Neurological Correlates

26 responses so far ↓

• 1 ItsTheWooo // Apr 4, 2009 at 8:51 pm

  This is bullcrap, and right away I know it is bullcrap because the best way to reduce inflammation in human beings is to go on a avery high fat low carbohydrate diet. If the problem is inflammation, then eating a low carb, high fat diet is part of the answer.

  Scientists have a way of blaming dietary fat for things which are actually caused by insulin or hyperglycemia or any number of metabolic sequellae related to the metabolic state conducive to obesity. This is because feeding fat to lab rats generally induces the metabolic syndrome and weight gain. Humans are not rats, and humans do not eat what lab rats are fed either.

  First of all, type of fat matters a lot. Omega 6 oils are more prone to cause this problem. That is because they are inflammatory. Omega 3 fats actually correlate with weight loss because they are antinflammatory.

  Second, carbohydrate and calorie content of the diet dramatically affects how fat behaves.
  If you’re on a very low carb or ketogenic diet, OR if your calories are very low, guess what inflammation is going to be very low.
  If carbs rise in the diet, suddenly fat seems to contribute to inflammation (especially the omega 6 fats and sometimes saturated fats)… and it is worse than if it were an uncomplicated high carb diet.

  It’s all very complicated but it eventually comes down to insulin sensitivity, glucose tolerance, free fatty acids and things of that nature. Fats tend to antagonize glucose oxidation, so a combined meal of fat and carb is often most insulinogenic because the fat is inhibiting glucose oxidation at the same time as glucose is rising from carbohydrate.

  Controlling insulin is the key to controlling systemic inflammation, and this most likely applies to “diet induced inflammation of the hypothalamus”.

  My blood pressure is like 80/50, my blood does not clot, I am thin, I have low white blood cells, my CRP is like 1 or something… I achieve this by eating an extremely low carb diet with moderate calories and high fat. All indicators suggest I am calorie restricted, but I actually eat quite a bit for my size. The key is controlling insulin. I only eat foods that are very minimally insulinogenic (e.g. peanuts and other very high fat, particularly monosaturated fats with moderate protein) and I avoid foods that ramp up blood sugar (carbs, particularly carb/fat combination foods).

• 2 ItsTheWooo // Apr 5, 2009 at 10:17 am

  I just wanted to say that I apologize if I sounded hostile… I didn’t mean to say your post was BS (your posts are always very informative and interesting), my hostility was entirely directed at the researchers and scientists studying obesity. They are totally going in the wrong direction and it is a subject that is personally meaningful for me because I have had extreme obesity.

• 3 swivelchair // Apr 5, 2009 at 10:19 am

  ITW, and I know you know from what you speak, yet how do you explain the pair feeding experiment? Same caloric intake but one was predominantly from fat.

  There are gut signals that go to the brain after eating a fatty meal and dial up satiety signals in the hypothalamus, (“Obesity news: Blood lipid signaling causes satiety. More obesity news: Oprah hits 200 lbs and feels guilty,” Neurological Correlates, December 10th, 2008 ). Despite direct dietary insulinogenic interference — when you eat the fat and carb diet, where the fat inhibits glucose oxidation while glucose is rising from the carbs — there are also separate brain signals just from, apparently, blood lipid levels.

  So I can see how a fatty diet selectively produces specific gut signaling molecules that go to the brain (“NAPES”or their breakdown product, oleoylethanolamides, I’m not clear which goes to the brain). If you eat too much fat, there are too many signalling molecules, and perhaps these overwhelm the hypothalamus and burn out the TLR4 receptors (the receptors reported to modulate immunological leptin/insulin resistance and also, maybe by a separate pathway, cell apoptosis).

• 4 swivelchair // Apr 5, 2009 at 10:27 am

  Our posts crossed in the mail, but no need to apologize at all. I didn’t read it that way, so I’m going to retract your apology for you.
  But, if you have complaints, please post!
  Readers: If you have complaints, please post. I’m quite proud to have been called a conspiracy mongerer by no less than the NYT (New York Times Sez Neurological Correlates Sustains Crazy Goldman Sachs Conspiracy Theory).
  If enough readers complain, I’ll put up a separate page called, “Cancel my subscription!” , something I saw in a magazine some time ago, but thought was a great idea.

