Low Fat Challenge?
The Ancestral Weight Loss Registry is running a contest. Find an RCT where LF bests LC. Here are the criteria. The proceeds go to prizes and NuSI.
- Randomized Control Trial comparing a low fat, calorie restricted diet to a low carbohydrate diet, with or without a calorie limit.
- Statistically significantly greater reduction in weight and/or fat in the low fat group as compared to the low carb group
- Low fat diet must be similar in macronutrient composition to standard american diet encouraged by the USDA, ~50-60% carbohydrates, 20-25% fat, 20-25% protein
- Low carbohydrate diet group must be encouraged to limit their carbohydrate intake to < 100 grams of carbohydrates per day, with or without calorie restriction
- Sample size should contain no less than 15 subjects in the experimental group (or 15 total if it is a crossover design).
My challenge for which you will receive a lifetime weekly Cherry Pickin' Martini (virgin or $toli) in the Asylum Lounge (sorry no substitutions) is to identify what is wrong with this challenge. I have several thoughts in mind.
Given that it is the "ancestral" weight loss registry, I wonder if peer review studies of ancestral cultures with no history of obesity or diabetes would be considered. Oh ... like ... what the Pima really ate? Naah ...
In LC trials, low-fat are always crappy diet providing 10-15g of fibers. That means that the low-fat group are eating high-sugar, processed food. I'm averaging 50g of fiber a day on my high-carb, lowish-fat (10-15%) diet.
LC brings water loss that low-fat don't.
LC usually result in greater lean mass loss (carbs are protein-sparing).
Here's a funnier challenge for them. Show a metabolic ward calories, protein controlled study where LC has any magic. Duh, done mutltiple time already, no magic.
LC will also most likely worsen most health markers in a non-sick, overweight, ie healthy population.
The criteria are overly restrictive. Almost all the "low-carb diets" in clinical trials are 20-30% carb, so at least 100 g/day. The few trials with carbs less than 100 g/day have been small and have not had a low-fat control group, rather a SAD control group typically eating 50% carb, 15% protein, 35% fat.
Worse yet, I'm wondering who or what body does the accounting for donations. I said in the past that Louis C.K. made at least a million dollars when he took his 'stand-up show' to the web and charged admission through PayPal. Read what happened:
Now, Louis has promoters, agent, accountant, etc. I'm wondering how all of this 'donate now' on the web stuff works for Ancestral Weight Loss Registry? If you ever find the guy living in the basement of his mom's house, with a post office box for 'Ancestral Weight Loss Registry,' let me know....
I'm left wondering where the other 60% goes!
I'm still wondering, although the first sentence of this paragraph claims that no donations will go to the AWLR, whether there is any accounting. Is there an address, for example, beyond an e-mail?
(Trad Pima diet: 70%-80% carbohydrates.)
Frank makes a great point about fiber too. Most of the LF diets are full of processed foods and bread and grains ground to dust and made into flakes and such are just not the same.
Eating just a standard mixed diet of vegetables, tubers and meat reached a much higher fibre number. Similarly, with even a calorie restricted McDougall or Fuhrman menu, one is looking at a very high fibre number around the 50+ gram figure.
I am also intrigued by the whole carcass mantra vis a vis fat consumption. Wild animals do not tend to have nicely marbled muscles or large fat pads. Except for brains and intestines, the organs are generally low fat as well.
Thus I don't know of any "high fat" diet that has been tested either. Even that study where they were supposed to aim for 50% they fell short and I think most who were included in the analysis were around 45% fat.
