Anyone done the Whole9 30 day challenge (Paleo diet)?

[DSeid]

@Renee

… disagree with DSeid …

Renee, could please clarify for me what you disagree with me on?

My points have been:

The actual diets of Paleolithic modern humans was high in game (marrow and organs inclusive) and various aquatic species, and some portion of gathered vegetables and fruits when available. Some at more plants, some less, some more total fat, some less.

None of them ate all that much SFA. Game (marrow and organ meat inclusive) and aquatic species are fairly low in SFA and relatively high in MUFA/PUFA/omega 3’s. All diets that consist of mostly game and aquatic species have been shown to have relatively low SFA, including those that include chewing on whale blubber and drinking rendered seal fat. Paleolithic humans did not eat much SFA and per unit protein they ate quite little. Any media savvy guru who states otherwise is misrepresenting what the science is. Ample cites for this have been provided. Anyone who claims otherwise should volunteer exactly from what source those ancestral peoples were getting all that saturated fat since it was not from the game or from the aquatic species in their diet.

Modern grain fed beef, butter, lard, etc., OTOH are all extremely high in SFA and low in MUFA/PUFA/omega 3’s. Compared to game they are low in protein. Eating lots of that is doing a poor job of replicating Paleolithic dietary habits.

Multiple expert panels have reviewed the huge breadth of studies on fats in the diet and they have all concluded that a diet high in SFA and low in MUFA/PUFA/omega 3 is harmful compared to a diet low in SFA and high in MUFA/PUFA/omega 3. A diet of modern grain fed beef, especially one that adds in extra full fat cheese and lard is extremely high in SFA and very low in MUFA/PUFA/omega 3’s; not very Paleolithic and according to current expert consensus, very likely very harmful. (If I stated that imprecisely in post 105, I aplogize.) Certainly SFA are not the single factor in CHD. Large amounts of simple carbs may even be worse. Trans fats certainly are (but no, typical home cooking with modern canola or olive oil does not result in large amounts of trans fats … not eating at home often does). Neither of those points alters the fact however that adding lots of saturated fat (rather than adding modest portions of MUFA/PUFA/omega 3s, which was I thought clearly implied in that post) is indeed harmful.

That said high fat/low carb diets (not similar to what most pre-agricultural humans ate) can “work” for some people. The “Paleo” diet that is the subject of this thread’s op is, minimally, a huge step up from the usual American crap. If it works for you that is a wonderful thing. But remember that at least a modest amount of vegetables and berries and nuts are part of his plan too. Grass fed beef. Lots of fatty fish.

Still the article I just posted above, that very large prospective cohort study, should give one pause about staying on such a diet forever. Minimally it demonstrates that the demonization of a vegetable predominant low carb high protein diet (inclusive of beans and tofu) as much more harmful than an animal based one, is false.

What part of that do you disagree with and what is the reasoning behind that disagreement?
My suspicion is that a diet high in complete protein (be it from game, fish, dairy, or a combination of plant sources, or all of them put together), low in SFA, high in MUFA/PUFA/omega 3’s (from animal or plant sources), high in antioxidants from plants (and other beneficial phytochemicals), low in simple carbs, high in fiber, and relatively low in salt, will be healthy. And that does happen to be the ancestral nutritional profile. Today’s meat just travels with bad company so getting to that diet with large amounts of fatty meat, let alone added lard, is not gonna happen. I choose to do it with modest amounts of lean meats, game when I can, poultry, fish, nonfat dairy (Greek yogurt and whey powder), tofu, beans, lots and lots of nuts and seeds (mostly raw and unsalted and with dried fruits), lots of vegetables and other fruits, sweet potato, seiten (wheat gluten), olive and canola oil, and only small portions of breads and starches. With some flexibility. And exercise, HIIT of wide sorts, weight training, and long runs/bike rides (but the latter two more just because I enjoy it). I take fish oil caps and turmeric caps too. And add some ground flax seed and chia to my yogurt (along with nuts or raw sunflower or pumpkin seeds, dried cranberries or cherries or fresh berries, maybe some “Go Lean” high protein high fiber cereal and sometimes some raw unsweetened cocoa). That’s what works for me and I am a foodie. I just find my vegan meals often more interesting, tasty, and fun, than my meat based ones. Others would find that unpalatable. Do what works for you.

[Renee]

Actually, you’re right, I don’t disagree with much of that. I apologize, I was caught up in how irritated I was with Stoid’s attitude that I didn’t read carefully. Your current diet sounds very much like what I used to eat 6 months ago, but I still struggled with cravings for bread and sweets, and always felt like I was dieting. I’ve have seen a lot of improvements in my health since I gave up grains, so I do think there is something to the grains aren’t great thing, and I think it’s ideal to give up processed sugar completely. I realize this is anecdotal, but one’s personal experience does tend to be powerful. After reading “Good Calories, Bad Calories” (have you read that? What did you think?) it seems that the science on fat/saturated fat is extremely muddled and misinterpreted, and that it is difficult for scientists to see past the demonization of fats that has been going on for decades.