• 5 Sandra // Apr 8, 2009 at 1:13 pm

  According to the study, the high-fat rats and mice were also low-carb. However, the fats were, apparently, all saturated.

  Could this be the difference between the heavies who top out in the overweight or mild obese categories, and those who go beyond that? When I eat badly, I overeat carbs (esp sugar), not fat. When I watch the programs on TV about the morbidly obese, I see them eating so much greasy food and not so much cake, cookies, and candies.

• 6 ItsTheWooo // Apr 8, 2009 at 4:43 pm

  Before I look at the study I just want to mention that when scientists consider a rodent “low carb” usually what they mean to say is “we replaced a very small amount of carbohydrate with dietary fat, thus replicating the sort of diet most americans eat and become obese on”. Very rarely do scientists use a real low carb diet – i.e. 10-15% calories of carbohydrate, with the rest being fat and about 20-25% protein.

  As I expected, this diet was the typical macronutrient composition of 45% carb and 20% protein with 35% fat. In other words, this is a standard american diet, the very same sort that americans become hugely obese on. This is not a low carb diet. At all.

  The fact the scientists are calling this a high fat diet, when the mice are actually only eating 35% fat and 45% carb ought to raise eyebrows.

  Try the sort of diet I eat – 65% fat, 10% carb, and then see what happens.

• 7 ItsTheWooo // Apr 8, 2009 at 4:44 pm

  Oh, and I just noticed all of the fat was saturated. Why? That’s totally unnatural. Most natural fats (from animals) are mostly monosaturated with saturated in equal or lesser proportion. It is known monosaturated has a glucose-tolerance enhancing effect, whereas saturated fats can be inflammatory particularly if insulinogenic conditions exist (i.e. a 45% carbohydrate diet).

  This research is more typical garbage, and it is why people will never become thin and I will continue to be one of the only obese people to actually control their condition using diet alone.

• 8 swivelchair // Apr 8, 2009 at 4:59 pm

  ITW how do you explain the results? There seems to be an inflammatory response, is that just artifactual? Or could there be saturated fat metabolites in the gut entering the systemic circulation and headed up to the brain where they’re supposed to signal the hypothalamus for satiety, but instead put the whole system on overload?

• 9 ItsTheWooo // Apr 8, 2009 at 5:04 pm

  swivelchair – I can explain it easily. This is very typical in fraud obesity research.

  It is known that an extremely low fat, high carb diet is usually less insulinogenic and glucose-intolerance producing than is an equal calorie moderate fat, high saturated fat, moderate carb diet. This is not new. It is always true that if carbs are around 30-50%, fat intakes that are around 20-30% will be the most fattening of all possible diet conditions, and that is because the higher fat intake will antagonize glucose uptake from the carbs you’re eating and so compensatory insulin resistance and hyperinsulinemia sets in, which leads to inflammation and systemic damage that promotes obesity and altered feeding behavior (note, altered feeding behavior comes AFTER obesity, not before it, as one is getting fatter and storing more fat in tissue, one begins to eat more, much in the way growth hormones during childhood lead to a relatively larger increase in energy / metabolism … but, the feeding does also cause obesity because if youa re feeding on the same foods causing this hormone imbalance that leads to fat accumulation and white adipocyte hyperplasia/hypertrophy, you are going to store even MORE fat, which leads to eating even MORE of the food, which promotes MORE hormone imbalances, which promotes MORE body fat cell/size increase, over and over until you are 500 pounds. I mean, assuming you have the genetic vulnerabilities for that, of course. NOt everyone does, most people don’t).

  Assuming a constant sufficient protein level, in order, the most fattening diets are these:
  1) Moderate, fat, moderate carb (35-45/ 35-45/ 20)
  2) High carb, low fat (>60, <20, 20)
  3) High fat, low carb (60, 20)

  Researchers CONSISTENTLY compare the moderate fat-moderate carb diet to the high carb low fat diet and then say “SEE HIGH FAT DIETS MAKE YOU FAT”. I’m tired of this bogus research.