Unfortunately there will no bling-bling for me because it wasn't low fat enough. Can I still get money for saving Nutsci a bunch of time and money? :D
"Choose a diet that provides no
more than 30 percent of total calories from
fat." from (page 26): http://www.cnpp.usda.gov/Publications/DietaryGuidelines/1995/1995DGConsumerBrochure.pdf
That's from the 90s. From the 2010 guidelines they've expanded the range a bit: "adult ages 19 years and older: 20–35%"
from (page 24): http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2010/PolicyDoc/PolicyDoc.pdf
I don't know if the USDA ever recommended a diet with a fat content of 20-25%. I imagine that studies are using the USDA guidelines to define low fat, so they will all by definition contain 30% fat. It seems the Ancestral Weight Loss Registry people have set us at an impossible task and I figure they know it.
you can get an idea of how much fiber you eat - if you eat some bananas, blueberries, frozen cherries, sweet potatoes you will get much more fiber than you think.
You can have all the markers, I will keep the quality of life, thanks.
I don't buy too much into the malnutrition in formative years thinking because a) it is very hard to define and varies; highly subjective and far too trivial towards u-curves and j-curves. And b) I have seen too many contrary anecdotes in my own life, even if I don't claim to carry as much experience as others. If that model was refined and actually studied in detail rather than lots of jibber jabber over epidemiology, then we'd certainly have something to talk about. However, as it stands, this model is still a template for those people over at 180degreehealth to interpret gestinational diabetes as good - fatter baby as high IQ Übermensch - brostatic levels of speculation that is just baffling.
Durian rider probably s*its like a rabbit except more messy.
Are you telling me you don't think proximate markers of health are important? That's about the best we can do with short-term RCTs in nutrition. You'll never get a long-term, low-fat vs low-carb study with mortality. So we're stuck with epidemiological evidences and proximate markers of health in humans and animal studies.
But if you are healthy, ie non-overweight, with TC under 150mg/dl, great glucose control, going LC will most likely worsen your markers (which you seem to think are irrevelant)
If you look at this paper for example
Cholesterol feeding from eggs results in an increase from inflammatory markers only in the insulin sensitivive individual, not in the insulin resistant individual.
In the kanwu study, SFAs impairs IS in healthy individuals.
Since i'm healthy, nonobese and have a very good IS, have low LDL level, I see no reason to consume nutrients/food that are shown to worsen my IS, increase my inflammation markers and increase my LDL levels. That to me is quality of life because i've never known worse.
Insulin sensitivity determines the effectiveness of dietary macronutrient composition on weight loss in obese women.
Cornier MA, Donahoo WT, Pereira R, Gurevich I, Westergren R, Enerback S, Eckel PJ, Goalstone ML, Hill JO, Eckel RH, Draznin B.
Department of Medicine, University of Colorado Health Sciences Center, Denver, CO, USA.
To determine whether macronutrient composition of a hypocaloric diet can enhance its effectiveness and whether insulin sensitivity (Si) affects the response to hypocaloric diets.
RESEARCH METHODS AND PROCEDURES:
Obese nondiabetic insulin-sensitive (fasting insulin < 10 microU/mL; n = 12) and obese nondiabetic insulin-resistant (fasting insulin > 15 microU/mL; n = 9) women (23 to 53 years old) were randomized to either a high carbohydrate (CHO) (HC)/low fat (LF) (60% CHO, 20% fat) or low CHO (LC)/high fat (HF) (40% CHO, 40% fat) hypocaloric diet. Primary outcome measures after a 16-week dietary intervention were: changes in body weight (BW), Si, resting metabolic rate, and fasting lipids.
Insulin-sensitive women on the HC/LF diet lost 13.5 +/- 1.2% (p < 0.001) of their initial BW, whereas those on the LC/HF diet lost 6.8 +/- 1.2% (p < 0.001; p < 0.002 between the groups). In contrast, among the insulin-resistant women, those on the LC/HF diet lost 13.4 +/- 1.3% (p < 0.001) of their initial BW as compared with 8.5 +/- 1.4% (p < 0.001) lost by those on the HC/LF diet (p < 0.04 between two groups). These differences could not be explained by changes in resting metabolic rate, activity, or intake. Overall, changes in Si were associated with the degree of weight loss (r = -0.57, p < 0.05).
