Quotable Quotes: Tei¢holz and Taube$
I normally only share this stuff on social media these days, but the hypocrisy and irony here is too much. This book is stocked full of ironic and just downright hilarious contradictions and inconsistencies. So many ... not enough time ... :-)
Kindle Location for Teicholz quote: 652-657
Comments
Cheers.
This is not really on-topic but as long as we were sharing quotes I wanted to put this up where someone could appreciate its true awesomeness, other than the three prehistorians on my Facebook feed who are also familiar with the X-men.
You may now carry on with your current business.
original source: http://io9.com/peta-tries-to-pretend-dairy-products-have-something-to-1582896128
The IMPACT model found that in the United States between the years of 1980 and 2000, a time at which coronary heart disease mortality was reduced by about half, the decline in serum cholesterol, largely due to changes in diet, could explain approximately 24% of this reduction, compared to only about 12% for the decline in smoking prevalence.
http://www.ncbi.nlm.nih.gov/pubmed/17554120
See Stamler et al 1998:
“It is a reasonable inference that the sizable decline in per capita egg consumption in the United States in recent decades, and hence in per capita total cholesterol intake, has been one important component of the improved dietary patterns leading to a fall in mean serum cholesterol concentration in the adult population from ~ 6.08 mmol/L (235 mg/dL) in the 1950s to ~ 5.30 mmol/L (205 mg/dL) in the 1990s, and to the concomitant sustained marked reductions in mortality rates from CHD, all cardiovascular diseases, and all causes.”
IMPACT model has made it clear that in those nations which experienced the most dramatic declines in heart disease mortality in the world, such as Finland and the former communist nations of Eastern Europe, large dietary induced declines in serum cholesterol has typically explained a very significant portion of the decline ( ~ 50%). The changes in serum cholesterol levels took place prior the wide-scale adoption of cholesterol lowering agents. The changes in serum cholesterol can be almost completely explained by large reductions in SFA intake.
http://www.biomedcentral.com/1471-2458/11/641
In 1989 Epstein examined the changes in coronary heart disease mortality in 27 countries during the previous 10 to 25 years, noting that:
In almost all of the countries with major falls or rises in CHD mortality, there are, respectively, corresponding decreases or increases in animal fat consumption...
Thematic review series: The Pathogenesis of Atherosclerosis. An interpretive history of the cholesterol controversy: part I
http://www.jlr.org/content/46/2/179.full
Thematic review series: The Pathogenesis of Atherosclerosis. An interpretive history of the cholesterol controversy: part
II: the early evidence linking hypercholesterolemia to coronary disease in
humans
http://www.jlr.org/content/46/10/2037.full
Thematic
review series: The Pathogenesis of Atherosclerosis. An
interpretive history of the cholesterol controversy, part III:
mechanistically defining the role of hyperlipidemia
http://www.jlr.org/content/47/1/1.full
Thematic review series: The Pathogenesis of Atherosclerosis. An interpretive history of the cholesterol controversy, part
IV: The 1984 Coronary Primary Prevention Trial ends it—almos
http://www.jlr.org/content/47/7/1339.full
Thematic
review series: The Pathogenesis of Atherosclerosis. An
interpretive history of the cholesterol controversy, part V: The discovery of
the statins and the end of the controversy
In the second link, Steinberg cites three "well-designed" pre-1970 dietary studies - ODHS, LA Veterans and FMHS.
To anyone who has read the Oslo study would realize this involved massive dietary changes. The experimental group increased their EPA/DHA and vitamin D intake through seafood and cod liver oil, reduced their intake of trans fat, increased their nut, fruit, vegetable intake and restricted their intake of refined grains and sugar. Yet Steinberg ignores all this and claims that it was the drop in cholesterol level that was responsible for the protective effect.
Steinberg to his credit realizes that the primary endpoint of the LA Veterans was not statistically significant. The only statistically significant result was a post-hoc pooled endpoint, which is invalid. Despite no significant difference in the primary endpoint including CHD death and total mortality, Steinberg states that it "stands as one of the most important and persuasive studies of the prestatin era". What? and this is not even taking into consideration that there were confounders in favor of the experimental group.
The FMHS may just be one of the worst dietary trials ever conducted, so it is mind-boggling that he describes it as well-
designed! In fact, some meta-analyses exclude it because of its inapproprate design and large confounding.
Steinberg left out many studies in his review, and in general, dietary trials do not support his case taken collectively.
In the fourth link, speaking of the LRC-CPPT trial, Steinberg claims that the use of the one-tailed test was appropriate. Actually, the issue here is not really a one-talied test, but the fact that it was never prespecified and used such a low standard (one-tailed at 0.05 rather than 0.025). Using conventional statistics, the primary endpoint of the trial was not statistically significant, and the decrease in CHD death was nowhere near statistical significance including no decrease in the objective endpoint of total mortality. Also, the drug used may have pleiotropic effects. Despite all of this Steinberg somehow finds the results convincing as evidence to lower cholesterol. Also in the fourth link, Steinberg mentions the POSCH trial, but nowhere does he mention that it was a trial of surgical weight loss, neither does he mention that the results were not statistically significant at the formal end and instead cites an observational follow-up.
