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EventsThe margarine giant gives up: butter wins
Gigantic margarine manufacturer Unilever is starting to give up the fight. Fewer and fewer people want artificial margarine, and fewer and fewer people are still unnecessarily afraid of all-natural butter.
In many countries – including the US – the sale of margarine is plummeting, while the sales of butter are increasing more and more.
In a new strategy, Unilever in Germany (and Finland), now blends butter into its cheap margarine – new TV commercial above.
Quartz: The war against butter is over. Butter won.
Bloomberg: I Can’t Believe It’s Butter in My Unilever Rama Spread
“Margarine has become a marker for cheap, processed, artificial, unhealthy food,” says Marion Nestle, a New York University nutrition professor. “The irony is hilarious. Unilever went to a lot of trouble to formulate healthy margarines, but the zeitgeist has caught up with them.”
More
The Real Association Between Butter and Heart Disease in Sweden
“Butter Better than Vegetable Oils”
Heart Doctor: time to Bust the Myth about Saturated Fat and Heart Disease
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in San Luis Obispo, California on March 1st, 2014.
The info is here:
http://www.ccnutritionconference.com/Home.html
All the best Jan
How unhealthy is Vitalite (sunflower margarine) ?
Im lactose intollerante.. and there are a lot of lactose free butter/dairys for us.. at least in scandinavia!
I am eating the butter all of my life (65) but there is one big problem about the "all must eating the butter": Can you guess which one is this? There is no butter for 7 billion people on the Earth!
They first must eat the margarine to halve the population and after that maybe the rest of us will get some of butter!!
Thank you for attention and good luck!
P.S.
There is no need to worry about the healthy population or like is someone is worry about lot of guy people. It is natural way to lower the population on Earth!
The population on Earth is far greater problem than obesity and health!
Look around you everyday. There is no day that someone not push you or tell you something bad!
Leave them with their sugar and bread to live to their fate!
Sunflower margarine would contain lots of unhealthy omega-6!
Ghee was proposed and here are simple instructions how to make it from real butter.
Try 1/4 pack of butter first time!
http://www.everydaymaven.com/2013/how-to-make-ghee/
Ghee has both lactose and casein removed so it should be just fine !
If you still have problem it could be due to long term low fat eating which makes the bile from the liver thick and full of stuff ready for disposal. A few charcoal tablets before fat intake helps to absorb such stuff and bring it "to drain" to minimize re-circulation into the bloodstream.
If a tendency for constipation exists take magnesium together with the charcoal. Try 1 tabl and increase 1 per day until loose and scale back. No harm with too much magnesium.
Olive oil, coconut oil and Beef tallow are other good fats, the last one my favorite. It can be hard to get real olive oil as there seem to be a lot of illegal mixing and ignorant authorities, so I for one avoid it unless I one day come to a farm where it is made in small scale.
Good Luck !
Its more of an selection of different good fat sources?
The best source of monosaturated fats in scandinavia is oxlard!
And we are eating more olive oil in scandinavia too!
Where can I get any "non-artificial" margarine. And dipping into olive oil doesn't count.
I've never liked margerine, much like my newfound (LCHF) change where sugar and starch is not appetizing, I'd forego things if I wanted butter and there was only margerine.
The problem with sugar is it tends toward overload. Sweet is sweet. But when you don't OD on sugar, your cravings, appetite, whatever get right and you desire the right things.
The cat didn't like it.
https://www.youtube.com/watch?v=xzzezDYvIFU
I trust the cat!
Isn't it strange that as soon as one is convinced about something and shares what he/she has discovered, to those who do not share his beliefs - or more specifically who do not have an open mind, ready to consider ideas that are not what they have chosen to believe, then whatever is written, regarless of the science backing it, becomes an "evangelical rant".
It ain't. I have watched what doc Einfeld writes for a while and he is on the contrary quite nuanced, insisting on countless occasions that correlation does not mean causation and always backing up his arguments with sound, well done research.
After finishing a MPH, I can certify that doc Einfeld does know what he is talking about and that his arguments are sound. But then it must be mentally straining to even consider that what one thought as the truth may not be so true in the end. It is much more easy to make a blanket statement to the effect this is an "evangelical rant".