The state of Si determines the effectiveness of macronutrient composition of hypocaloric diets in obese women. For maximal benefit, the macronutrient composition of a hypocaloric diet may need to be adjusted to correspond to the state of Si.
He eats 92 grams of fibre a day in my analysis
low fat has its demerits on markers as well. As careful a researcher as Chris Gardner (who ran the biggest blinded RCT trial on garlic supplements) listed some near the end of his talks on the ATOZ diet.
The evidence in favor of HDL keeps weakening
Individual with genetically high HDL level don't have decrease risk of CHD, whereas individual with genetically high LDL level such as in familial hypercholesterolemia die of incredebly young age from CHD.
There was another recent study showing no reduce CHD event from higher HDL but I can't find it at the moment.
I agree about high triglycerides certainly not being a good thing. I'll keep monitoring mine but so far they are fine, I might just add some mono/poly-rich food back at some point if it gets too high.
I still think that the evidence are pointing toward lowering LDL/TC as the main effective prevention strategy. Just the case of familial hypercholesterolemia is pretty damning when you think about it. These people have very high TC level, and they can die as young as in their 20' from CHD.
A Low-Glycemic Load Diet Facilitates Greater Weight Loss in Overweight Adults With High Insulin Secretion but Not in Overweight Adults With Low Insulin Secretion in the CALERIE Trial
Anastassios G. Pittas, MD1, Sai Krupa Das, PHD2, Cheryl L. Hajduk, MS, MPH, RD2, Julie Golden, MD2, Edward Saltzman, MD2, Paul C. Stark, SCD3, Andrew S. Greenberg, MD12 and Susan B. Roberts, PHD2
1Division of Endocrinology, Diabetes, and Metabolism, Tufts-New England Medical Center, Boston, Massachusetts
2Energy Metabolism Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston, Massachusetts
3Institute for Clinical Research and Health Policy Studies, Tufts-New England Medical Center, Boston, Massachusetts
In a 6-month controlled feeding trial in healthy overweight adults with normal glucose tolerance, we tested the hypothesis that individuals with higher insulin secretion lose more weight when randomized to a low–glycemic load diet compared with a high–glycemic load diet.
The main finding from this pilot study was that healthy overweight women and men with relatively greater insulin secretion in response to a standard oral glucose tolerance test lost more weight when assigned to a low–glycemic load hypocaloric diet than to a high–glycemic load diet, but there was no differential effect of the two diets on weight loss in individuals who had relatively lower insulin secretion.
Data from human studies on whether insulin secretion predicts future weight gain (4,6,27–29) or affects the ability of overweight individuals to lose weight in response to a hypocaloric diet (7,30) are controversial. However, the influence of postchallenge hyperinsulinemia on weight loss may be particularly important for specific dietary compositions, in particular diets that differ in glycemic load or glycemic index, as suggested by animal studies (31–33). High–glycemic load diets increase postprandial hyperinsulinemia, which favors fatty acid uptake, inhibition of lipolysis, and energy storage leading to weight gain (34). High–glycemic load diets also lead to other postprandial metabolic changes, including a lower glucose nadir and increase in counterregulatory hormones that may explain increased hunger and increased energy intake in the postabsorptive period, presumably leading to weight gain over time (32). All of these mechanisms may be exacerbated in individuals with high insulin secretory capacity at baseline, which makes them more susceptible to weight gain upon exposure to a high–glycemic load diet (35). These individuals can be hypothesized to do best on low–glycemic load diets, a hypothesis supported by our present findings.
He seems to think he's a wiz kid that's going to bring The Truth to the ignorant world. First he talks about his iPhone app that will overcome the inaccuracy of self-reporting in diet studies. Then he talks about how great his self-reported (and self-selected) registry is. (Apparently all LCers lose weight effortlessly without hunger as opposed to LFers.)
Then I self-selected to not finish watching.