Obviously, diet is an extremely difficult thing to study in humans, and the paleo movement is so varied and new that I’m not sure any of the current studies really address it. You’re right that today’s meat travels with bad company, which makes the affects of high saturated fat difficult to separate out from the effects of crap carbs.

I will say that I don’t consider paleo to be a low carb diet. It is lower carb than the standard American diet, but there is a strong emphasis on eating a lot of vegetables, and depending on who you ask, starch. There is also a strong emphasis, which I think is universal among the paleo crowd, on omega-3s, including fish and grass-fed ruminants. It is not Atkins.

I need to get offline now, but I did want to ask about the turmeric. I know it’s good for joint health, is that why you take it or is it something else?

[abderian]

@Stoid

Seriously, that is so not true, as I’ve demonstrated in this thread.

As I said, I won’t get into a study-for-study tit-for-tat, but I do not see that anything has been demonstrated here at all, other than the zeal of a true believer in the latest dietary trend.

And the mocking tone of the words do not prove you are correct, but rather suggest that you feel defensive and attacked at the suggestion that this way of eating may not be “The Answer”.

[DSeid]

Thank you Renee. No, I’ve not read “Good Calories, Bad Calories”. I’ve read reviews but that is not the same. My understanding is that I agree with some of what he says and disagree with some too. Probably not a surprise.

Certainly, I think the science is usually more complicated than many initially think. There has been a mainstream appreciation that the lowering fat by raising simple carbs is not a good thing. There is a greater understanding that some fats are actually good fats and that some fats are very much not. In short hand that translates to saturated fats as bad guys and MUFA/PUFA/omega 3’s as good guys, but of course that really means that excess SFA are bad and also, when one drills in, particular saturated fats may be neutral or, possibly, depending on how they are packed, of some benefit (we’ll see how the work with the MCTs of coconuts shakes out over the years), and certain PUFAs are excellent to have more of, and others are potentially harmful. I also agree with Taubes purported basic thesis: not all calories are the same and a focus on calorie restriction alone is wrong-headed. Nuts may be high calorie but they take energy to burn and the calories are not always completely absorbed; they also are very satiating and tend to decrease how much people otherwise eat. Added sucrose and HFS causing sugar spikes and crashes, etc., is conversely calories that can cause lots of harm. Bodies also change their metabolism in response to dietary changes. The system is much more complex than “a calorie is a calorie”. My personal take has been that the focus on the scale is wrong headed. Developing healthy habits that are associated with long term good health outcomes is the goal.

Still, the mainstream scientific consensus is consistently clear: diets high in fat from red meat coming from modern grain fed cattle and pork and from butter and lard are associated with all sorts of long term worse outcomes; lots of vegetables and fruits and foods rich in fiber are associated with better outcomes. Pollard’s mantra of “Eat real food; not edible food-like substances” is a good one. Taking in many more calories than one burns off will cause weight gain. Those who take from “The Paleo Movement” that they should eat as much grain-fed beef, visible fat, lard and cheese as they can (because “Paleolithic Man ate animals!”), are misguided (I know you are not one of them), and some of the “gurus” are partially culpable for that. But we’ve beaten this discussion to death.

Turmeric. Lots of very suggestive evidence out there that it does worlds of good in many venues. In multiple animal models it lowers LDL, and decreases LDL oxidation. There are many studies suggesting that turmeric (to be more precise, it seems to be the curcumin) helps decrease cancer risks. I though started taking years ago however based on what I found to be convincing enough evidence that regular intake lowers risks of Alzheimer’s Disease. The evidence of benefit is not conclusive, but I think it seems likely enough, coupled with its no known risk of harm and low cost, that taking one or two a day seems like a reasonable choice for me.

[DSeid]

Abetter article about Alzheimer’s and curmumin.

[Stoid]

Regarding:

[QUOTE=Dseid]
studies like this one are informative…but it does falsify the proposition that an animal based low carb approach is clearly superior.
[/QUOTE]

"Folks adhering the most to the animal-based diet were **more likely to smoke and had higher BMIs **than the best adherents of the Vegetable Group. Along with influencing mortality outcomes, this suggests the Animal Food group, in the highest decile, may have been somewhat less health-conscious than the dieters lumped into the highest decile for the vegetable category. And that’s the type of thing that has repercussions for other diet and lifestyle choices that weren’t measured in the study.

For the Vegetable Group, cancer and cardiovascular mortality was lower in the tenth decile than the first decile, even though both deciles ate exactly the same amount of red meat and nearly the same amount of total animal foods. This suggests animal products aren’t the driving force behind differences in mortality rates.