In the fifth link he talks about statins. In his book he asks: Is the effect of the statins on coronary event rates all due to the extent to which they lower LDL? Or do their so-called pleiotropic effects (i.e. effects independent of cholesterol lowering) also play a significant role? The implication with these questions is that the pleiotopic effects may be responsible for only part (not all) of the benefits. The problem is that Steinberg never proved that the benefits of statins are due to LDL lowering per se in the first place, and so there is the third possibility that the pleiotropic effects are responsible for all the benefits. Futhermore, the benefits of statins are modest and only seem to be benefical in a select population, so even if we assume the pleiotropic effects are responsible for only part of the benefit, the role of LDL per se has to be very small and couldn't be a "major cause". I could say a lot more on statins that Steinberg does not go into, such as the design and conduct of some trials, but I'll leave it there.
Steinberg is very clear on the fact that dietary trials make up just a one part of the evidence for diet-heart. It's preponderance of evidence that counts.
The relative failure of smoking cessations trials can be considered a very good example of why all forms of evidence need to be considered when evaluating a hypothesis, not just a few data points from randomized controlled trials from homogeneous populations. The lack of statistically significant favourable findings in the group that received counselling on smoking cessation has been explained by a lack of follow-up time sufficient to achieve the maximum benefits of smoking cessation (which is believed to be more than 2 decades), lack of participant size, a smaller than anticipated number of participants in the group that received counselling that quit smoking, and a greater than anticipated number in the group that did not receive counselling that quit smoking. These limitations are very similar to those that plague the trails that attempted to test the diet-heart hypothesis. For example the authors of WHI-trial stated:
"The intervention was designed to focus on lowering rates of breast and colorectal cancer by reducing total dietary fat. DM-I women reported saturated fat and cholesterol intakes that were <10% of total energy and <300 mg/d, respectively. However, the declines in saturated and trans fat intakes were small, and intakes of polyunsaturated fat also declined. These are the primary dietary determinants of LDL cholesterol. When the equation of Mensink and Katan (29) was applied, the observed changes in LDL cholesterol were as predicted.
“Because there are no apparent changes that would have mitigated a potentially favorable effect on CVD, the lack of an appreciable CVD effect maybe attributable to the limited decrease(only 2.7 mg/dL [0.07 mmol/L]) in LDL-C level, as well as the modest differences in other potentially favorable dietary components. Based on a large body of evidence from LDL-C–lowering trials, this magnitude of change in LDL-C level would be predicted to produce only a small (2%-4%) decrease in CVD risk, a value far below the power for detection in the current study . As delivered, the dietary intervention was not expected to have substantial effects on lipoprotein levels, but it is possible that a diet specifically lower in saturated and trans fat combined with increased intakes of vegetables ,fruits, and grains might have led to a decrease in CVD risk.”
One compelling line of evidence for diet-heart comes from the LDL receptor theory as elucidated by Brown and Goldstein who stated:
"Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl. In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels. Second, the LDL level in newborn humans is approximately 30 mg/dl, well within the range that seems to be appropriate for receptor binding. Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies".
The thing is, the evidence as a whole does not support him. There are limitations to every type of evidence, but Steinberg only points them out when it suits him. The LDL receptor hypothesis is irrelevant (or too simplistic) when you have a substance such as saturated fat decreasing receptor activity yet not causing increases in CVD and overall mortality -- as demonstrated in almost every prospective cohort and randomized trial.
Complaining about the lack of evidence (based on unproven ad hoc explanations) is not the same as providing evidence for your claims. This has nothing to do with smoking which is a completely different substance. Nevertheless, the real link here is that smoking and cholesterol may be related to CHD through the same oxidative mechanisms.
A Preliminary
Evaluation of Chowdhury Meta-Analysis on the Association of Fatty Acids with
Coronary Risk
http://www.drmcdougall.com/misc/2014nl/apr/chowdhurypart2.pdf
Evaluation of Chowdhury
Meta-Analysis on the Association of Fatty Acids with Coronary Risk, Part 2
http://www.drmcdougall.com/misc/2014nl/may/chowdhuryp3.pdf
Evaluation of the Chowdhury
Meta-Analysis on the Association of Saturated Fatty Acids with Coronary Risk,
Part 3
http://www.drmcdougall.com/misc/2014nl/may/chowdhurysupp.pdf
Evaluation of the 20
SFA-Intake Studies Used in the Chowdhury Meta-Analysis on the Association of
Saturated Fatty Acids with Coronary
Risk
In the RANDOMIZED comparison the WHI found no difference between the groups. What you cite is an observational analysis subject to major bias. This illustrates a common problem with people holding your views, citing inferior evidence when there is better evidence available saying the opposite -- even in the same study!