Of note there, "The favourable effects of substituting a monounsaturated fatty acid diet for a saturated fatty acid diet on insulin sensitivity were only seen at a total fat intake below median (37E %)."
Once again, it is quantity that matters most. Yet to be a big hit on the internet, you have to take an extreme position so that you stand out from the herd - and you end up as a VLC or VLF food-banner.
That's an isoenergetic diet, btw.
1) Um, unless they are calorie-alike this seems like a huge problem. Just pick one non-calorie controlled LF and one calorie controlled LC and boom.
2) They even note that hundreds of studies show no difference, this means that by selecting two to compare and ignoring the rest is classical file drawer problem. Heck the more times you run a similar study the more likely that one will show statical significance by accident and significance should be evaluated in light of the other studies as well.
3) The linked document is hardly SAD and does not show an ideal macro breakdown
4) Very loose guidelines for what counts as "low carb" makes it easier to drum up some study
5) Tiny study side when they fully admit that there are hundreds of studies that show no difference. A group of 15 would hardly show statical significance.
Just reading some of the rest of the page and it's scandalous how far they take this. Classical conspiracy thinking of pattern matching to previous events. They pinpoint dietary recommendations to americans, but their charts show a global change in obesity rates that are near proportional, that tells me that the FDA's recommendations can NOT be the source but some other out side factor.
Their quote from Percy was the fact that dietary choices should be a personal matter, yet they go on to insinuate that LC should have been chosen.
I swear people get on the LC wagon and their brain shuts down.
Effects of Dietary Composition on Energy Expenditure During Weight-Loss Maintenance
After achieving 10% to 15% weight loss while consuming a run-in diet, participants consumed an isocaloric low-fat diet (60% of energy from carbohydrate, 20% from fat, 20% from protein; high glycemic load), low–glycemic index diet (40% from carbohydrate, 40% from fat, and 20% from protein; moderate glycemic load), and very low-carbohydrate diet (10% from carbohydrate, 60% from fat, and 30% from protein; low glycemic load) in random order, each for 4 weeks.
Compared with the pre–weight-loss baseline, the decrease in REE was greatest with the low-fat diet (mean [95% CI], –205 [–265 to –144] kcal/d), intermediate with the low–glycemic index diet (–166 [–227 to –106] kcal/d), and least with the very low-carbohydrate diet (−138 [–198 to –77] kcal/d; overall P = .03; P for trend by glycemic load = .009). The decrease in TEE showed a similar pattern (mean [95% CI], −423 [–606 to –239] kcal/d; −297 [–479 to –115] kcal/d; and −97 [–281 to 86] kcal/d, respectively; overall P = .003; P for trend by glycemic load < .001). Hormone levels and metabolic syndrome components also varied during weight maintenance by diet (leptin, P < .001; 24-hour urinary cortisol, P = .005; indexes of peripheral [P = .02] and hepatic [P = .03] insulin sensitivity; high-density lipoprotein [HDL] cholesterol, P < .001; non-HDL cholesterol, P < .001; triglycerides, P < .001; plasminogen activator inhibitor 1, P for trend = .04; and C-reactive protein, P for trend = .05), but no consistent favorable pattern emerged.
Among overweight and obese young adults compared with pre–weight-loss energy expenditure, isocaloric feeding following 10% to 15% weight loss resulted in decreases in REE and TEE that were greatest with the low-fat diet, intermediate with the low–glycemic index diet, and least with the very low-carbohydrate diet.
"Our results do not confirm the findings of the KANWU study (7), which also used an IVGTT and a similar dietary prescription to replace SFAs with
MUFAs for 3 mo"
"the difference between treatments was of borderline statistical significance (P = 0.053). Further analysis suggested a significant difference (P = 0.03) in subjects who consumed ,37% of energy as fat during the study period, but the justification of conducting this post hoc comparison is questionable (30) because there was no evidence that the treatment effects differed in the different subgroups (P = 0.26; Lars Berglund, personal communication, 2008)."