Similarly, at the fifth decile, the Vegetable Group had a lower cardiovascular mortality hazard ratio than the Animal Group (0.99 versus 1.21), even though the Vegetable Group was eating a slightly greater proportion of animal foods (33.3% versus 29.9% of total energy for women; 32.9% versus 31% for men)"

From an Annals of Internal Medicine editorial regarding the study which also includes the whole study:

Newer observational studies and systematic reviews, however, have absolved fat (with the exception of trans fat) as a detriment to health, and some have implicated refined sugars and starches instead

Observational studies have great strengths but also significant limitations that can complicate claims to causality if not addressed by design or analysis. A previous analysis of the Nurses’ Health Study cohort illustrates the challenge of generating valid causal inferences in observational studies. That study found that use of postmenopausal estrogen plus progestin replacement therapy was protective for nonfatal myocardial infarction or death due to coronary heart disease (CHD). Subsequently, the Women’s Health Initiative-a large, multisite, randomized clinical trial-found that combination hormone replacement therapy** may actually increase risk for CHD**.Of interest, the diet aim of the Women’s Health Initiative **also refuted previous observational studies suggesting that reducing fat intake would improve health outcomes **

Well-documented criteria exist for assessing the strength of causation between an exposure and an outcome (5, 14). One of the most important criteria is the strength of association found between the exposure and the outcome of interest. This study reported a hazard ratio of 1.23 (CI, 1.11 to 1.37). Such a result would be notable if comparing one low-carbohydrate diet score decile to the next lower (or higher) decile but becomes **less impressive **when comparing extreme deciles.

Fung and coworkers (9) did not show a clear dose-response relationship in that there was not a clear progression of risk moving up or down the diet deciles.

Finally, imbalance in observed covariates across the diet deciles in this study raises the specter of unobserved confounding and detracts from the sensibility of the association. For example, men in the highest decile of animal-based low-carbohydrate diet score were 3 times more likely to smoke and half as likely to exercise than those the lowest decile. With frank differences such as this on observed characteristics, there could be marked differences between these groups in unobserved characteristics, which could misattribute mortality differences to diet and result in incorrect inference

Unobserved confounders to consider include:
[ul]
[li]race, [/li][li]income, [/li][li]wealth, [/li][li]education, [/li][li]health insurance status, [/li][li]family history of CHD, [/li][li]blood pressure, [/li][li]serum lipid levels, [/li][li]social support, [/li][li]local food prices, [/li][li]local availability of healthy food options, [/li][li]and having a regular health care provider.[/li][/ul]

Also, several dietary assessment and classification issues cloud interpretation of this study…Perhaps the most important dietary points to contend regards classification. The participants in the highest decile of low-carbohydrate diet score (that is, those eating the least amount of carbohydrate) actually had a moderately high carbohydrate intake (37.2% of daily energy intake).

it turns out that participants in the highest decile of the vegetable score consumed similar amounts of fat and protein from animal sources as did participants in the upper deciles of the animal score.

In sum, this well-written study addresses a critical, unresolved public health question of diet but cannot satisfy us with a definitive answer. …The current state of the evidence is such that **no one can legitimately claim that a low-carbohydrate diet is either harmful or safe with any degree of certainty **until a large-scale, randomized study with meaningful clinical end points is done

This is why it is so important to read the research itself, vs. assuming an abstract or a press release is telling the truth about what it says and what it means. Any commitment to intellectual honesty demands it.

@DSeid

None of them ate all that much SFA. Game (marrow and organ meat inclusive) and aquatic species are fairly low in SFA and relatively high in MUFA/PUFA/omega 3’s. All diets that consist of mostly game and aquatic species have been shown to have relatively low SFA, including those that include chewing on whale blubber and drinking rendered seal fat. Paleolithic humans did not eat much SFA and per unit protein they ate quite little. Any media savvy guru who states otherwise is misrepresenting what the science is. Ample cites for this have been provided. Anyone who claims otherwise should volunteer exactly from what source those ancestral peoples were getting all that saturated fat since it was not from the game or from the aquatic species in their diet.

When The Conclusions Don’t Match The Data: Even Loren Cordain Whiffs It Sometimes, Because Saturated Fat Is Most Definitely Paleo (Updated)

First example: in the subsection “Fatty domestic meats”, they claim that wild game is much leaner than feedlot cattle (this is true)—and then claim it is much lower in SFAs (saturated fatty acids), which is false according to their own data!

In Fig. 6, showing seasonal variation in caribou body fat, caribou at their leanest (in April) contain 9% saturated, 8% monounsaturated, and 2% polyunsaturated fats—a fat profile of 47% SFA, 42% MUFA, and 11% PUFA. At their fattest (in October), they contain 33% SFA, 29% MUFA, and 5% PUFA, or a fat profile of 49% SFA, 43% MUFA, and 8% PUFA.

Here are their claims:

“Because subcutaneous and abdominal body fat stores are depleted during most of the year in wild animals, PUFAs and MUFAs ordinarily constitute most of the total carcass fat (11). [False: half the carcass is SFA. 47%/53% and 49%/51% equal 1/2 within the precision of their data set.] MUFAs and PUFAs are the dominant fats in the edible carcass of caribou for all 12 mo of the year, as illustrated in Figure 6 (11, 60-65). [False again: as shown above, there is as much SFA as MUFA and PUFA combined.] Because of the seasonal cyclic depletion of SFAs and enrichment of PUFAs and MUFAs, [What seasonal depletion? 49% to 47% is insignificant, being well within the rounding error of the percentages they use in the table] a year-round dietary intake of high amounts of SFAs would have not been possible for preagricultural hominins preying on wild mammals. [False again! The table of fat content Cordain uses assumes that hunters selected an animal purely at random from the herd, which is nonsensical.]