Siri-Tarino showed that their results were very robust AFTER taking into consideration dietary assessment and adjustments for cholesterol. For fatal CHD the relative risk was weak and non-signifcant. Furthermore, Siri Tarino is not the only one to find a lack of association between safa and CVD. They are only one of at least five different reviews finding no association, which is really not surprising given the lack of evidence from individual cohorts.
"Had they included the additional 4 studies in their analysis perhaps
their estimate would have shown an even stronger relationship"
Cherry-picking again. They are also many studies not in their analysis that if added would have further weakened the relationship.
Overadjustment is a problem in all observational research, BUT residual confounding is also a major problem which you ignore.
"Moreover, I did not claim tobacco and SFA are identical subjects. I
claimed that both, trials that tested whether smoking cessation
influences lung cancer risk and diet trials face similar problems due to
design and overall the nature of chronic disease that take several
decade's to develop before any clinical manifestations can be verified."
Do you understand that the best observational evidence and randomized
trial evidence available are both CONSISTENT with each other?
You are trying to cast guilt on safa by comparing it to smoking. The fact that you are even making this argument shows just how little evidence you have against safa. The totality of the evidence for smoking causing lung cancer is MILES stronger than the evidence against safa. The evidence against safa is almost non-existent and when the rare association is found it can be explained by probable residual confounding. The evidence against smoking can stand on its own, but apparently you are now admitting that the evidence against safa can't.
Richard, I get the impression that you think that randomized trials are the only evidence skeptics take into consideration. This is just false. It's the totality of the evidence that shows that safa is probably not harmful and lowering cholesterol is a waste of time.
You are looking at the evidence with the assumption that safa and cholesterol are guilty and interpreting the evidence accordingly, rather than taking an objective look. Steinberg does this also, as I've shown above.
no major differences in regards to CHD incidence was found between the group that received their 20min of counseling the intervention arm because there were no differences in major risk factors as the authors of the WHI study explained. To provide you with some international perspective, the intake of SFA at the highest fifth of consumption was 3 grams / per day less in rural Japan in the 1970s compared to lowest quartile of SFA consumption in the baseline of Nurse's Health Study in 1980s.
Nearly all of the prospective cohorts studies were launched after the great structural change in the diet that occurred in all developed countries and which led to major reductions in serum cholesterol levels. In Chowdhury paper the SFA intake was in the 5-10%. This about 1/2 level of the intakes that persisted in the 1950s in most developed countries.
The SFA-Fatal CHD RR of 1.32 as reported by Stamler (2010) is higher than the RR for passive smoking - lung cancer which is typically found to be around 1.27. And that being said, the meta-analysis doesn't take into account the methodological strengths of individual studies, this is extremely important caveat in diet-heart as the number of poorly done studies exceeds the number of well done studies. In fact, professor Frank Hu recently elaborated why pooled analysis is much more reliable opposed to the meta-analysis concept in regards to the diet-heart (see Jacobsen et al 2009).
The critics (Scarborough et al 2010) pointed out that the individuals studies in S-T meta-analysis seemed to be mostly of 2 type:
a) those which had over-adjusted serum lipids, and
b) those that did not have any information of serum lipids
The authors of S-T meta-analysis reported the RR's separately for the studies that a) had adjusted for serum cholesterol levels and for the studies that b) had no information of the serum cholesterol levels. The authors of the meta-analysis did not look at the raw data of the individual studies in an attempt to un-adjust the over-adjusted serum lipids as you seem to believe. The whole point of diet-heart is that SFA influences the risk of CHD via the LDL lowering mechanism. If most of material over-adjust serum cholesterol levels, a null association is to be expected.
Persistently elevated LDL causes CHD in every mammalian specimen, and to this day there's not a single experimental model which would indicate that the regression of atherosclerosis is possible while simultaneously elevating LDL cholesterol. The totality of evidence very strongly suggests that there is substantial benefit in LDL lowering and that this can be seen even when systematically pooling together results from different medications, diets, hormone therapies and even surgical treatments
http://www.ncbi.nlm.nih.gov/pubmed/17697899?dopt=Abstract&holding=f1000,f1000m,isrctn
Your cholesterol "skepticism" has been contradicted in hundreds of various experimental animal studies in which exogenous LDL infusions, hypercholesterolemic diet and/or genetic modifications have all been shown to be directly atherogenic. You seem to openly enunciate that every public health organization in the world gets the story wrong.