They MUST be isocaloric diets.
“Other than simple curiosity about our ancestors, why do we care whether an adult from 4,000 years ago could drink milk without getting a stomachache? The answer is that these samples are revolutionizing our ideas about the speed at which our evolution has occurred, and this knowledge, in turn, has made us question the idea that we are stuck with ancient genes, and ancient bodies, in a modern environment. We can use this ancient DNA to show that we are not shackled by it.”
“In short, we have what the anthropologist Leslie Aiello, president of the renowned Wenner-Gren Foundation for Anthropological Research, called “paleofantasies.” She was referring to stories about human evolution based on limited fossil evidence, but the term applies just as well to the idea that our modern lives are out of touch with the way human beings evolved and that we need to redress the imbalance. Newspaper articles, morning TV, dozens of books, and self-help advocates promoting slow-food or no-cook diets, barefoot running, sleeping with our infants, and other measures large and small claim that it would be more natural, and healthier, to live more like our ancestors. A corollary to this notion is that we are good at things we had to do back in the Pleistocene, like keeping an eye out for cheaters in our small groups, and bad at things we didn’t, like negotiating with people we can’t see and have never met.”
“Grinding and cooking grain is a practice that goes back perhaps as far as 30,000 years. By contrast, brussel sprouts appear to be just a few hundred years old and until the 16th century Native American populations were the only people eating tomatoes or hot peppers. None of which is to say that adopting a paleo diet won’t “work.” Any sufficiently stringent, somewhat arbitrary set of dietary restrictions is likely to lead you to snack less and be more mindful of what you’re eating. But the paleo concept is a marketing gimmick that doesn’t have much basis.”
“Four years ago, biology professor Marlene Zuk was attending a conference on evolution and diseases of modern environments. She sat in on a presentation by Loren Cordain, author of “The Paleo Diet” and a leading guru of the current craze for emulating the lifestyles of our Stone-Age ancestors. Cordain pronounced several foods (bread, rice, potatoes) to be the cause of a fatal condition in people carrying certain genes. Intrigued, Zuk stood up and asked Cordain why this genetic inability to digest so many common foods had persisted. “Surely it would have been selected out of the population,” she suggested.
Cordain, who has a Ph.D in exercise physiology, assured Zuk that human beings had not had time to adapt to foods that only became staples with the advent of agriculture. “It’s only been ten thousand years,” he explained. Zuk’s response: “Plenty of time.” He looked at her blankly, and she repeated: “Plenty of time.” Zuk goes on to write, “we never resolved our disagreement.””
” generalizations about the typical hunter-gatherer lifestyle are spurious; it doesn’t exist. With respect to what people ate (especially how much meat), the only safe assumption was “whatever they could get,” something that to this day varies greatly depending on where they live. Recently, researchers discovered evidence that people in Europe were grinding and cooking grain (a paleo-diet bugaboo) as far back as 30,000 years ago, even if they weren’t actually cultivating it. “A strong body of evidence,” Zuk writes, “points to many changes in our genome since humans spread across the planet and developed agriculture, making it difficult at best to point to a single way of eating to which we were, and remain, best suited.”
Social and family relationships, too, vary greatly. But to draw conclusions about ancestral hunter-gatherers by examining diverse forager communities existing now, as some anthropologists do, is dubious in itself. Tribal people, too, have had tens of thousands of years to evolve. And unlike paleolithic hunter-gatherers, they live on the margins of developed societies and are almost always affected by them in some way.
Furthermore, the fossil record of the Stone Age is so small and necessarily incomplete that its ability to tell us about paleolithic society is severely limited. Consider this: For all we know, the first tools were not stone implements but woven slings designed to allow a mother to carry an infant while foraging; it’s just that stone happens to survive longer than fibers.
