A Question about the latest diet study ...
As you may have heard there's a new LC vs. LF diet RCT out there. I'll have more to say about that when some time frees up, but I have had a chance to look at the full text and it is quite the horribly conducted study -- at least by the description put forth in a fairly highly regarded peer review journal. (disturbing ....)
In any case, the LC group was instructed to keep carbs under 40g per day. If you arm a person with some tables of carb content or links to online databases, etc., this is a pretty straight forward and "simple" task. By that I mean, disregarding any issues with compliance, the task remains an easy and straightforward one.
The LF group was instructed to reduce total fat to a maximum of 30% of calories and sat fat to a maximum of 7%. We are then told that no calorie goals were specified (for either group).
Pray tell, how does the LF group accomplish their goal?
Comments
But why the saturated fat restriction? Meat restriction is already guaranteed by the low fat requirement. I suspect another vegetarian sponsored study which means more than usual scrutiny for dirty tricks.
Does the study show what was actually chosen for the menu? Many fish including some shellfish are low fat. and it would interesting to see if that is a food choice. For either group.
When or where can we read about this study? 40 grams of carbs is a true low carb diet but I wonder if 70-100 grams in the LC is more in keeping in spirit with 30% fat for the LF group. 30% per cent fat is in the range of popularly accepted healhy fat ranges while 40 grams is considered by many as being too low for health (in the long run). In other words, it looks like a moderate LF diet vs an extreme LC diet. So the question is, what is exactly being tested?
I don't think animal protein had to be restricted much to get to 30% fat. It's at the truly low fat levels that you have to forgo at least some animal protein. To get to 30% you probably have to cut back on deep fried foods and processed packaged foods.
"At 12 months, mean total energy intake on the low carbohydrate diet was 1,448 kcal/day with 23.6% from protein, 40.7% from fats, and 34.0% from carbohydrate versus 1,527 kcal/day with 18.6% from protein, 29.8% from fats, and 50.0% from carbohydrate on the low fat diet."
Guess it was the calorie restriction that caused the weight loss.
How many studies have shown a negative effect from a long-term low carb diet?
Not one... there are no long-term controlled studies of a low carb diet - so when people talk about this issue as if they know what "healthy" is, they are really talking out their ass.
Shouldn't we focus on the important issue here - the LOWER carb diet beat the LOWER fat diet in basically every heart disease correlate/risk marker (kinda shocking given both diets seem heavily calorie restrictive - even though they didn't restrict either group)
(1450 and 1527 are both very low)
I would also point out that the carbs actually consumed were well above a low carb diet at 35% per commenter below.
It also sounds like you are asserting the lead researcher had some goal to reach this conclusion - read her CV - it's full of papers on cholesterol and fat's role in heart disease as well as quite a few on fruits and vegetables role in preventing it. (Standard lipid hypothesis CV)
^The person who ran the study talking about the study (lowish fat vs. lowish carb).
OK, now try again without the total calories ... which was the point of the question.
I haven't even commented on the research yet. I have hinted that I think the journal write up is poor. I'll expand on that when I discuss the study/article, but for now I'll say that the raw data is hopelessly obscured.
Not one... there are no long-term controlled studies of a low carb diet - so when people talk about this issue as if they know what "healthy" is, they are really talking out their ass<<<
(1) If there are such studies, why is Nina Teicholz going on any program that will have her claiming that such diets have unequivocally been proven to be healthier? The answer is that she is being dishonest in portraying the Shai diet trial as a test of any sort of low carb diet.
(2) Not only have there been no long term studies on this diet, but statistically zero human beings have ever eaten it. Ever. Meanwhile, there are billions of humans who have consumed upwards of 80% of their diets as carbohydrate, and many of the longest living cultures on the planet eat a higher percentage than we do. The LCHF diet is NOT the diet of the Inuit or the Masai.
Therefore it is those who are talking about LCHF as "healthy" who are really talking out of their asses. The burden of proof is on them to demonstrate that it is a healthy diet for the long term, not the other way around.
A VLC diet will leave you lethargic, constipated, sleep-deprived, insulin-resistant and unable to do any strenuous activity, along with screwing up your thyroid function... but you'll live. Keto advantage!