If it makes you feel better, continue thinking what your mama and your dietitian trained by Coca Cola told you was the truth, eat tons of carbs and margarine. I wish you good luck on such a diet.
oh dear your frantic frantic attack and defensive post , is obviously not evangelical rant lol
The "doc" post numerous ridiculous exaggerated claims the facts are that this huge upsurge in butter consumption means that a whopping 1% of the market is butter with 99% margarine. So making a claim that butter won is downright silly. Personally I wouldn't use margarine to shine my shoes let alone put it in my mouth but facts are facts and rants are rants.
As for your " eat tons of" post what do you think would happen if you ate tons of butter and animal fat , especially if you followed the first sentence posted in the site" Do you want to eat real food (as much as you like) and improve your health and weight?"
http://www.dietdoctor.com/lchf
Your reaction and that of other evangelists is akin to a fanboy of a game or particular brand, no matter what the reality you can not accept any challenge that may affect your "faith" in what you believe. A lot of the LCHF stuff is pretty sound with decent scientific back up and though we all know that a calorie is not necessarily the same as another calorie ,for those attempting to lose weight their is no magic wand other than eat less than you burn, so one way or another they are going to have to reduce quantity of food eaten and types of food eaten . To suggest otherwise is downright wrong and bordering on unethical.
There are literally dozens of non scientific points of views posted both by the doc and the followers:
a few examples
How about dramatic points made with zero scientific back up, a test based on one biased subject lol
http://www.dietdoctor.com/is-pepsi-max-bad-for-your-weight
with a follow up lol , wonder what the fan boys/ followers/ evangelists thought happened
http://www.dietdoctor.com/update-on-the-pepsi-max-test
The headline posts made here too often look like the kind of mad claims seen on the fronts of tabloids . The posts against fruit etc are nonsense humans have been eating fruit for 10s of thousands of years ,eons before butter appeared
LCHF works. for weight loss. For many migraines.For many cases of asthma. For resistant epilepsy in children. To improve the biochemical profile of people. and to reverse type 2 diabetes (tsearch Jason Fung in youtube: he's a nephrologist who reverses type 2 diabetes with LCHF and partial fasting for breakfast. It's also good for cardiac disease... It simply works. In my case, it cured my overweight problem and my sleep apnea. For my wife, it cured her migraine headaches and her asthma. How do we know? This is the only thing we changed.
And as far as artificial sweeteners, they are truly bad for a number of reasons, including the fact that they increase the odds of suffering from a stroke.
I honestly think doc Einfeld is doing a pretty good job. His blog is not popular by accident: He provides info that truly change the life of many people. This may sound too evangelistic for you. But I truly do not care. Tough my editorial choices may be different than his, I always read him with great pleasure. I'd rather read an enthusiastic text than a boring one.
Was I defensive? Probably. I simply hate when people, hiding under a pseudonym, make sweeping statements with absolutely no nuance. Feel free to start a blog of your own. Much more difficult than making caustic comments. It puts you in the spotlight, You may even be subject to attacks.. If you ever do decide to start a blog (not evangelical of course), please let us know of the address so we all can visit.
... The posts against fruit etc are nonsense humans have been eating fruit for 10s of thousands of years ,eons before butter appeared"
Well, that is a dramatic point. The evidence is that hominids lost the fructase enzyme during the long phase inhabiting the savannahs and can no longer metabolize fructose directly for energy. What evidence is there that hominids were eating fruit, much less out of season?
Butter is just separated breast milk. I expect the evidence will be that our ancestors have been consuming breast milk since they became mammals. So it is hardly foreign to the human metabolism. Unlike fruit, there is no evidence we went eons without it and lost the genes for critical enzymes. Indeed, the adaptation on chromosome 2 for adult lactase has been identified as the most strongly selected of human-specific genes. And you don't even need that gene to eat butter.
None is a knock down proof, but they are all evidence.
http://www.youtube.com/watch?v=E57cFhjpxgw
Dr Sikaris specialises in cholesterol and is chair of the International Federation of Clinical Chemistry Committee on Analytical Quality, so he should be on top of the latest research. The powerpoint slide shown at 13:36 is instructive. The slide chronicles the evolution of the leading thinking in research into heart disease.
The view 30 years ago was that total cholesterol mattered.
This was later rejected and the view 20 years ago was that there is “good” cholesterol (in HDL particles) and “bad” cholesterol (in LDL particles).