  Why don’t they use real low carb high fat diets? You know, >60 fat, <20 carb?
  Oh, that’s right, because the high carb diet would be shown for the fraud that it is.

  The research is out there.

  Besides, rodents are not furry little humans. Their metabolism are significantly different from our own. Even if we assume an ultra high fat ultra low carb diet also ruined the brains and metabolisms of these creatures it has little relevance to how it might affect a human being.

  There is a reason gastric bypass doctors are like “oh, and now that you’ve had gastric bypass, completely avoid sugar and minimie starch and drink lots of protein shakes”.

  Everyone who gets gastric bypass gains the weight back when the post-surgery inability to eat leaves them. The ones who keep it off are the ones who actually continue to follow the low carbohydrate diet outlined by the doctors.

  This obesity treatment and research business is such a scam it literally disgusts me. Pfft.

  Regarding the hypothesis that an excess of satiety molecules overwhelm the hypothalamus… I don’t think this is true, because obesity would involve a “pre-illness ” period of extreme satiety. This would produce a compensatory decrease in eating behavior, which would probably terminate any “overload” condition because you would eat less fatty food.
  As someone who is obese I can tell you that there is no “extreme satiety” state – as you are getting fat, you are also insatiably hungry. There is no satiety what so ever.Either these receptors burn out so quickly that you never even register their effect (unlikely) or burned out satiety receptors from high fat eating has little to no role in obesity.

  Actually, a hypothesis I rather like is that hypertriglyceridemia after eating an insulinogenic meal blocks leptin passage into the blood brain barrier, which in turn blocks a significant amount of anorexogenic effects of weight gain and eating food. This would explain why induction of a very low carb diet rapidly induces normal satiety and an intuitive “feeling” like your body can finally “see” all of the fat it has. That is exactly what it felt like when I went on the very low carb diet… within a day I felt like my brain could suddenly realize how much fat I had, and if I tried to eat I became nauseated because I was just emptying my fat cells which were overfull due to years of hyperinsulinemia.

  I am also quite sure glucose and insulin negatively affect dopamine receptor concentration/signalling and this is a significant part of altered fat burning, weight gain, lethargy and lack of attention/motivation that is so common in obesity. It is shown obese rats and humans have little dopamine d2 binding. It is known neuroleptics that block d2 receptors lead to obesity and metabolic syndrome. It is known restricting food, NOT weight loss, increases the density of d2 receptors, and food restricted animals are hypersensitive to stimulant dopaminergic drugs but not to opioidergics.
  Insulin upregulates teh dopamine transporter, which is to say it clears dopamine out of the synapse. This may be why junkfood diets correlate with ADHD and why first line treatment is to get ADHD kids on higher protein lower carb/sugar diets.

  There is also new research that simulant drugs can actually improve metabolic syndrome and obesity. People will scoff and say “duh, crackheads and coke addicts are thin” but this is ignorant and does not understand the intimate role of impaired dopaminergic signalling involved in obesity. Personally I think this can be significantly improved by going low carb, and may be a symptom of carb intolerance (along with obesity) but people like drugs and I think this is actually a good solution because it addresses the underlying defect that leads to altered metabolism of food and eating behavior (as opposed to bariatric surgery, which does nothing, other than make one temporary intolerant of eating due to mutilating the gastrointestinal tract).

  BTW, thank you for not taking offense to my vitriol-tinged response… it was all meant for the idiot obesity researchers, none of which can scratch their heads and understand / grasp event he FUNDAMENTAL defects which cause obesity. They’re so focused on molecules, and potential drug targets, they can’t even see the big picture: it’s insulin, it’s carb intolerance, and while I”m not against drug therapy, focusing on appetite is like focusing on cough as it pertains to tuberculosis. Appetite does not cause obesity, obesity causes appetite.

• 10 Sandra // Apr 9, 2009 at 10:20 am

  I don’t think this is fraudulent research. Whether or not it applies to humans is certainly open to question, but ItsTheWooo you seem to be taking both sides. You adamantly state that this study doesn’t apply to humans because the subjects were rodents, and yet you justify your other opinions by referring to studies which used rodents as subjects. I also find it odd that you are so quick to condemn high carb diets but refuse to acknowledge that high fat (esp high saturated fat) can also be problematic.