As concluded by Stamler (2010) in a response to authors overlooking the experimental data:
"To neglect this fact in a review about humans is to imply that the Darwinian foundation of biomedical research is invalid and/or that there is a body of substantial contrary evidence in humans. Neither is the case”.
http://ajcn.nutrition.org/content/91/3/497.full
As I already wrote in previous post, The most relevant models for human atherosclerosis come from experiments done with non-human primates. It has been observed that the long-term feeding of cholesterol and saturated fat has resulted in heart attacks, sudden death, development of gangrene, softening on the bones and numerous other serious complications in nonhuman primates. For example, it has been shown that when diets rich in cholesterol and saturated fat are fed to monkeys of the genus Macaca, including the rhesus monkey and the crab-eating macaque, they experience heart attacks at approximately the same rate as high-risk populations living in developed nations. It has also been demonstrated that the cessation of a cholesterol-rich diet and the subsequent lowering of serum cholesterol results in the regression of atherosclerosis in various mammalian and avian species, including herbivores, omnivores, carnivores and nonhuman primates. In one experiment Armstrong and colleagues induced severe atherosclerosis in rhesus monkeys by feeding a diet with 40% of calories from egg yolks for 17 months. The egg yolks were then removed from the monkeys diet and replaced with a cholesterol-free diet with either 40% of calories from corn oil or low-fat chow with 77% calories from sugar for three years, resulting in a reduction of serum cholesterol to <140 mg/dl and a marked regression of atherosclerosis.
Great, the double-stand king is telling me I've got double standards? Maybe you should point out where.
"This is known to bias studies towards finding an association between a higher intake of cholesterol and saturated fat and lower blood cholesterol levels. This would also likely similarly bias the results for the association between intake of cholesterol and saturated fat and the risk of cardiovascular disease."
Do you even see what you're doing? Not once have you provided any credible evidence to show that saturated fat is harmful. All you have done is cherry-pick and complain about the lack of evidence claiming bias in one direction (bias can go both ways!) all the while comparing the evidence against smoking to the evidence against saturated fat, which all logically leads in your mind to the conclusion that saturated fat is harmful? What? You don't even realize that the total evidence for both is different or that your comparing a substance with toxic chemicals to one with beneficial nutrients?
Let's ASSUME for the moment that the evidence for smoking and saturated fat is the same (which is BS). Even then it still does not follow that saturated fat is harmful. The fact that you are even making this argument is itself an admission that you don't have any credible evidence against it.
Also, since your claim is that safa is harmful by raising cholesterol, do you realize that you first have to prove that increased cholesterol levels are necessarily harmful? If increased cholesterol levels do not necessarily translate into increased harm then your argument falls apart right from the start, which is the case here.
increased levels of cholesterol have been shown to directly harmful. Increased levels of cholesterol in mid-life have not only been strongly tied to CHD but also to aggressive lethal prostate cancer, impotence, alzheimer, dementia, infertility in women, etc. Western people have about 2-3 the level of LDL cholesterol that is physiologically normal, and that is measured in free-ranging mammalians. The people that comsume paleo-like fad diets have much higher LDL cholesterol that what is Western norm.
Anyways, I think it's a good starting point that we agree that SFA elevates serum cholesterol. Finally we agree on something.
“The molecular basis for the effects of dietary saturated fat on plasma LDL cholesterol levels is well understood. Saturated fat influences the LDL receptor activity of liver cells as described by Brown and Goldstein, dietary saturated fat suppresses messanger RNA synthesis for the LDL receptor. This decreases hepatic LDL receptor activity and slows the removal of LDL from the blood, thus increasing the concentration of LDL cholesterol in the blood. Dietary cholesterol augments the effects of saturated fat further suppressing the hepatic LDL receptor activity and raising the plasma LDL cholesterol levels”.
–Heart Disease, Environment, Stress and Gender [proceedings of the NATO Advanced Research Workshop on Increase in Coronary Heart Disease in Central and Western Europe: Stress and Gender Related Factors, 20-24 May, 2000, Budapest, Hungary]
What relevance does this have if saturated fat does not cause anything?
I don't know if you noticed, but the evidence against safa being harmful is so bad, that the question has changed from:
is safa harmful?
TO
what can we replace safa with?
Many researchers believe that refined carbohydrates and omega-6 pufa to be worse than safa.
For example, I recall you mentioned Jakobsen et al earlier. Did you know that his analysis found that replacement of saturated fat with high-GI carbohydrates
significantly increased the risk of MI, no association with medium-GI, and a nonsignificant inverse association with low-GI?
How about unrefined carbs? Fruits, tubers, legumes and *whole* grains (as in the whole grain give or take some bran removal in some) vs. pulverized dust and isolated starch?
This is what -- first two on the list -- is mainly done in paleo RCT's.
I've been looking at that LA Vet study -- thanks to Steven H of paleo premise and Seth Y from science of nutrition -- there are actually 3 papers totalling over 60 pages. Don't really expect to find much on comparing the fats because they replaced 40% mostly sat with 40% mostly poly unsat ... which even the researchers were concerned was "unnatural". It would be nice if the current bunch pushing 80% fat diets had such reservations!! On the flip side the detail in the reporting of patient characteristics and risks is mind numbingly extensive -- it makes Teicholz dismissal vs. her glorification of Shai all the more absurd.
replaced 40% mostly sat with 40% mostly poly unsat ... which even the
researchers were concerned was "unnatural"
Yea, the quality of all fats are important, but people often use this study to argue against saturated fat or for cholesterol lowering when it does not necessarily support it. If one wants to argue based on non-significant results with no reductions in total mortality, it can be taken to mean that increasing omega-3, vitamin E intake and reducing trans fat (check Ramsden) is beneficial. The problem is that both sides take this study and interpret it according to their bias rather than looking at all possible interpretations. BTW, adherence was poor with both these crappy diets.