This was later rejected and the view 10 years ago was that it only glycated (sugar-damaged) LDL and oxidized LDL (mostly from vegetable oils) that matter. The small dense LDL particles are the most prone to oxidation, as they have LESS cholesterol per particle and cholesterol is an anti-oxidant! (All cholesterol is good cholesterol!)
The current view is that it is triglycerides that matter. What causes triglycerides to rise? Primarily the fructose in sugar. The liver converts dietary fructose into triglycerides and packs them into VLDL particles that eventually become LDL particles.
Dr. Sikaris suggests it is only dietary fructose that matters, but Drs. Phinney and Volek (artandscienceoflowcarb.com) cite research that high carbs in general (over 40% of calories, for most people) significantly increase triglycerides, even carbs from starch (glucose). It seems that once the muscles and liver are replete with glycogen to capacity, then the liver has to start converting glucose into triglycerides, which eventually go into LDL particles. So the body can tolerate a lot more glucose than fructose, but only to a point (depending on the rate at which one uses the glycogen in the muscles and liver).
Indeed, by coincidence the following report came out on the prevalence of atherosclerosis in Egyptian mummies "despite" their diet heavy in grains, fruit and vegetables and with limited meat and saturated fat. (Seems the ancient Egyptians also invented the food pyramid.) No junk food or tobacco to blame. But applying what Dr. Solaris is reporting from leading metabolic research, this is entirely consistent with a diet high in grains and fruits leading to rampant atherosclerosis.
http://www.npr.org/2011/04/09/135269340/egyptian-mummies-diagnosed-wi...
There is lots of metabolic evidence that indicates fructose is toxic to humans if too great a portion of daily calories comes from fruit. The only real issue is what is the safe dose for one's particular metabolism, which appears to be age dependent, among other things.
Br J Nutr. 2011 Aug;106(3):390-7. doi: 10.1017/S000711451100033X. Epub 2011 Mar 22.
Prevention and reversal of diet-induced leptin resistance with a sugar-free diet despite high fat content.
Shapiro A, Tümer N, Gao Y, Cheng KY, Scarpace PJ.
Author information
Abstract
Chronic consumption of a Western-type diet, containing both elevated sugar and fat, results in leptin resistance. We hypothesised that fructose, as part of the sugar component of Western-type diets, is one causative ingredient in the development of leptin resistance and that removal of this component will prevent leptin resistance despite high fat (HF) content. We fed rats a sugar-free (SF), 30 % HF (SF/HF) diet or a 40 % high-fructose (HFr), 30 % HF (HFr/HF) diet for 134 d. The HFr/HF diet resulted in impaired anorexic and body-weight responses to both peripherally (0·6 mg/kg, assessed on day 65 of the diet) and centrally (1·5 μg/d, assessed on days 129-134) administered leptin, whereas SF/HF-fed rats were fully leptin responsive. At day 70, half the HFr/HF-fed animals were switched to the SF/HF diet, reversing the leptin resistance (assessed 18 d after the diet switch). The HFr/HF diet elevated serum leptin and reduced adiponectin, and levels were restored abruptly at day 3 after switching to the SF/HF diet. These data demonstrate that a diet containing both HFr and fat leads to leptin resistance, while an isoenergetic SF/HF diet does not. Moreover, removal of fructose from this diet reverses the leptin resistance and the elevated leptin, suggesting a cause-and-effect relationship. These data suggest that fructose is the bioactive component of a HF/high-sugar diet that is essential for the induction of leptin resistance.
It is interesting to hypothesize. Suppose an animal comes up to a seasonal source of fruit (a tree or a berry bush), having been on a high-fat pre-fruit season diet. The animal starts at the fruit tree and this shoots up fructose. Given the lingering fat in the small bowel (fat being only taken up according to need through homeostatic regulation of bile production, so there should be plenty of fat there from earlier eating), this results in high-fructose, high-fat signalling to override appetite control by leptin. The animal enters a gorge phase of unrestrained appetite (say 6-8 tangerines or more per sitting, as per field observations by Galina), creating lots of triglycerides and storing fat for winter.
What is the natural check on this phase? Likely the supply of fruit. There is competition for fruit in a brief window of ripeness. Then, about three days after leaving the fruit grove, and back to regular high-fat low-fructose diet, normal homeostatic appetite signalling restores. Thus plants and animals have evolved symbiotically. Plants program the flesh around seeds to be high in fructose when the seed is ready to be dispersed (the fruit ripens) and animals are programmed to crave and become addicted to the sweet fructose, with loss of appetite restraint, in order to gather, take away and eat as much bounty as possible while available.