“The primary use made of reindeer [note: reindeer = caribou] was, of course, nutritional. The autumn hunts indicated by the dental eruption sequences at Pincevent and Verberie would be designed to exploit the prey in its best condition of the entire year. The summer forage would have fattened up the herd to its maximum annual weight, and even more importantly, to its highest fat content. Both meat and marrow are important for the diets of reindeer hunters. Speth and Spielmann’s arguments (1983) about the desirability of fat in the diet are particularly pertinent for cold climate hunter/gatherers in the winter. The fat in marrow can supply twice as many calories per gram as protein can, and can allow efficient metabolism of the protein from meat. There are no whole bones in the faunal assemblages from Pincevent or Verberie. There are abundant impact fractures, systematically placed to open the medullary cavities for the extraction of marrow.” [Note: marrow is very high in fat.] - Subsistence strategies and economy in the Magdalenian of the Paris Basin.
In: R.N.E. Barton, A.J. Roberts and D.A. Roe, eds., The Late Glacial of Northwest Europe: Human Adaptation and Environmental Change at the End of the Pleistocene, pp. 63-71.
Council for British Archaeology Research Reports 77, London.

Finally, I note that caribou hunting is a recent adaptation: Homo sapiens didn’t reach Europe or East Asia at all until perhaps 40,000 years ago. Quoting the original paper again, “Larger mammals generally maintain greater body fat percentages by weight than do smaller animals.” Recall that preagricultural hominins preferentially hunted megafauna: mammoths, mastodons, giant ground sloths, giant tortoises, gomphotheres, chalicotheres, giant hartebeest, giant bison, woolly rhinoceri, and the myriad other megafaunal species that our ancestors drove extinct during the Quaternary period. Even modern American bison (let alone ancestral bison) are many times larger than caribou.

Such animals would have contained a much greater percentage of carcass fat, which would therefore have comprised a much greater percentage of the human diet. Taking caribou as typical representatives of the hunter-gatherer diet is somewhat disingenuous, as humans didn’t even reach the area where caribou lived until perhaps 40,000 years ago.

[QUOTE=Dseid]

Modern grain fed beef, butter, lard, etc., OTOH are all extremely high in SFA and low in MUFA/PUFA/omega 3’s. Compared to game they are low in protein. Eating lots of that is doing a poor job of replicating Paleolithic dietary habits.
[/QUOTE]

According to the USDA’s food information database, the fat profile of grain-fed beef is approximately 46% SFA, 50% MUFA, and 4% PUFA.* In other words, grain-fed beef has a slightly lower percentage of saturated fat than wild caribou—and we have disproven another of the authors’ key claims about saturated fat. (“Marbled meat results from excessive triacylglycerol accumulation in muscle interfascicular adipocytes. Such meat has a greatly increased SFA content…” [which we’ve just proven false])

In fact, based on Table 5 of this Cordain paper, the fat of wild game averages approximately 45% SFA (saturated fat).

Finally, the fact remains that hunter-gatherers ate all portions of the animal. Hunters did not trim their steaks—and they ate the fatty parts of the carcass, such as brains and visceral fat, that modern humans throw away! Therefore, the fact that modern muscle meat is fattier is balanced by the fact that we throw away much of the fat which Paleolithic humans consumed with relish.

The rest of the article is indeed correct,** including their subsequent conclusions about the PUFA profiles (n-3 vs. n-6) of wild game vs. feedlot beef**—but their conclusions about saturated fat are simply a regurgitation of disproved theories which are contradicted by their own data, as well as recently but clearly established science.

Therefore, though it is an excellent paper overall, we can safely discard all its conclusions relating to relative intake of saturated fats.

[Stoid]

And to help people try to understand all this a little better, from here I summarize the following:

RESEARCH METHODS
To understand the use of statistics, one needs to know a little bit about experimental design or how a researcher conducts investigations. A little knowledge about methodology will provide us with a place to hang our statistics. In other words, statistics are not numbers that just appear out of nowhere. Rather, the numbers (data) are generated out of research. Statistics are merely a tool to help us answer research questions. As such, an understanding of methodology will facilitate our understanding of basic statistics.

Validity

A key concept relevant to a discussion of research methodology is that of validity. When an individual asks, “Is this study valid?”, they are questioning the validity of at least one aspect of the study. There are four types of validity that can be discussed in relation to research and statistics.

**Statistical Conclusion Validity: **…" Essentially, the question that is being asked is - “Are the variables under study related?” or “Is variable A correlated (does it covary) with Variable B?”. If a study has good statistical conclusion validity, we should be relatively certain that the answer to these questions is “yes”. Examples of issues or problems that would threaten statistical conclusion validity would be random heterogeneity of the research subjects (the subjects represent a diverse group - this increases statistical error) and small sample size (more difficult to find meaningful relationships with a small number of subjects).