Who knows.
What I do know is that the diet world in low carb corners has gone absolutely batshit crazy with the keto stuff. On the one hand you have some going potatoes over starch and OTOH you have this 80% fat pile on the butter, eat it by the stick, put it in your coffee bunch.
The thing is, while there may not be examples of full vegan cultures, there ARE examples of largely plant based cultures whose diets and general health can be verified rather than divined from tooth markings, carbon isotopes etc.
Refined fats -- e.g. oils -- and refined carbs -- e.g. sugar/sweets -- were always and forever at the top of the food pyramid. Even Westman says don't fear unrefined fats.
absolutely batshit crazy with the keto stuff. On the one hand you have
some going potatoes over starch and OTOH you have this 80% fat pile on the butter, eat it by the stick, put it in your coffee bunch."
Definitely, because saturated fat is not harmful does not mean that eating a ****load isn't harmful. As in many cases the dose makes the poison. I do not go out of my way to increase safa intake, but nethier do I go out of my way to avoid it.
Pepper Culpepper is the founder of Culpepper Culinary Creations: Food for
Thought and is a writer, photographer and graphic designer. She
currently resides in Pensacola, Fl. Her main objective is teaching
others how to overcome and successfully manage chronic illness symptoms
through creative cooking. Planning ahead and shopping for healthy foods
can be overwhelming for those fighting disease, but Pepper shows them
how. Pepper lives with Bipolar Disorder, Panic Disorder, Agorabphobia,
Cervical Osteoarthritis, Bursitis, Herniated Disc and a pinched nerve.
She also manages her Interstitial Cystitis, an incurable disease of the
bladder, through functional medicine and food therapy.
I took 10 min. out of life and checked some of the recipes; I found the use of sugar, evaporated coconut sugar, ah, it's still sugar. "real" maple syrup, yes sugar, the evil fruits, Splenda, say what? And last but not least bakery pastry dough, Oh my!
Also - please define exactly what you mean by low carb?
From your website
http://zenpaleoliving.wordpress.com/2014/05/31/lean-green-summer-smoothies/
protein powder is NOT paleo - even if it's plant based - as it is a processed food that "paleo" man would have no access to
In fact - NOTHING in these smoothies is paleo AND since "paleo" man would have had no access to a blender smoothies are - by definition - not paleo!
http://zenpaleoliving.wordpress.com/2014/05/29/15-bread-recipes-that-are-low-carb-and-gluten-free/
" a significant percentage of the population is now intolerant to gluten."
define significant and provide proof
NONE of these low carb recipes are paleo in any sense of the word!
You've also said - "mental illness associated with wheat and sugar consumption." Again - please provide proof
Please provide ANY studies which show that our ancestors ate a LOW CARB diet.
"I'm not here to tell you that you should stop your crusade, I'm just here telling you that there is no one size fits all approach to weight loss. "
Well thank you for that news flash. Now ... did you have anything relevant to add to the conversation here?
the take-home message of diet-heart trials is replacing SFA with PUFA and low GI carbs is likely to be very beneficial. Taken to the totality of evidence there are very good reasons for the government to promote low SFA diets. You are a pathological denialist and you are distorting the message of every single study you manage to find in order to promote your ideology.
The diet employed in Lyon is similar to that promoted by nearly every public health institution.
Frank Hu, the third co-author of S-T meta-analysis in 2011:
"Prevailing dietary recommendations focus on reducing and eliminating unhealthy food components, such as saturated and trans fats, sodium, and added sugar. This is an important way to improve overall diet quality…..plant-based foods have significant health-benefits”
The intervention arm in Lyon ate much low amount of of SFA and dietary cholesterol as did the controls. The trials was not designed to show an effect of serum cholesterol since both groups, intervention and controls where jacked in statins, diuretics, anti-clotting medicine, etc. In fact statins where more widely used among the controls. Yet, cholesterol levels in these people where HIGHLY predictive for cardiac events throughout the trials as the authors in the paper clearly stated.
Anyways, I'd like to make few mentions about the 7CS, since this study is vital to understand the roots of diet-heart. When Keys (1988) decided to analyze the participants of the large Israel Ischemic Heart Disease study in the form of small groups based on place of birth, he found a strong correlation between the intake of saturated fat and serum cholesterol levels. This association did not exist when the participants were analyzed as an individual basis. Some information is always lost with the use of medians, however, by using and comparing medians, the researchers can effectively eliminate the effect of spontaneous variation within individuals and the large individual differences in dose-response and the statistical fallacy brought by such large differences between individuals. The differences in the intake of saturated fat explained 89% of the variation in serum cholesterol levels between the 16 different cohorts used in the 7CS. The differences in the intake of SFAs were large, from 3 percent (of calories) to 22 percent (of calories). The lowest mean serum cholesterol levels at the baseline was measured in one of the Japanese cohort (143mg/dl) and the highest in one of the Finnish cohort (262mg/dl). These ecologic correlations described the real world in much greater accuracy than did the poorly conducted population studies from homogeneous cultures.