  I am fascinated by this study and thought about it all night and all this morning. I always wondered why there are people who top out in the overweight or mildly obese categories, and others who top out in the moderate, severe, or morbidly obese categories. I have little doubt that genetics are a reason, but I’m now beginning to think that what you overeat is also a factor. So there needs to be different approaches to weight loss based on the individual’s cause of obesity, it’s not just about cutting calories and exercising (though those will always be success factors).

  Let’s say the study is valid and it does apply to humans, then we might expect to find that people who overeat a diet high in saturated fat are heavier than those who overeat a more balanced diet, and possibly more than those who overeat a high carb diet. Then we could say to the people who are overeating the high saturated fat diet (if it’s not too late !) “You can eat the same number of calories, we’re just asking you to eat different foods”. I don’t know many obese people who would object to a weight loss diet that didn’t ask them to cut calories.

  I also want to add that even when I was heavier and well into the mild obesity category I DID have periodic satiety. I did not eat all day long, I did not want to eat all day long. I’m talking about satiety with respect to both stomach hunger and cravings.

  I think we can no longer lump all obese people into a single category. There are too many differences … innate variety among humans due to genetics, epigenetics, environment, etc … and, now, diet.

• 11 swivelchair // Apr 9, 2009 at 1:16 pm

  Sandra, thank you for your comments, which I always read and by now have stopped spraying diet soda into the screen while I disagree with your more outre statements.

  Be that as it may, guess what? We agree. The causes of obesity are many. My guess is that it’s a lot of background noise for about 80% of the people who are obese, or getting there because you can jump upstream and dial down appetite, and reset everything, at least for a while.

  Whether the source of the calories matters directly, who knows. There probably is a neuroimmunological effect somewhere along the line. Sugar gets into the systemic circulation pretty quick from the gut, and fat get stored. But, breaking a carbon bond will release the same number of calories whether it’s in a celery stick or in a lemon drop martini, if those have any organic material in them.

• 12 ItsTheWooo // Apr 9, 2009 at 1:18 pm

  Actually sandra the main reason I don’t think this study applies is because the diet was not high fat, it was actually a 45% carb 35% fat diet, which is the exact composition of food KNOWN to be most fattening. The researchers are arbitrarily calling this a high fat diet when it is not a high fat diet. The diet I eat is a high fat diet – 65% fat, 10-15% carb.
  This is the main problem I have with the research.

  I do not think rodent research always translates to humans either, but the stuff I was talking about (e.g. dopamine & dopa receptors being downregulated by insulin/food) this has also been demonstrated in obese humans. A few retards (err, researchers) originally thought the low activity dopamine receptors in obese people was surely evidence of compulsive eating, in much the way low dopamine receptors in coke addicts is evidence of coke binging. As if food were as potent as cocaine. Ha. Fortunately it is now becoming thought that the poor dopaminergic tone in brain is not the result of addictive use of food, but rather it is part of the metabolic abnormalities that lead to obesity. Sort of how changes in animals (e.g. melatonin production with seasons) affect their seasonal metabolism and reproductive patterns, it also seems a downregulation of d2 receptors is part of the genetic program to gain weight and go into a sort of “hibernation” mode. This applies to humans too. Less dopamine, more melatonin (these exist on an axis BTW) seems to cause some kind of “winter adaptation program” and gaining weight, becoming lethargic/sleepy, deterioration of blood glucose (higher levels) are all part of it.

  My money is on it being triggered by increased glucose, as increased glucose indicates to the brain it is early fall, which then logically means winter is coming. The reason carbohydrate is fattening is because peak carbohydrate consumption occurs during the months preceding winter in a natural environment.

  But I am really going on a tangent here. Heh.

• 13 ItsTheWooo // Apr 9, 2009 at 1:29 pm

  Sandra – genetics are absolutely required to become overweight. Here is an interesting exercise. Stand outside an amusement park or a tourist trap and watch parents and children together. It is amazing, the kids look like little clones of the parents. The way their body fat is stored, AS WELL as their level of fatness, is identical generation to generation. When I did this once, it became so clear to me that weight is entirely hormonally and genetically determined.