Internal Validity: Once it has been determined that the two variables (A & B) are related, the next issue to be determined is one of causality. Does A cause B? If a study is lacking internal validity, one can not make cause and effect statements based on the research; the study would be descriptive but not causal.

Construct Validity: One is examining the issue of construct validity when one is asking the questions “Am I really measuring the construct that I want to study?” or “Is my study confounded (Am I confusing constructs)?”. For example, if I want to know a particular drug (Variable A) will be effective for treating depression (Variable B) , I will need at least one measure of depression. If that measure does not truly reflect depression levels but rather anxiety levels (Confounding Variable X), than my study will be lacking construct validity. Thus, good construct validity means the we will be relatively sure that Construct A is related to Construct B and that this is possibly a causal relationship. Examples of other threats to construct validity include subjects apprehension about being evaluated, hypothesis guessing on the part of subjects, and bias introduced in a study by expectencies on the part of the experimenter.

**External Validity: **External validity addresses the issue of being able to generalize the results of your study to other times, places, and persons. For example, if you conduct a study looking at heart disease in men, can these results be generalized to women? Therefore, one needs to ask the following questions to determine if a threat to the external validity exists: “Would I find these same results with a difference sample?”, “Would I get these same results if I conducted my study in a different setting?”, and “Would I get these same results if I had conducted this study in the past or if I redo this study in the future?” If I can not answer “yes” to each of these questions, then the external validity of my study is threatened.

Types of Research Studies

**Observational research: **There are many types of studies which could be defined as observational research including case studies, ethnographic studies, ethological studies, etc. The primary characteristic of each of these types of studies is that phenomena are being observed and recorded. Often times, the studies are qualitative in nature.

Correlational research: In general, correlational research examines the covariation of two or more variables. For example, the early research on cigarette smoking examine the covariation of cigarette smoking and a variety of lung diseases. These two variable, smoking and lung disease were found to covary together.

It is important to not that correlational research is not causal research. In other words, we can not make statements concerning cause and effect on the basis of this type of research. There are two major reasons why we can not make cause and effect statements. First, we don¹t know the direction of the cause. Second, a third variable may be involved of which we are not aware. An example may help clarify these points.

Correlational research is often conducted as exploratory or beginning research. Once variables have been identified and defined, experiments are conductable
True Experiments: The true experiment is often thought of as a laboratory study. However, this is not always the case. A true experiment is defined as an experiment conducted where an effort is made to impose control over all other variables except the one under study. It is often easier to impose this sort of control in a laboratory setting. Thus, true experiments have often been erroneously identified as laboratory studies.

…
A special case of the true experiment is the clinical trial. A clinical trial is defined as a carefully designed experiment that seeks to determine the clinical efficacy of a new treatment or drug. The design of a clinical trial is very similar to that of a true experiment. Once again, there are two groups: a treatment group (the group that receives the therapeutic agent) and a control group (the group that receives the placebo). The control group is often called the placebo group. The independent variable in the clinical trial is the level of the therapeutic agent. Once again, subjects are randomly assigned to groups, they are tested simultaneously, and the experiment should be conducted double blind. In other words, neither the patient or the person administering the drug should know whether the patient is receiving the drug or the placebo.

Quasi-Experiments: Quasi-experiments are very similar to true experiments but use naturally formed or pre-existing groups. For example, if we wanted to compare young and old subjects on lung capacity, it is impossible to randomly assign subjects to either the young or old group (naturally formed groups). Therefore, this can not be a true experiment. When one has naturally formed groups, the variable under study is a subject variable (in this case - age) as opposed to an independent variable. As such, it also limits the conclusions we can draw from such an research study. If we were to conduct the quasi-experiment, we would find that the older group had less lung capacity as compared to the younger group. We might conclude that old age thus results in less lung capacity. But other variables might also account for this result. It might be that repeated exposure to pollutants as opposed to age has caused the difference in lung capacity. It could also be a generational factor. Perhaps more of the older group smoked in their early years as compared to the younger group due to increased awareness of the hazards of cigarettes. The point is that there are many differences between the groups that we can not control that could account for differences in our dependent measures. Thus, we must be careful concerning making statement of causality with quasi-experimental designs.

As no random assignment exists in a quasi-experiment, no causal statements can be made based on the results of the study.

[twickster]

@Stoid

This is why it is so important to read the research itself, vs. assuming an abstract or a press release is telling the truth about what it says and what it means. Any commitment to intellectual honesty demands it.

And yet you didn’t – the quotes you cite are from ablog post.

Don’t do this again, Stoid.

twickster, Cafe Society moderator

[DSeid]

Stoid, while I know that engagement with you will not be productive, I will point out a few things:

1. You have appear to misattributed a quote. No, your first quote box does not come from that linked editorial. It comes from this blog post. In point of fact, the study’s numbers not only controlled for confounding factors in a wide variety of ways, they estimated how big an unobserved confounder would have to be to drive the result down to statistical insignificance:

… the unmeasured confounder would have to have a prevalence of 40% among those at the highest decile of the animal score and a hazard ratio of 2.0 with total morality to attenuate the association to non-statistical significance. In NHS, the corresponding parameters for the unmeasured confounder would have to be 20% prevalence and HR of 2.0 to attenuate the association to non-significance. Since important confounders for the analyses of total and disease-specific mortality were controlled for, it is unlikely that such strong confounding would remain to explain the observed associations.