"The intervention arm in Lyon ate much low amount of of SFA and dietary cholesterol as did the controls."
Every saturated fat trial that did not employ multiple interventions have failed. It is then completely illogical to think that reductions in saturated fat in a multi-interventional trial were responsible for the benefits. This is the height of bias.
"The intervention arm in Lyon ate much low amount of of SFA and dietary cholesterol as did the controls."
What was the difference in safa intake between the groups? Waiting for your answer.
"The trials was not designed to show an effect of serum cholesterol since both groups, intervention and controls where jacked in statins,
diuretics, anti-clotting medicine, etc."
This is irrelevant. The randomized comparison showed massive reductions in CHD death and total mortality that had nothing to do with lowering cholesterol. What don't you get about that? Whatever drugs were used is irrelevant to that fact. Also, the fact that statins were used more in the control group would mean that the reductions in mortality were underestimated, if anything.
"Yet, cholesterol levels in these people where HIGHLY predictive for
cardiac events throughout the trials as the authors in the paper clearly
stated."
This was an observational analysis made after pooling the two groups, not a randomized comparison. The authors themselves do not believe that cholesterol causes anything and agree with me, not you.
...
Woah! Sorry. Ate some wheat there and lost my mind. All good now.
If you look at our wild ape cousins you will see fat intake is only around 5% of their calories.
OH - maybe giving up booze and pain meds had something to do with it - since alcoholics tend to eat lots of candy, etc.
Thanks for any clarification.
you are right. Mediterranian diet high in canola oil based margarines, free vegetable oils and heart healthy whole-grains and low in artery clogging saturated fats seems to induce mortality benefits for patients at standard care. This means that when the Mediterranean diet is administered at the top of extensive cascade of various cardiovascular drugs, and the comparison is made next to control patient group in extremely high risk for another cardiac event, there seems to be a benefit that the traditional good o'le LDL cholesterol cannot entirely explain. The patient group is quite challenging and usually made of old people with history of heart disease.
However, we need to differentiate between a) atherosclerosis as process within the artery wall and b) eruption of plaque build-up resulting in clinical manifestation of the atherosclerosis process.
Regression of atherosclerosis as a process within the artery wall seems to be possible only when aggressive cholesterol lowering scheme is present. For example, the intervention arm in Ornish celebrated study showed nearly 40% reduction in LDL in just 12-weeks which is comparable to atorvastatin (known as Lipitor in the US). These results have been replicated in multiple hospital sites which have utilized the Ornish program. The Mediterranean diet seems to protect patients from plaque eruption at least for those that have already experienced a cardiac event next to controls when administered at the top of drug therapy. However, the med diet has not been shown to induce regression of the atherosclerotic plaques within the coronary arteries.
The intervention arm eat a diet that contained 8% of calories from SFA and 203mg dietary cholesterol (the equivalent digits for the controls were 11% and 312mg). The intervention group was asked to use the canola oil based margarine and ditch butter.
The chief inspector of the Lyon study, de Lorgiril is indeed the last medical expert in cardiology who is in cholesterol denial. You won't find anyone else in the field at the same level who does not embrace the lipid theory. However, de Lorgiril is advocating a low SFA Mediterranean diet and thus cannot be put to the same category as the low-carb authors pushing for diets high in animal fats.
and 203mg dietary cholesterol (the equivalent digits for the controls
were 11% and 312mg). The intervention group was asked to use the canola
oil based margarine and ditch butter."
So is this difference in safa intake between the groups sufficient to cause benefits?
'Replacing saturated and trans with natural vegetable oils can greatly reduce the risk of heart disease and diabetes.'
'In the Nurses’ Health Study II we have seen that women who consume high amounts of red meat and high-fat dairy foods during their early adult years are at increased risk of developing breast cancer.'
'And keep in mind that too many calories from both fat and carbohydrate will lead to weight gain, which will increase risks of breast cancer, colon cancer, and heart disease.'
I see anti-SFA, anti-red-meat, and pro-CICO positions in that order. I understand that you follow a low-carb Paleo approach, and that's fine, but reading these statements on the page to which you linked, would you say that the Harvard School of Public Health agrees with your dietary paradigm overall and would be a good source to cite in support of your diet ?
Today, people eat about 30 more pounds of vegetables and 25 more pounds of fruit per year than they did in 1970, according to Sturm's calculations.