I look around and I see oceans of fat people suffering from chronic diseases resulting from chronically high sugar and insulin levels which in turn result from low-fat, low calorie diets they try to follow and the inherent substitution towards sugar and refined grain they cause.
It may be that a plant based diet is healthier - but the fact that everyone seems to "know this" and doesn't follow it, seems to indicate alternate messages need to be put forward.
" If the rule you followed brought you to this, of what use was the rule?"
-Cormac McCarthy
I always ate ridiculous amounts of food prior to high fat. (I would often eat an entire deep dish Giordano's pizza after work in college)
(If you've been to Chicago you know how much food that is)
I still do eat a lot:
1 cup heavy whipping cream a day. (Spread throughout - in coffee and drunk straight - love the taste)
2-4 table spoons coconut oil.
6-8 eggs yolks, 2-3 egg whites, boursin cheese (half pack) and shredded cheese on top with hot sauce.
2-3 pieces of bacon
Half a rotisserie chicken for lunch (split with coworker) - some days.
1 pound ribeye (costco) for dinner with a half stick of garlic butter and sparing amounts of boursin.
Occasionally small amounts of almonds (not daily)
The other thing I noticed was how easy it was to put on muscle - nobody apart from my girlfriend (who sees me workout) can believe I only workout 5 minutes or less a day - not sure if my results are due to higher testosterone from all the cholesterol in my diet but I'll sure take em' whatever it is.
People really shouldn't talk bad about ketosis until they've tried it for a few weeks. It's just like a runner hitting the wall - the more times you've gone through it and the longer you stay in it - the easier it becomes.
Odd Aside:
(runners hitting the wall is actually switching from glucose to FFA's and Ketones - so its the same process - indeed you hear the long-term runners talk about how much shorter the wall lasts the more you go through it)
A. You don't know that. (you don't know what all humans throughout history have eaten)
B. Native Americans in the plains often ate only Pemmican for vast periods of time (buffalo protein with tallow dripped into it) for months (particularly in the winter) - they were nomads so the only time in the northern midwest that food could be obtained from plants was what they could scrounge from the prairie when it was available. (Buffalo always were).
C. Inuits - even more-so.
D. I eat like that.
(I can't speak for Nina since I haven't read her book but I'd imagine her argument is more along the lines that we don't know, and that the evidence points to the low-fat diet as wrong and the high fat one as healthier - far from unequivocal - I assume like Taubes she urges us to do more science.
On Twitter, Thomas Dayspring stated that roughly 20-25% of people he's seen go on keto diets exhibit the hypercholesterolemia that Jimmy does -- at times TC > 400 , LDL-P > 3000, LDL-C > 300. NOBODY can say that this is not associated with increased risk just because fasting trigs and HDL are good.
This is my big problem with the promoters of this wholly untested diet, which the current trial doesn't even come close to resembling. For all the nonsense about how a low fat diet is untested, it remains nonsense. The vast majority of cultures favor a much lower fat intake than we even consider "low" (30% is a joke to call low fat). The advice is potentially dangerous.
You are also making assumptions that folks like myself have never been in ketosis and that would be highly erroneous. I don't experience any elevated mental function, rather the opposite as it is difficult to function on only 4 hours of interrupted sleep.
C -- The Inuit diet is roughly 45% protein, 55% fat on average and involved seasonal "starvation" with very low fat intakes. They were rarely in ketosis.
B -- Still statistically zero as you'll find most of the northern central plains Indians also consumed a lot of wild rice and potatoes that were preserved for the winter. There were many many more tribes besides the one that is highlighted in low carb lore, including tribes for whom maple sugare was a major dietary component. Let's not forget the rest of the continent either.
A -- No, it is not wildly unscientific. If you say that we can't know what humans ate in the paleolithic, I'd agree. Which is why you cannot *GUESS* that they were keto and claim this supports your diet. Of the cultures whose dietary traditions have been documented, there are isolated pockets that get up to perhaps 60% fat. Such diets were not keto.
So, like I said, it is irresponsible to recommend such a diet to others without expressing the necessary reservations. It is fraudulent to pass off short term trials that don't even test anywhere near the diet as support for the keto extreme.