The actual editorial is primarily making an argument for a true large scale randomized controlled trial by pointing out that nothing short of that can be definitive. No argument there.

2. The editorialist actually is however badly mistaken when (s)he claims that the upper decile of the vegetable low carb group had similar amounts of animal fat and protein as the animal low carb group. The table is available on the pdf. (S)he must have been looking at the wrong column.

For women animal group 10th decile: animal protein (AP) 18.5%; animal fat (AF) 26.3%. Women vegetable group: AP 12.7%; AF 17.2%

For men animal group 10th decile: AP 18.8%; AF 27.4%. Men vegetable group: AP 12.6%; AF 17.1%.

Those are not similar amounts. Yes, actually reading the study, not just what others said about it, even editorialists, is good practice.

Again, I completely agree, and already stated, that a single study, even a very large prospective one like this one, cannot definitively declare that the vegetable group is in a superior position to the animal group. Once again however, it is enough to falsify the proposition that demonizes vegetable sources of protein as harmful, something many of the Paleo gurus do (avoid tofu and beans!) And the data is highly suggestive that the vegetable group has better outcomes.

Now onto the data about the diet of of Paleolithic humans. You may want to look at the actual article yourself as well. Here is figure 6. Averaging over the year the complete edible carcass (brain, organs, marrow inclusive) would have 17.5% of its energy from SFA. Even if the share of hunted meat in the average Paleolithic human’s diet was 70% (no aquatic species, and a full 70% of total energy coming from animal sources, higher than most typical estimates) that would result in only about 12.25% of energy coming from SFA. Which is still less than the typical 15% that the average Americans eats. And of course if the experts in human evolution are correct, then: over 30% of the diet at most latitudes was gathered and of the animal source at least 40% of it came from fish. In Northern climes the gathered sources go down and the animal sources go up, but so does the share that is from fish sources. Consequently the hunted portion never goes over 40% of energy as fish replaces gathered plants. So from hunted game a top level of only 7% of the diet coming from SFA. Fatty fish? Pretty low in SFA, salmon for example about 8% of its total energy … and of course high in omega 3s.

[DSeid]

What your blogger missed in his mission to prove his preferred conclusion is that Cordain had not “miffed it”, that the edible carcass number includes all the high fat regions, and that the amount of protein in game per unit fat is much higher. On average 62% of total energy from the whole edible carcass, including marrow, brain, organs, was from protein, and only 38% from fat. Again, from game (meat, marrow and organs) a total of 12.5% of total energy from SFA. In comparison a rib eye even trimmed of all visible fat and broiled, provides 40% of its energy from protein and 60% of its energy from fat, with less of it, as your blogger appreciates, in healthier n-3. A total of 22% of its total energy from SFA.

[DSeid]

Error in the above noticed after edit window, 17.5, not 12.5. Point remains as stated.

[Amasia]

Just an additional point on saturated fats- an article came out in the last two weeks demonstrating in yet another way how saturated fats promote diabetes type 2 development, while the omega-3 type fats act as an inhibitor. Study text here. This is actually pretty groundbreaking stuff, so if anyone previously denied that saturated fats can be unhealthy, now is the time to jump on board!

**Dseid, ** don’t be afraid to give a large prospective study some credit If properly done and controlled for, it’s one of the best epi tools out there. Of course, there is always a chance of missing a confounder or incorrect data reporting, but science-minded people who value rational thought are not freaked out at the idea of one day being demonstrated to be wrong. It’s part of the process! The wonderful thing about science is that it is an evolving understanding of the world.

[Stoid]

@twickster

And yet you didn’t – the quotes you cite are from ablog post.

Don’t do this again, Stoid.

twickster, Cafe Society moderator

Don’t do what?

Link to the whole study for anyone who is interested to read, vs. a short abstract with no links to anything complete?

Quote from AND link to the editorial critique of the study pointing out the multiple reasons the study is basically worthless?

Or are you telling me to stop accidentally deleting the line with the link to the blog post identifying it as the short and snappy version for those who don’t want to slog through the heavy science verbiage?

Your statement to me reads as you accusing me of quoting the blog then claiming the blog quote is from the editorial critique, and that would be dishonest - not something I’m known for.

It also makes no sense. Only the first quote block, the one preceding the link which accurately attributes the quotes that follow it, was from the blog post and (due to my error) lacks attribution, it’s not MIS-attributed to anything: I’m sure you understand that a colon at the end of a sentence specifically refers to what comes after that sentence, not what comes before:

From an Annals of Internal Medicine editorial regarding the study which also includes the whole study:

And of course my habit (as well as forum convention!) is to give my attributions before the quotes, not after.

On top of everything else, the blogpost snappy summary of the editorial is, as far as I could see, perfectly accurate, making all my information entirely consistent, attribution of sources notwithstanding.