Two problems these days. Humans lack fructase, which diminishes binge tolerance. Two, global supply chains, CO2 warehouses, and freezers have made fruit available all year round, so the escalation of appetite and serum triglycerides in response to fructose is chronic for many people.
A rat study, of course, says nothing about dose in humans. But it does elucidate the metabolic pathways to explain what is happening metabolically to people who are plainly exceeding long-term safe doses of fructose.
Liquid fructose downregulates Sirt1 expression and activity and impairs the oxidation of fatty acids in rat and human liver cells.
Rebollo A1, Roglans N2, Baena M2, Sánchez RM2, Merlos M2, Alegret M2, Laguna JC3.
Author information
Abstract
Fructose ingestion is associated with the production of hepatic steatosis and hypertriglyceridemia. For fructose to attain these effects in rats, simultaneous induction of fatty acid synthesis and inhibition of fatty acid oxidation is required. We aimed to determine the mechanism involved in the inhibition of fatty acid oxidation by fructose and whether this effect occurs also in human liver cells. Female rats were supplemented or not with liquid fructose (10% w/v) for 7 or 14days; rat (FaO) and human (HepG2) hepatoma cells, and human hepatocytes were incubated with fructose 25mM for 24h. The expression and activity of the enzymes and transcription factors relating to fatty acid β-oxidation were evaluated. Fructose inhibited the activity of fatty acid β-oxidation only in livers of 14-day fructose-supplemented rats, as well as the expression and activity of peroxisome proliferator activated receptor α (PPARα). Similar results were observed in FaO and HepG2 cells and human hepatocytes. PPARα downregulation was not due to an osmotic effect or to an increase in protein-phosphatase 2A activity caused by fructose. Rather, it was related to increased content in liver of inactive and acetylated peroxisome proliferator activated receptor gamma coactivator 1α, due to a reduction in sirtuin 1 expression and activity.
In conclusion, fructose inhibits liver fatty acid oxidation by reducing PPARα expression and activity, both in rat and human liver cells, by a mechanism involving sirtuin 1 down-regulation.
Role of immunodeficient animal models in the development of fructose induced NAFLD.
Bhattacharjee J1, Kumar JM2, Arindkar S1, Das B1, Pramod U1, Juyal RC1, Majumdar SS1, Nagarajan P3.
Author information
Abstract
Cellular and humoral immunity had been implicated in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). This study was designed to assess if T, B and natural killer (NK) cells are involved in the progress of NAFLD in mouse models after chronic fructose treatment. Mouse models that are deficient in either T cells, B cells or NK cells or lacking both T and B cells were fed with 30% fructose solution for 12 weeks. Typical features of NAFLD, including the relative body weight, food and water intake, biochemical analytes, liver histology, NAFLD activity score, and glucose tolerance and insulin tolerance test were characterized. Further, the percentage of CD3, B220 and NK cells in peripheral-blood mononuclear cell, terminal deoxynucleotidyl transferase dUTP nick end labeling assay, immunodetection for hepatic apoptosis (p53) and for inflammation (TNFα) and quantitative real-time polymerase chain reaction for putative and inflammatory genes involved were determined. Our results conclude that mice deficient in T cells or NK cells fail to develop fructose induced NAFLD whereas the immunocompetent mice and mice with B-cell-specific defect developed NAFLD.
Taken together, these data support that the onset of fructose-induced NAFLD is associated with involvement of T cells and NK cells in mice.
this is a nice review, I am sorry I am unable to post full paper but you can get a copy at your local University.
Prog Lipid Res. 2013 Dec 18;53C:124-144. doi: 10.1016/j.plipres.2013.12.001. [Epub ahead of print]
Regulation of energy metabolism by long-chain fatty acids.
Nakamura MT1, Yudell BE2, Loor JJ2.