  But, yes what we eat is the determining factor, genes just give us the potential, what type of diet we eat determines if I am 260 pounds like my mother or 125 pounds like myself. I store weight exactly like my mother, I am like her in so many ways, and my high weight was 280 (I actually surpassed her high weight, probably because I was eating more carbs than she eats)… but I was able to escape that fate by educating myself in depth and learning about what truly causes obesity for the vast majority of people. And for the majority of people it is carbohydrates that primarily lead to obesity. I stopped eating carbs, and switched to eating fats, and it is only this way I am able to be thin.

  You don’t always have to cut calories to lose weight. I am telling you, though, that cutting sat fat calories and replacing them with carbs is the most inefficient way to go. For most people this is only going to produce more fat storage and more hunger because the underlying defect in obesity is hyperinsulinemia and deficient glucose oxidation capacity.

  I agree with your surmisation that what you eat matters. I not only agree, but I have known this first hand (anecdotally) as well as logically (through research).

  My problem is with the idea that fat, or even sat fat, is the major issue – the major issue is carbohydrate, fat is a passive actor which is only significant in that it worsens the insulinogenic effects of carbohydrate.

• 14 ItsTheWooo // Apr 9, 2009 at 1:49 pm

  Swivelchair – the problem with the idea that “all food contains the same amount of energy” is that it neglects to consider our body does not just handle all food the same. Eating is not like dumping coal into a furnace – our hormones control what happens to that energy. Our hormones determine if we make ATP, heat, muscle, bone, or visceral fat, or white adipose tissue. And let me tell you, it ain’t even remotely similar.

  Eat a 160 calorie twinkie.

  What you are putting in your body is a bolus of vegetable omega 6 fatty acids coupled with insulinogenic glucose/fructose from the sugar and starch. The omega 6 fats will produce an inflammatory reaction, especially coupled with an insulinogenic meal (e.g. the high starch/sugar content) since insulin seems to encourage more bioactivity of omega 6 PUFA via delta 6 desaturase and delta 6 desaturase is the “window” by which omega 6 reaks its havoc on the body.
  Now, to get to the nitty gritty of what the starch and sugars do. Glucose rises from the glucose portion, while the fructose portion gets TO BIDNESS telling your liver to make fatty acids. You know what that means. More fats in the blood stream, reduced glucose uptake and oxidation (cuz, ya know, mitochondria sort of like not being killed off by fatty acid toxicity and insulin resistance is the compensation, because higher insulin levels will hypothetically lower free fatty acids in a normal metabolism). This is an elaborate chemical way of your body saying “holy hell, partition all of this glucose and fat back into the adipose STAT before we kill off our already strained mitochondria”.
  So the insulin rises, fat-making enzymes rise, fat breaking enzymes decrease. We start laying down a nice and good pad of fat on our bodies.

  And then we get hungry. Even though we just ate a god damned twinkie an hour ago (which, correlates, with maximal phase 2 insulin release).

  Of course whether or not this actually happens inside of YOU depends on whether or not you are vulnerable to obesity… which is determined by a nebulous sea of genes affecting our physiology (neurotransmitters, hormones, receptors, blah blah blah). Some people can eat twinkies and feel energetic/full. People like me? Forget it. Lethargic and ravenous, within 1.5 hrs.

  Now, eat 160 calorie tin of sardines.

  What happens? The absence of carbohydrate means there is very little glucose rise after eating – only that which is related to an increase in fatty acids producing compensatory insulin resistance (and, this is minimal indeed since the fatty acids in sardines are omega 3s and monosaturates, which tend to enhance glucose disposal). There is minimal glucose, fructose, or omega 6 or sat fat… so glucose disposal and insulin levels remain normal.

  The bolus of protein means you have the building blocks to maintain muscle and bone, which tends to increase metabolic rate without leading to fat accumulation due to a favorable balance of glucagon/insulin from a protein food… whereas all the twinkie gave you was sugar, a big fat saggy bag of it. Your body can’t do anything with sugar except use it for energy, and if you didn’t eat sufficient proteins, your metabolism is going to be lower because there isn’t the substrate to maintain muslce/bone mass, which means the sugar has to be shunted into fat tissue (and, uncoupling proteins are suppressed by anything which so heavily weights toward insulin and away from glucagon, like a carbohydrate… whereas heat-producing uncoupling proteins are increased from protein food).