Unfortunately, they're eating more of everything else, too. The average adult consumed about 2,100 calories in 1970, but in recent years that number has risen to more than 2,500.
this is straightforward as it can. Claiming that dietary cholesterol has not an effect on serum cholesterol would be akin to saying that whiskey has no effect on cognitive function and then test this hypothesis on a bunch of alcoholic people who are already drunk. The dietary cholesterol story has been dead clear already since the 1970s. The low-carbers and their favorite, obese lipid researchers have just missed the bandwagon. Moreover, as concluded by Jeremiah Stamler (2010) there is evidence from prospective cohort studies which indicate that dietary cholesterol influences CHD risk over and above its effect on plasma cholesterol.
http://ajcn.nutrition.org/content/91/3/497.full
The point is that dietary cholesterol clearly affects serum cholesterol levels but the effect is dependent on the baseline intake.
Effect of dietary cholesterol on serum cholesterol: a meta-analysis and review
"Serum cholesterol concentration is clearly increased by added dietary cholesterol but the magnitude of predicted change is modulated by baseline dietary cholesterol. The greatest response is expected when baseline dietary cholesterol is near zero, while little, if any, measurable change would be expected once baseline dietary cholesterol was > 400-500 mg/d. People desiring maximal reduction of serum cholesterol by dietary means may have to reduce their dietary cholesterol to minimal levels (< 100-150mg/d) to observe modest serum cholesterol reductions while persons eating a diet relatively rich in cholesterol would be expected to experience little change in serum cholesterol after adding even large amounts of cholesterol to their diet. Despite modest average effects of dietary cholesterol, there are some individuals who are much more responsive (and others who are not responsive). Individual degrees of response to dietary cholesterol may be mediated by differences in cholesterol absorption efficiency, neutral sterol excretion, conversion of hepatic cholesterol to bile acids, or modulation of HMG-CoA reductase or other key enzymes involved in intracellular cholesterol economy, each ultimately resulting in changes of plasma LDL cholesterol concentration mediated primarily by up- or down-regulation of LDL"
http://ajcn.nutrition.org/content/55/6/1060.long
see also egg feeding studies on the Tarahumare indians who had low cholesterol intake and low serum lipids at the baseline.
"The lack of relationship between dietary cholesterol and plasma cholesterol concentration in Americans with these relatively high intakes....Under conditions of similar high dietary intake the wide range of plasma cholesterol levels in Iowa children indicates the impact of genetic-metabolic factors in setting homeostatic level of the plasma cholesterol level and not the cholesterol in the diet as it is. When populations consuming low-cholesterol, low-fat diet are looked at the same perspective, a completely different pattern emerges" .
"Apparently the level dietary cholesterol intake in the Tarahumaras is below the so-called treshold level above which differences in intake do not affect plasma-cholesterol concentrations. We suggest from various metabolic-studies that this treshold may well be in between 100-300mg/day of dietary cholesterol"
"Since in the experimental dietary cholesterol is sine qua non for the development for the experimental atherosclerosis, especially among the sub-human primates, the finding of linear association of dietary cholesterol intake and plasma cholesterol concentrations in man further undergirds the evidence relating dietary factors to hypercholesterolemia and atherosclerotic coronary heart disease".
http://ajcn.nutrition.org/content/31/7/1131.long
my bad. The controls ate 12% of their calories from SFA; 8% vs. 12%.
Great points. You are correct. I would not say that Harvard agrees with my approach. I posted it because I wanted to point out that low fat diets aren't working to help American's lose fat. You see, Trae, I drank my way to IR in my 20's, having no idea the harm it would cause in the long run because I just naive enough to think beer and alcohol was ok because it didn't have any fat. I'm much older and more educated now and know better. I'm in recovery as well. I think each person responds differently to low carb.
"I'm good enough. I'm smart enough. And doggone it, people like me."
https://www.youtube.com/watch?v=-DIETlxquzY
This an assumption made by numerous people before. Low fat does not mean highly processed foodstuff labeled low fat. Low fat means eating real whole foods that are naturally low in fat. Vegetables, fruits, lean meats and grains all fall into this category. The challenge for most is that they equated Fettucini Alfredo, pizza and processed foodstuff as suitable alternatives. Not to mention the hydrogenated oils & trans fats fiasco!
Low fat & low calories are probably the best established dietary nutrient proftocol enjoyed by studied long lived societies. I think it would be a challenge to find a long lived society that eats high fat or low carb consistently.
As a side note Ancel Keys lived to be 100!
You have yet to comment on a post regarding the paleo diet.
You have yet to add to a discussion here in any meaningful way.
Trust me, my readers are all well aware of the claims about miracle cures and deadly toxicities associated with eliminating or eating various foods.
I'm going to politely ask you to leave if you have nothing to contribute to the conversation. Alternately you can take the time to find a post in which your diatribes might fit.
I deleted ONE comment regarding my ESR podcast because it was a personal attack. I considered responding in kind but thought the wiser of it.
Do you have ANY relevant commentary to THIS post you'd like to share?
in the long run because I just naive enough to think beer and alcohol
was ok because it didn't have any fat."
This is such bull shit it boggles the mind
Healthy diet: Mostly whole minimally processed foods, mostly plants. Sufficient protein so not fearing animal foods, but more for their protein and nutrients than fats. When that is at the base, the rest absent real intolerances can be rounded out with other foods, including even so-called "junk" from time to time.