Author information
Abstract
In mammals, excess energy is stored primarily as triglycerides, which are mobilized when energy demands arise. This review mainly focuses on the role of long chain fatty acids (LCFAs) in regulating energy metabolism as ligands of peroxisome proliferator-activated receptors (PPARs). PPAR-alpha expressed primarily in liver is essential for metabolic adaptation to starvation by inducing genes for beta-oxidation and ketogenesis and by downregulating energy expenditure through fibroblast growth factor 21. PPAR-delta is highly expressed in skeletal muscle and induces genes for LCFA oxidation during fasting and endurance exercise. PPAR-delta also regulates glucose metabolism and mitochondrial biogenesis by inducing FOXO1 and PGC1-alpha. Genes targeted by PPAR-gamma in adipocytes suggest that PPAR-gamma senses incoming non-esterified LCFAs and induces the pathways to store LCFAs as triglycerides. Adiponectin, another important target of PPAR-gamma may act as a spacer between adipocytes to maintain their metabolic activity and insulin sensitivity. Another topic of this review is effects of skin LCFAs on energy metabolism. Specific LCFAs are required for the synthesis of skin lipids, which are essential for water barrier and thermal insulation functions of the skin. Disturbance of skin lipid metabolism often causes apparent resistance to developing obesity at the expense of normal skin function.
Have I got it right that this suggests it would be better to have resveratrol in dry red wine than pomegranate juice? And I should limit fructose when I am aiming for the benefits of ketones and ketosis?
I have that trouble with my mom. She was always proud to live a healthy life-style, did her exercises and walked a lot daily, she never had cookies and sweets at home, didn't eat cakes even during festivities, ate only sourdough rye bread. However, the huge amount of fruits, root vegetables and vegetable salads she consumed was just impossible to imagine for a regular person. Needless to say, her belly was growing and blood pressure rising, even though she is much healthier than SAD junkies, there is no question about it. So,my annoyance with the mantra "fruits and vegetables are good for you" has a personal note. I manage to convince her to start LCarbing and drop rye bread and breakfast oatmeal and go really easy on potatoes, but fruits remain a problematic theme. Actually, to binge on any food is bad, period. I don't live on meat and eggs, vegetables are a tasty addition to my diet, but fruits are very limited.
http://www.huffingtonpost.com/2014/01/10/butter-consumption_n_4568064...
In 2010, American consumed (data from the very "evangelical pro LCHF" USDA...)
Butter: 4.9 lbs / person
Margarine 3.7 lbs/person
And, very unfortunately, salad and cooking oils, a whooping 53.6 lbs.
So it appears, and the graph makes it quite clear, that butter is winning the war against that crap chemically processed spread known as margarine BUT there is still a very long ways to go to win the battle against those supposedly "heart healthy" omega-6 rich, totally devoid of omega-3 oils. The use of these omega-6 rich oils may help promoters of the low fat craze to state that high fat creates heart disease. In an article, they simply have to forget to identify the fat source. While the heart disease problem is clearly an excess of carbs and omega-6, we will read statements that "a ketogenic diet induces carotid artery stiffness" in kids, while the authors forgot to state that the fat that was used was omega-6 rich vegetable oils.
There definitely is a role for this blog and the exchanges going on, to get facts straight.
Anyway,I think rye bread is much better than the wheat one - its gluten is weaker, not so genetically modified like modern wheat,especially when fermented several days in a refrigerator. According to Weston Price, some isolated groups of people had an exceptional health eating small amounts of rye bread with a lot of grass-fed cheese and butter.
The assertion that butter is just 1% of the sales of margarine seemed unreliable. I'll go with the USDA figures until someone comes along with something demonstrably more reliable.
"Per-capita butter consumption hit a 44-year high in 2012, according to U.S. government data, while margarine is at a 70-year low. In Germany, butter outsells margarine by a three-to-one ratio, according to data tracker IRI."
http://qz.com/168276/the-war-against-butter-is-over-butter-won/
As for tabloid style evangelical headlines I am afraid that still stands a number of the posts look like they came from the Daily Mail .My point was not that I do not see the advantages of LCHF eating but rather the type of wild claims { such as posting "results" of a lets have a giggle and call it an experiment with diet pepsi and one biased subject looking for a specific reaction, that is as bad as science gets
As for the headlines here, I view most of them as delightfully hopeful camp. Much of the LCHF trek has been debunking conventional wisdom and method and trying to discover the facts, as science has not been forthright and uninfluenced in these areas. This can be draining and dispiriting, so some humor and delightful over-enthusiasm is just what the good doctor has prescribed. Works for me. Lots of opportunity for critical rumination along the way..