So accusing me of claiming that the first block is from the same source as everything that comes after, and for the purpose of being dishonest to boot, seems like a quite a ways to go to find something to moderate. At least to me, and leads me to ask again: exactly what is it I’m supposed to not do again, apart from make absolutely sure that I never make any kind of mistake that ***in no way ***alters the accuracy and truth of what I’ve posted?

[twickster]

Stoid, don’t make posts that you imply are from one source when they are from a different source. If this was done mistakenly, be more careful. If this was done deliberately, stop doing it.

twickster, Cafe Society moderator

[Stoid]

@DSeid

Stoid, while I know that engagement with you will not be productive,

Have to admit I’m curious aboutyour definition of productive.

1. You have appear to misattributed a quote.

Incorrect. I failed to attribute the quote at all. That’s meaningfully different than misattributing.

The rest, as accurately attributed originally, was printed in the Annals of Internal Medicine and was authored by:
William S. Yancy Jr., MD, MHS; Matthew L. Maciejewski, PhD; and Kevin A. Schulman, MD From Veterans Affairs Medical Center and Duke University Medical Center, Durham, NC 27705.

Two MDs and a PhD made all those critiques. I have no idea if they are any good at what they do, but they their critique was published. I don’t think yours or mine would be. At least not in the Annals.

[QUOTE=Dseid]
In point of fact, the study’s numbers not only controlled for confounding factors in a wide variety of ways, they estimated how big an unobserved confounder would have to be to drive the result down to statistical insignificance.I will point out a few things:
[/QUOTE]

All I can tell ya is what the docs had to say:

To address potential unobserved confounding, the authors did sensitivity analyses by using propensity score adjustment, but this method deals only with confounding from observed variables and cannot account for confounding from unobserved variables (15, 16). Without statistical adjustment for unobserved confounding through instrumental variables or other methods, it is unknown whether the consistency of main results and sensitivity analyses is evidence of both results being right (unbiased) or both results being wrong (biased).

And we’ve already seen how badly they blew it with the observed variables (three times more likely to smoke???) and the critical number and variety of UNobserved variables looks pretty meaningful to me.

The actual editorial is primarily making an argument for a true large scale randomized controlled trial by pointing out that nothing short of that can be definitive. No argument there.

I don’t argue either. But you were the one who felt this was a pretty definitive “falsification”, not me.
And for those who don’t want to go look, this is what they said in reference to the argument for a controlled trial:

The goal of our assessment is not to refute the utility of observational studies but to clarify the need for a large-scale clinical trial to provide a more definitive answer to the largest public health crisis in the United States: the effect of diet on obesity, chronic disease, and mortality. The current state of the evidence is such that no one can legitimately claim that a low-carbohydrate diet is either harmful or safe with any degree of certainty until a large-scale, randomized study with meaningful clinical end points is done. Such a study would require input from experts in administering each of the diets to minimize bias, and it would require an innovative design to enable completion of the study in a reasonable time frame for an achievable study budget. The authors claim that such trials are not feasible because of difficulties with follow-up and with dietary adherence. However, such a design is more feasible today than ever before given the possibility of a ubiquitous health information infrastructure emerging in the United States. Furthermore, a likely major detractor to dietary adherence is the plethora of mixed messages society receives about what and what not to eat. Isn’t adherence likely to be higher if we had greater certainty about which dietary patterns are healthy and which are not?

[QUOTE=Dseid]
Again, I completely agree, and already stated, that a single study, even a very large prospective one like this one, cannot definitively declare that the vegetable group is in a superior position to the animal group. Once again however, it is enough to falsify the proposition that demonizes vegetable sources of protein as harmful, something many of the Paleo gurus do (avoid tofu and beans!) And the data is highly suggestive that the vegetable group has better outcomes.
[/QUOTE]

Pardon? A very sincere question, (skepticism doesn’t mean I’m not sincere) on what basis do you arrive at the idea that the study cannot be considered definitive for A, but it can for B?

And B has done some of that morphing I referred to earlier. It used to be:

[QUOTE=Dseid]
but it does falsify the proposition that an animal based low carb approach is clearly superior
[/QUOTE]

And now it is:

Once again however, it is enough to falsify the proposition that demonizes vegetable sources of protein as harmful.

The “once again” is a very compelling clue that you somehow consider

-an animal based low carbohydrate approach is clearly superior
and
-vegetable protein is harmful

to mean identical things. Do you?

[Stoid]

@twickster

Stoid, don’t make posts that you imply are from one source when they are from a different source.

Since the attribution I gave was correctly worded, placed and punctuated, in a manner consistent with most if not all of my own posts as well as other people’s, I reject any suggestion that I implied anything at all. At most my error created a small degree of confusion, which, as noted previously, still changed nothing.

So with every bit of the respect that is due: your inference is not my implication.

But you can bet I sure will be extra-careful in the future, ma’am, yes I will.

[DSeid]

Stoid, I linked the pdf. Look at the table for the numbers yourself. It’s not too difficult. (You funny. Read the actual studies you say, not what people say about them. Unless the actual study contradicts what you want to believe. Then you can’t be bothered.) As to the three times more likely to smoke, yes, that is between different deciles among the animal predominant group, men only. Women animal predominant lowest decile to top decile high to low 27 to 32; men animal predominant 5 to 14. OTOH the difference between the top decile between animal and plant predominant was not so impressive. And was accounted for in the analysis. I don’t see a problem here.

