular disease.<br />"It's very difficult to know in clinical studies how diets affect vascular health," says senior author Anthony Rosenzweig, MD, Director of Cardiovascular Research in BIDMC's CardioVascular Institute and Professor of Medicine at Harvard Medical School. "We, therefore, tend to rely on easily measured serum markers [such as cholesterol], which have been surprisingly reassuring in individuals on low-carbohydrate/high-protein diets, who do typically lose weight. But our research suggests that, at least in animals, these diets could be having adverse cardiovascular effects that are not reflected in simple serum markers."<br />Rosenzweig and his coauthors found that the increase in plaque build-up in the blood vessels and the impaired ability to form new vessels were associated with a reduction in vascular progenitor cells, which some hypothesize could play a protective role in maintaining vascular health.<br />"A causal role for these cells has not yet been proven, but this new data is consistent with the idea that injurious stimuli may be counterbalanced by the body's restorative capacity," he explains. "This may be the mechanism behind the adverse vascular effects we found in mice that were fed the low-carb diets."<br />The study's first author Shi Yin Foo, MD, PhD, a clinical cardiologist in the Rosenzweig laboratory at BIDMC, first embarked on this investigation after seeing heart-attack patients who were on these diets - and after observing Rosenzweig himself following a low-carbohydrate regimen.<br />"Over lunch, I'd ask Tony how he could eat that food and would tell him about the last low-carb patient I'd admitted to the hospital," says Foo. "Tony would counter by noting that there were no controls for my observations."<br />"Finally," adds Rosenzweig, "I asked Shi Yin to do the mouse experiment - so that we could know what happens in the blood vessels and so that I could eat in peace."<br />The investigators proceeded to study a mouse model of atherosclerosis. These "ApoE" mice were fed one of three diets: a standard diet of mouse "chow" (65 percent carbohydrate; 15 percent fat; 20 percent protein); a "Western diet" in keeping with the average human diet (43 percent carbohydrate; 42 percent fat; 15 percent protein; and 0.15 percent cholesterol); or a low-carb/high-protein diet (12 percent carbohydrate; 43 percent fat; 45 percent protein; and 0.15 percent cholesterol).<br />"We had a diet specially made that would mimic a typical low-carb diet," explains Foo. "In order to keep the calorie count the same in all three diets, we had to substitute a nutrient to replace the carbohydrates. We decided to substitute protein because that is what people typically do when they are on these diets."<br />The scientists then observed the mice after six weeks, and again at 12 weeks. Consistent with experience in humans, the mice fed the low-carb diet gained 28 percent less weight than the mice fed the Western diet. However, further probing revealed that the animals' blood vessels exhibited a significantly greater degree of atherosclerosis, as measured by plaque accumulation: 15.3 percent compared with 8.8 percent among the Western diet group. (As expected, the mice on the chow diet showed minimal evidence of atherosclerosis compared with either of the other two groups.)<br />"Our next question was, 'Why do the low-carb mice have such an increase in atherosclerosis?'" says Foo. Searching for an explanation, she and her coauthors proceeded to measure the usual markers thought to contribute to vascular disease, including the animals' cholesterol and triglyceride levels, oxidative stress, insulin and glucose, as well as levels of some inflammatory cytokines.<br />"In each case, there was either no difference in measurements compared with the mice on the Western Diet [which contains the same amount of fat and cholesterol] or the numbers slightly favored the low-carb cohort," she adds. "None of these results explained why the animals' blood had more atherosclerotic blockages and looked so bad."<br />Since there was no difference in the noxious or inflammatory stimuli that the animals' blood vessels were exposed to, Foo wondered whether the restorative capacity of the animals might be contributing to the difference. The investigators, therefore, looked at the animals' endothelial or vascular progenitor cell (EPC) counts. Derived from bone marrow, the EPC cells may play a role in vessel regrowth and repair following injury.<br />"Examinations of the animals' bone marrow and peripheral blood showed that the measures of EPC cells dropped fully 40 percent among the mice on the low-carb diet - after only two weeks," says Rosenzweig. "Although the precise nature and role of these cells is still being worked out - and caution is always warranted in extrapolating from effects in mice to a clinical situation - these results succeeded in getting me off the low-carb diet."<br />Even more important, he notes, the findings point out that there can be a disconnect between weight loss or serum markers and vascular health, and that vascular health can be affected by macronutrients other than fat and cholesterol - in this case, protein and carbohydrates.<br />"Understanding the mechanisms responsible for these effects, as well as the potential restorative capacity that may counteract vascular disease, could ultimately help guide doctors in advising their patients," adds Rosenzweig. "This issue is particularly important given the growing epidemic of obesity and its adverse consequences. For now, it appears that a moderate and balanced diet, coupled with regular exercise, is probably best for most people."<br />Source: Beth Israel Deaconess Medical CenterPeterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.com