  Because insulin never increases ridiculously after eating your sardine snack, 1.5 hours later you are actually very full and energetic. You are not storing fat, but burning it more efficiently, as your low insulin levels liberate fat from fat tissue and glycogen. Your hypothalamus is detecting a bounty of nutrition; appetite is decreased accordingly, spontaneous activity increases as the natural result of having more energy substrate 1.5 hrs after a meal.

  Yea.

  WHat you eat matters a lot.

  We are not furnaces. Dump 160 cals of a twinkie, 160 cals of sardines, big time difference. You can have a lethargic 500 pound person who is shunting all food into fat and conserving energy via natural lethargic behavior, or a wirey thin person who is shunting all food into energy/head production and natural energetic behavior.

• 15 swivelchair // Apr 9, 2009 at 2:17 pm

  ITW thank you for both comments, and it is interesting how you relate this to seasonality. Fertility ties into this too.
  This relates also to temperature — something in the news lately with the whole brown fat thing.

  If there is increased glucose to the brain when there is decreased brown fat (because, who needs high-energy burning fat in the winter, when food is scarce) then that would explain the seasonality.

• 16 swivelchair // Apr 9, 2009 at 2:27 pm

  ITW, I thought there was just a study demonstrating that it was the total number of calories?
  NEJM Vol 360:859-873 February 26, 2009 Number 9; Comparison of Weight-Loss Diets with Different Compositions of Fat, Protein, and Carbohydrates; Frank M. Sacks, M.D., et al
  But even people who read that article don’t believe it. Here ‘s was the NEJM poll:
  On the basis of your reading of this article, do you believe that the composition of one’s diet with regard to fat, carbohydrates, and protein has an effect on one’s ability to lose weight?

  * Yes 46%
  * No 54%

  Will the research results reported in the article influence your advice to patients about weight loss?

  * Yes 51%
  * No 49%

• 17 Sandra // Apr 9, 2009 at 2:45 pm

  Wow, these statistics tell me that health care professionals, including physicians, are ignoring actual data. I do hope that people who advise others about diet and weight loss comprise 100% of the 51% who said that the article will influence their advice!

  So if you are on a calorie-deficit diet (these people ate 750 cals less than required to maintain their weight), composition doesn’t really matter. And if you overeat, composition does (or at least might) matter. Seems reasonable.

  This is very fascinating. Swivelchair, I can’t thank you enough for your web site, the stuff you post here is really fabulous.

• 18 swivelchair // Apr 9, 2009 at 9:59 pm

  Thank you Sandra. I do appreciate your comments, although your Stalinesque approach to pharmaceuticals and junk food puts you up there with the Soup Nazi. In Sandra-land, we would not have any anti-obesity meds, and the food in the grocery would all be cream of wheat.

• 19 ItsTheWooo // Apr 9, 2009 at 11:49 pm

  Hi SC,
  My understanding of brown fat thus far is it is actually most active in cold environments; the point of brown fat seems to be to produce heat to protect vital organs. That is why infants have so much brown fat – the homeostatic thermoregulation of infant nervous system is immature so brown fat substitutes as a way to help prevent vulnerable infants from succumbing to temperature. Infants become dehydrated and hypothermic extremely easily. Animals that hibernate also have a lot of brown fat.

  Regarding the study showing it is all “just calories” – more bad science from a bunch of obesity researchers who made their careers based in promoting the low fat lie. Now that it is blatantly obvious low fat is bullsh*t, cuz like all the most modern science shows carbohydrate reduction and consumption of fats like monosaturates and omega 3s are the most potent way to reverse metabolic syndrome and obesity, these guys are holding on tot he last bastion of credibility by defaulting to a more neutral position that all which matters is calories.

  They fanagled these results by using diets which really werent much different. The “high protein” group is going from 15% to 25%. The “high fat” group is going to a mere 40% (carbs are still a ridiculously high 35%).