If you haven't heard of ketosis-induced insomnia and lethargy, then you must have a black belt in confirmation bias. Google "ketosis insomnia." Thousands of threads about it (MDA, paleohacks, lowcarbfriends, myfitnesspal, etc., etc., etc.).
On a related note, this reminds me of when I left Christianity. So many Christians would talk to me as if I had never believed. I had to constantly remind them that I was a fundamentalist Christian for 40 years. So much polarity in religion, politics, sports and now, it appears, in friggin' diet! So tiring...
Now I self-appellate as an omnivore and have to explain that I am not a carnivore. I am going nameless soon.
I've tried both diets extensively (I once lost 30 pounds on 1000 calories a day and swimming 1000 meters each day) but eventually the hunger won over. (like I said - I have an incredible capacity to eat)
Low-carb is the only one that seems to regulate appetite effectively, this may lead to restriction and ultimate weight loss - but I'm not so sure since I saw my weight loss accelerate pretty massively when I kept eating what I was and turned the fat way up (more butter and coconut oil)
In the cases of the people who've seen my example (friends and coworkers) and did what I did, the number one reason was always fear of health risks (due to the perceived heart risk) as well as a firm belief in calories.
All who did it for more than a 2 months lost very significant weight and seem to have kept it off - even as they exempt whole days from the restrictions of the diet.
So the real answer to your question is that most people don't try it - and the ones who do invariably lose weight - this does not however mean that all stay on it.
" Among this sample of successful weight loss maintainers, maintenance of weight loss is associated with continued consumption of a healthy low-energy, low-fat diet."
http://www.nwcr.ws/Research/02.htm
The other massive issue that is overlooked is how the bacteria they find in the arterial macrophages along with the LDL of bypass patients is the same kind of bacteria that causes periodontal disease.
One thing I have noticed (along with my dentist) was how my teeth stopped developing plaque entirely on this diet. This of course is due to oral bacteria being unable to maintain numbers sufficient to quorum signal and form colonies using biofilm... perhaps the periodontal bacteria (different from the plaque bacteria) are somehow affected by the same process using simple sugars in the blood - I really wish they'd look at this more instead of perpetually treating people with statin drugs that show minimal efficacy and have skewed results due to the multiple interventions people engage in when they are prescribed. (i.e. lifestyle changes often accompany a diagnosis of heart disease as well)
I believe the only reasons that low fat diets ever show an improvement in heart disease mortality (its usually very small in real terms) is that they remove some of the things sugar can oxidize, but they only slow the process.
A simpler means may just be to get the sugar under some as of yet unknown threshold where the body can enzymatically manage glycation.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3342583/
My goodness! If a new healthy looking, normal weight patient showed up with an LDL-C ~ 230 mg/dL, we are all presuming that familial hypercholesterolemia is present. At the age of 54 we would be searching for arcus senilis, a sternotomy scar or xanthomata. Although there is no premature CHD, there are certainly cholesterol issues in her family. Although we do not have a baseline LDL-P or apoB, how can one go from a perfect lipid profile to a seeming very high risk one in a very short period of time? Can CV lipid/lipoprotein-related risk be worsened by the weight loss? Or perhaps the question is – does it matter what one consumes to lose weight? Is there a danger too low carbs/high fat in some people? Or how about this absurd question – can an LDL-P of ~2600 nmol/L not be associated with atherothrombotic risk? It has been reported for years that diets high in saturated fat raise TC and LDL-C and diets with reduced saturated fat lowers them (Evidence Level IA in NCEP ATP-III). MUFA and PUFA can be neutral or lower LDL-C. MUFA may raise HDL-C. Of course we now know what any therapy does to CV outcomes likely has little if any relationship to what that therapy does to HDL-C but the story that raising LDL-C is associated with or causal of atherosclerosis is widely accepted. I, other lipidologists, and many patients themselves, are starting to see that the above lipid response to a high fat diet as not being very rare response in people who abandon carbs and replace it with saturated fat, especially in those doing extreme carb restriction to achieve nutritional ketosis.