And while you might be surprised in what I have been published, it is immaterial. An editorialist is not an expert panel, (s)he is just another doc like me.

I see that you do not understand the difference between proving one thing an falsifying another.

Let me try to explain:

Proposition A: An animal based low carbohydrate diet is superior (for mortality rates) to a plant based one, that is the plant based proteins are harmful relative to animal ones.) Yes, same thing, A better than B, or B worse than A.

If that proposition is true then those eating an animal predominant diet should have clearly superior outcomes compared to those who eat a plant predominant one. A result that shows either no benefit and more so one that shows the opposite falsifies that proposition.

Proposition B: A vegetable predominant one is superior to an animal based one. This study does not falsify that proposition. But failure to falsify is not the same as definitive proof. It may be highly unlikely that there was an unaccounted for confounder that was present in 40% of the population or more that when present doubled mortality rate, but it is not impossible. That would bring them down to being statistically equal. *Unlikely *but not impossible.

Therefore Proposition A is falsified and Proposition B is supported.

Do you get that now? (Serious question, no snark intended.)

[Stoid]

@DSeid

Therefore Proposition A is falsified and Proposition B is supported.

Do you get that now? (Serious question, no snark intended.)

I don’t need to concepts explained to me, because I understood them to begin with.

What I understand is that if it’s a badly done study to begin with, then the answers you draw from it cannot be considered meaningful whether they are used to confirm or falsify. (“support” is not the antonym to “falsify”, by the way). All kinds of things may be suggested by the information, but that just means it’s time to do some serious testing.
You have demonstrated a propensity to refer to a wide variety of things as settled, proved, known, absolute in one way or another, when virtually none of it is even close to that, and a lot of it is quite some distance away. Now you appear to be trying to sell the idea that research which in no way proves anything, (and can’t, because of the nature of it) which you admit, somehow manages to definitely DIS-prove something else, and that makes zero sense. You say:

A result that shows either no benefit and more so one that shows the opposite falsifies that proposition.

But your problem is that you are presenting this as though the “result” has magically become reliable, believable, carefully arrived at through rigorous methods that cleared out any meaningful possibility of error, and should be accepted as reflecting pure truth we can all bet our lives on.

Which is, of course, hogwash.

the most you can say for a study like this, which is rife with truck-sized holes, is that it suggests areas for further study. Period.

[Stoid]

@Amasia

Just an additional point on saturated fats- an article came out in the last two weeks demonstrating in yet another way how saturated fats promote diabetes type 2 development, while the omega-3 type fats act as an inhibitor. Study text here. This is actually pretty groundbreaking stuff, so if anyone previously denied that saturated fats can be unhealthy, now is the time to jump on board!

That is too arcane for me to parse one way or another, but I did find this at http://science.niuz.biz/ which appears to be “hardcore nerds only” and having nothing at all to do with pushing a low-carb or paleo agenda.

This is the opposite of what my research has led me to believe.
However, I do agree that lard is unhealthy, but not that saturated
fatty acids (SFAs) are to blame (lard is about 40% saturated fatty
acid, so the obvious question is, why are the SFAs being blamed?).
There is no such thing as “saturated fat” as a scientific entity,
because no food item one can buy in a supermarket is 100% saturated
fatty acids. At the end of this report was a link to this study:…
Apparently, what the researchers did was to feed mice a lard-rich diet
and then they looked for markers thought to be important in certain
disease contexts. What most likely happened is that the lard produced
more liipid peroxidation than whatever the control group ate. They
may not have even measured markers of lipid peroxidation, which I’ve
in other such studies and strikes me as an indication of incredible
ignorance on the part of the researchers. Since SFAs can’t contribute
to lipid peroxidation but unsaturated fatty acids can (and are most
likely the culprits) the question arises again, why are they blaming
SFAs?

However, I could not access the part of the paper that actually
addressed what was done in this experiment without paying for it.
Thus, I would have to essentially fund research that is apparently
terribly flawed in order to examine it. Is this how certain people in
positions of power think they can “combat” critics like myself? I
doubt it. I think it’s probably just a “money grab.” There’s so much
scientific evidence against the “saturated fat is bad” claim that this
one paper, no matter how badly flawed it is, isn’t likely to matter
much in the “grand scheme of things.”

The writer is no fan of lard, as he says, but for reasons having nothing to do with saturated fat. He also appears to be a researcher working with fats, and is one of those people who doesn’t understand the purpose of quotes, which drives me nuts.

I couldn’t get far in tracking down the writer, and the site does not appear to have an option for public registration.

PS: “Another way sat. fat promotes diabetes development”? have we seen any way SFAs promote diabetes development before this?

[rhubarbarin]

I’m content to consider myself an ongoing experiment. Would anyone feel I’ve made some point if I’m hale into my 90s after 60+ years guzzling saturated fats (palmitic acid mostly)?