Why are we so intent on establishing how paleolithic people ate, exercised, coupled up and raised their kids? That’s a question Zuk considers only in passing, but she hits the nail pretty solidly on the head: “We have a regrettable tendency to see what we want to see and rationalize what we already want to do. That often means that if we can think of a way in which a behavior, whether it is eating junk food or having an affair, might have been beneficial in an ancestral environment, we feel vindicated, or at least justified.” Even if we wanted to live like cavemen, Zuk points out (noting that the desire to do so somehow never seems to extend to moving into mud huts), we couldn’t. In reality, we don’t have their bodies, and don’t live in their world. Even the animals and plants we eat have changed beyond recognition from their paleolithic ancestors. It turns out we’re stuck being us.”
“Genes continuously appear in and disappear from the human genome. Some remain for millions of years, others for much shorter periods, Zuk says. Evolution is a series of compromises and tradeoffs because genes have more than one function, and interact in complicated ways.
Some of the work Zuk and her students have been doing on crickets found in Hawaii shows that a completely new trait, a wing mutation that renders males silent, spread in just five years, fewer than 20 generations.
If we want to learn from evolution, Zuk says, we should study rapid evolution rather than “holding up our flabby selves against a vision – accurate or not – of our well-muscled and harmoniously adapted ancestors” to understand how we have adapted to relatively recent changes in our environment and how we may continue to adapt as our environment changes.”
Effect of 6-Month Calorie Restriction on Biomarkers of Longevity, Metabolic Adaptation, and Oxidative Stress in Overweight Individuals
A Randomized Controlled Trial
Intervention Participants were randomized to 1 of 4 groups for 6 months: control (weight maintenance diet); calorie restriction (25% calorie restriction of baseline energy requirements); calorie restriction with exercise (12.5% calorie restriction plus 12.5% increase in energy expenditure by structured exercise); very low-calorie diet (890 kcal/d until 15% weight reduction, followed by a weight maintenance diet).
Conclusions Our findings suggest that 2 biomarkers of longevity (fasting insulin level and body temperature) are decreased by prolonged calorie restriction in humans and support the theory that metabolic rate is reduced beyond the level expected from reduced metabolic body mass. Studies of longer duration are required to determine if calorie restriction attenuates the aging process in humans.
Energy requirements at baseline were individually calculated from measured energy expenditure. Menus were then prescribed for each participant within 100 kcal of his/her daily target intake. Menus were designed using Moore's Extended Nutrient Database (MENu 2000, PBRC, Baton Rouge, La) and ProNutra 3.0 (Viocare, Princeton, NJ). Participants were provided with all their food from the last 2 weeks of baseline through week 12. Participants ate 2 meals at the center each weekday, with 1 meal plus snacks packaged for take-out. During weeks 13 through 22, participants self-selected their diet based on individual calorie targets. During weeks 22 through 24, 2 meals per day were provided at the center, with 1 meal and snacks for take-out. All diets (except the very low-calorie diet) were based on American Heart Association recommendations (≤30% fat). The very low-calorie diet was 890 kcal/d (HealthOne, Health and Nutrition Technology, Carmel, Calif) given as 5 shakes containing 75 g of protein, 110 g of carbohydrate, 5 g of fat plus a 10-g bolus of fat per day. Once target weight loss (−15%) was achieved, participants in the very low-calorie diet group were slowly refed to an energy level that maintained body weight. Generally, target weight was achieved by week 8 in men and by week 11 in women.
The results of this study show that prolonged calorie restriction by diet or by a combination of diet and exercise was successfully implemented as evidenced by reduced weight, fat mass, fasting serum insulin levels, and core body temperature. This study is unique in that individual energy requirements were carefully measured at baseline and individualized diet goals were determined for each study participant. Furthermore, we observed that “metabolic adaptation” develops in response to energy deficit in nonobese humans at 3 and 6 months leading to reduced O2 per unit of FFM, even after weight stability is achieved. Finally, this study confirms previous findings that calorie restriction results in a decline in DNA damage. However, longer-term studies are required to determine if these effects are sustained and whether they have an effect on human aging.