  They won’t use a real low carb diet, because they know what will happen: the low carb diet will destroy the low fat diet, and that would be like knocking over an autistic child’s stack of toy cars. This is all they have. This is the result they WANT.

  Oh, and, even though they rigged the diets so that the changes between them were so slight that no meaningful differences could possibly result, the low carb/high protein diet still showed a trend of being superior to the other diets. Look at the graph:
  http://content.nejm.org/cgi/content-nw/full/360/9/859/F1

  It clearly shows a pretty significant advantage in weight loss for both the “high protein” and the “low carbohydrate” group. This is most apparent in participants who completed the study.
  The same trend was observed in waist circumfrence.
  Fat was pretty neutral (but, then again, the high fat group was eating a boat load of carbs so, that’s kinda like making it fight with one hand tied behind its back since fat makes carbs more insulinogenic).

• 20 Sandra // Apr 11, 2009 at 9:14 am

  I wouldn’t those differences significant. .6 pound in 2 years ? I think what it does tell us is that there isn’t one superior diet and there’s no need to force any particular diet on all dieters, because in the end the differences between them are very minimal. So choose what works best for you. ItsTheWooo, obviously the diet you’re on is working very very well for you and I’m sure many others too. And that’s a great thing. I couldn’t possibly do that diet, I would feel deprived and abnormal 24×7. I wouldn’t want to live like that. I need more carbs. I can still lose weight though, as long as I don’t overdo them. Diets can be tailored, that’s what this data tells us.

• 21 Sandra // Apr 11, 2009 at 9:19 am

  If we legalized drugs, made them available at every store 24×7, put them in the schools, encouraged parents to give them to their kids, and advertised them non-stop to encourage cravings … would we have an epidemic of addiction? I’m thinking it might end up like the so-called obesity epidemic, we’d zoom up to some max number of addicts and then taper off. Kids would be impacted the most.

• 22 swivelchair // Apr 11, 2009 at 10:20 am

  Thanks ITW. Maybe the data are hokeyed-up for publicity sake (I’m no big fan of NEJM), but still, you got me thinking about population genetics. There has got to be some genetic background in all of this because plainly, some populations are more prone to metabolic syndrome than others on a McWestern diet. One carb size doesn’t fit all.

  Think of Asian diet and body adiposity (in general) — lots of carbs (rice) and low fat, and low body fat. (Not to be biased, so please no one take offense, this is a sweeping generality. . . ). That seems to be increasing with the introduction of the McFood diet, high in fat and carbs. So this seems to have a genetic component.

  Here’s a paper on mice (ITW, are you a mouse? ) who lack a protein involved in the inflammatory cascade (phosphodiesterase 4B, “PDE4B”), and stay lean even when eating fat. This seems to support the “obesity as an inflammatory reaction” framework.

  I’m guessing: if there is a double dose of the PDE4B or some hyper-reactivity of the PDE4B pathway then you get hyperinflammation in white adipose tissue — increasing leptin production locally and in the systemic circulation.

• 23 Memo // May 4, 2009 at 12:00 pm

  Doesn’t fat also kill brain cells that get rid of fat?

• 24 swivelchair // May 4, 2009 at 5:32 pm

  Hi Memo. Yes, apparently so, per the above paper.

• 25 Harry Halina // May 29, 2009 at 1:08 pm

  I don’t think animal fat by itself causes the problem.

  The food industry has introduced bioengineering practices, antiobiotics, growth hormones, preservatives, etc. into the food supply chain.

  These toxic chemicals end up in the fat cells of our meat products – which eventually wind up in our bloodstream – poisoning our metabolic system.

  I think this is a BIG, BIG tragedy: the general population is led to believe that cancer and disease come from our genetics.

  So the medical industry continues to look for the “medicine” that will cure our ills – spending away all our money into fixing the disease after the fact.

  All we really need to do is FOCUS on PREVENTION.

  Stop the disease from occurring in the first place, simply by eating the way Mother Nature had designed it: free range chicken, grass-fed beef, and mercury-free seafood.

• 26 swivelchair // May 29, 2009 at 10:52 pm

  HH why do you think the prevention gig has been such a miserable failure? Why do you think people don’t exercise self control?

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