“Let’s get rid of the nonsense seen all over the internet that atherosclerosis is an inflammatory disease, not a cholesterol disease. That is baloney-with the reality being that it is both. One cannot have atherosclerosis without sterols, predominantly cholesterol being in the artery wall: No cholesterol in arteries – no atherosclerosis. Plenty of folks have no systemic vascular inflammation and have atherosclerotic plaque. However clinicians have no test that measures cholesterol within the plaque – it is measured in the plasma. It is assumed, that if total or LDL-C or non-HDL-C levels are elevated the odds are good that some of that cholesterol will find its way into the arteries, and for sure there, are many studies correlating those measurements with CHD risk. Yet, we have lots of patients with very low TC and LDL-C who get horrific atherosclerosis. We now recognize that the cholesterol usually gains arterial entry as a passenger inside of an apoB-containing lipoprotein (the vast majority of which are LDLs) and the primary factor driving LDL entry into the artery is particle number (LDL-P), not particle cholesterol content (LDL-C). Because the core lipid content of each and every LDL differs (how many cholesterol molecules it traffics) it takes different numbers of LDLs to traffic a given number of cholesterol molecules: the more depleted an LDL is of cholesterol, the more particles (LDL-P) it will take to carry a given cholesterol mass (LDL-C). The usual causes of cholesterol depleted particles are that the particles are small or they are TG-rich and thus have less room to carry cholesterol molecules. Who has small LDLs or TG-rich LDL’s? – insulin resistant patients! After particle number endothelial integrity is certainly related to atherogenic particle entry: inflamed endothelia have inter-cellular gaps and express receptors that facilitate apoB-particle entry. So the worse scenario is to have both high apoB andan inflamed dysfunctional endothelium. Is it better to have no inflammation in the endothelium – of course! But make no mistake the driving force of atherogenesis is entry of apoB particles and that force is driven primarily by particle number not arterial wall inflammation.”
Long-term weight loss maintenance
Results of random digit dial surveys indicate that ≈20% of people in the general population are successful at long-term weight loss maintenance. These data, along with findings from the National Weight Control Registry, underscore the fact that it is possible to achieve and maintain significant amounts of weight loss.
Findings from the registry suggest six key strategies for long-term success at weight loss: 1) engaging in high levels of physical activity; 2) eating a diet that is low in calories and fat; 3) eating breakfast; 4) self-monitoring weight on a regular basis; 5) maintaining a consistent eating pattern; and 6) catching “slips” before they turn into larger regains. Initiating weight loss after a medical event may also help facilitate long-term weight control.
Additional studies are needed to determine the factors responsible for registry participants' apparent ability to adhere to these strategies for a long period of time in the context of a “toxic” environment that strongly encourages passive overeating and sedentary lifestyles.
http://www.ncbi.nlm.nih.gov/pubmed/9550162
Persons successful at long-term weight loss and maintenance continue to consume a low-energy, low-fat diet
RESULTS:
Successful maintainers of weight loss reported continued consumption of a low-energy and low-fat diet. Women in the registry reported eating an average of 1,306 kcal/day (24.3% of energy from fat); men reported consuming 1,685 kcal (23.5% of energy from fat). Subjects in the registry reported consuming less energy and a lower percentage of energy from fat than NHANES III subjects did. Subjects who lost weight on their own did not differ from those who lost weight with assistance in regards to energy intake, percent of energy from fat, or intake of selected nutrients (iron; calcium; and vitamins C, A, and E). In addition, subjects who lost weight on their own and those who lost weight with assistance met the RDAs for calcium and vitamins C, A, and E for persons aged 25 years or older.
APPLICATIONS:
Because continued consumption of a low-fat, low-energy diet may be necessary for long-term weight control, persons who have successfully lost weight should be encouraged to maintain such a diet.
Any thoughts as to what that might be??
https://www.lipidcenter.com/pdf/Understanding_the_Entire_Lipid_Profile.pdf
http://plantpositive.com/
or this site also:
http://healthylongevity.blogspot.it/
CALORIE INTAKE IN RELATION TO BODY-WEIGHT CHANGES IN THE OBESE
So, with a 2,000-calorie intake and 35% of calories from fat -- participants would actually have to eat an additional 300 calories of carb & protein (whether they were hungry or not) in order to transform that 35% into 30%. It's a lower percentage, but still the same amount of fat & an extra 300 calories, to boot.
Obviously, I don't know for sure if this happened, but it seems plausible, and if it did, the methodology itself could have led the low-fat group to overeat. Not good.
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