"A low carb diet does not work when there is adrenal fatigue. (Or to put in more modern terms: HPA axis dysfunction).
A somewhat out-dated term, adrenal fatigue presents with abnormal DHEA and cortisol on saliva test. In reality, it’s more about the nervous system than the adrenal glands. The modern term is hypothalamic-pituitary-adrenal (HPA) axis dysfunction. Essentially, the nervous system is over-stimulated, and cortisol and DHEA struggle to keep up with that. The symptom of low blood sugar is common.
The adrenal-kind of “low blood sugar” is not a problem with insulin, but rather a problem with neurotransmitters and stress hormones. For those with HPA dysfunction, cortisol is both too low (daytime) and too high (night-time). Furthermore, the body may not be responding to cortisol the way that it should. (Thanks to Chris Kresser for making me aware of cortisol resistance.)
Other symptoms of HPA dysfunction include: Anxiety. Low or high blood pressure. Dizziness. Brain fog. Insomnia. It is sometimes associated with autoimmune thyroid disease.
Gentle Carbs calm the nervous system
What are Gentle Carbs? In a word, they are starchy foods that are not inflammatory. They do not spike insulin and stress hormones.
In contrast are the un-gentle Carbs: 1) Gluten grains and 2) Refined sugar. Single-handedly those two foods generate more inflammation, more impaired insulin response, more HPA dysfunction than any other food. But why should their crimes cast aspersions on their non-inflammatory carb-cousins rice and potato?
Gentle carbs are rice, potato, sweet potato, squash, beet. When combined with protein, fat and vegetables, rice of any kind is low glycemic. Not that I find GI a useful concept, but I just want to make the point that the rice does not need to be low GI basmati or brown. It can be white rice, but not a bowl of white rice with nothing else. A serving of rice with butter, lamb cutlets and broccoli (for example).
Let me say this: I think that for many people, rice is healthier than fruit (because it doesn’t contain fructose)."
"Dietz and a colleague analyzed trends since the 1970s and found that among adults, average daily energy intake rose by a total of 314 calories from 1971 to 2003, then fell by 74 calories between 2003 and 2010.
Seventy-four calories is a lot, and as I said before, we would expect to see a measurable impact on obesity," said Dietz.
The CDC released similar results last month for children: boys have cut their calorie intake by 150, and girls by 80, since 1999. Obesity rates for boys continue to increase, however, while holding steady for girls."
This goes against the LC/Paleo fantasy that has been repeated (last October here, e.g) that SFA somehow magically lowers LDL. This also goes against the idea that lots of SFA results only in bigger LDLs - here we see more LDLs. RISCK was an isoenergy study.
Also, low GI generally beat high GI. I don't see why GI became passe' in the world... maybe because the "lose weight by eating low GI" fad was a failure.
Maybe it's time to just stop doing studies based on self-reported consumption.
My main point about the study though was about the KANWU comments. The KANWU study is constantly cited as evidence that saturated fat impairs Si when really it shows no such thing.
Otherwise, just hedge all bets by eating a variety - unless a person has a really, really good reason to follow some extreme diet -- like an epileptic going for ketosis, or somebody tracking LDL-P and finding paradoxical results in their own case.
Or there's also this, since you mention GI: why not buy the old-fashioned oats and skip the quick-cook stuff, since you get possible benefits from the lower GI and there's no big accommodation required.
Wrt to these particular studies, they're talking about MUFA -- not about Olive Oil which has plenty of SFA anyway. I don't see myself searching out pure MUFA sources.
There is also this one from 2009: "Randomized clinical trial of standard dietary treatment versus a low-carbohydrate/high-protein diet or the LighterLife Programme in the management of obesity", where VLCD meal replacements gave a much greater weight loss than low-carb/high-protein (<40 g carbs/day) (-15.1 kg vs. -1.9 kg after 9 months).
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