Now. Take your entitled attitude to somewhere you are entitled to pontificate. Like your own blog.
There is no clear definition of exactly what constitutes a “low carb diet” and what is “low” for one person may not be “low” for the next.
An individual’s optimal carb intake depends on age, gender, body composition, activity levels, personal preference, food culture and current metabolic health.
People who are physically active and have more muscle mass can tolerate a lot more carbs than people who are sedentary. This particularly applies for those who do a lot of high intensity, anaerobic work like lifting weights or sprinting.
Metabolic health is also a very important factor. When people get the metabolic syndrome, become obese or get type II diabetes, the rules change.
People who fall into this category can’t tolerate the same amount of carbs as those who are healthy. Some scientists even refer to these problems as “carbohydrate intolerance.”
Did I say you were crazy for eating the way you eat? I don't give two flips what or how you eat!
Any nutrition book or, frankly, the USDA guidelines with a few tweaks (such as putting legumes and starchy veg with whole grains and emphasizing "whole") is a fine place to start.
THIS blog is not a food blog. It is not a weight loss blog. It does not promote a diet. I discuss the science here as much as I can and try to disseminate the truth about what does or does not cause or contribute to diabetes, etc.
Now I repeat. Do you have anything to contribute to the subject of this blog post or not? If not, leave.
"Now. Take your entitled attitude to somewhere you are entitled to pontificate. Like your own blog."
Translation:
"Now take your entitled attitude to somewhere you are entitled to pontificate, such as your own blog."
As to what I eat - my diet and supplement regimen is designed to stabilize and then regress the arterial plaque that I have.
It includes raw dairy, kefir, raw meat, fruits, veggies, nuts, seeds, grass fed protein powder, etc.
It includes supplements such as berberine, citrus bergomot, alma, vitamin c, vitamin d3, SloNiacin, etc.
It includes armour thyroid, testosterone injections and 10mgs atorvastatin/day.
It is what I use based on what I need and I would NOT recommend it to anyone else.
As to being in ketosis - the only way to know for sure is to measure it - just because you keep carbohydrate consumption to 50 grams/day DOES NOT mean you are in ketosis.
As to Kris Gunnars
http://authoritynutrition.com/about/
"My name is Kris Gunnars. I’m a medical student, personal trainer and
someone who has spent years reading books, blogs and research studies on
health and nutrition."
Big Whoop! - Not qualified at all.
Since "There is no clear definition of exactly what constitutes a “low carb diet” - then your opinions are just that - OPINIONS.
Pepper Culpepper
charles grashow
•
an hour ago
"Thank you for bringing that to my attention. I use coconut sugar VERY
sparingly, usually 1 tbs. in my coffee, and my diet contains 20-40g of
carbs each day from things such as lettuce, tomato, onion, spinach, etc.
My protein comes mostly from eggs and the fat I eat comes from extra
virgin olive oil."
You forgot the part about nuts, seeds, chicken, fish. Forget anything else??
It's from The American Journal of Clinical Nutrition, June 1995
"Mediterranean diet and public health: personal reflections." By Ancel Keys
http://m.ajcn.nutrition.org/content/61/6/1321S.full.pdf
URLs are so funnnn to type longhand on a cellphone. :-/
So - what is it - 20 grams to keep you in ketosis or enough to keep you out of ketosis?
I was banned :D
Blechhhh! |-P
2) These people are delusional - especially Dana
"Dana Carpender I
can't speak for Fred, but dropping from about 120 grams of protein per
day to somewhere between 60-80 grams, and adding extra fat, improved my
blood sugar. My HbA1c was normal, but my fasting BG was running just
slightly high, generally between 105-110. Doc told me it was from
gluconeogenesis driven by extra protein. Dropping my protein and
increasing my fat fixed it."
It is seriously sick in ketopia these days. NO humans ever ate an 80% fat diet. It is only recognized to treat epilepsy in children (doesn't work as well in few studies in adults) with strict adherence and SUPPLEMENTS to prevent things like kidney stones that are almost unheard of in children but rather common for kids on keto.
ROFLOL!
Fred's lunch ... pretty spartan!
Your problems are only partially dietary. The mental derangement that would exhibit these symptoms are rooted more in long-standing behavioral than biological problems. I would consider seeing a therapist and going on an SSRI, if you can tolerate it. Seriously, I'd do something about it. Mental issues can have biological issues but behavioral problems rooted in past events and traumas need to be "hashed" quite differently. I strongly encourage you to seek the counsel of mental health professionals.
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I’m no scientist Evelyn, but here’s a bit of advice. Reduce the starchy carbs and sugar, reduce the calories, spend as much time exercising as you do running others down, and you will be as slim as a whip, instead of an obese and bitter whinger."
Great rant Eddie! Loved it. I discovered Evelyn on accident and wish I had been hit by a train full of wasps on crack and then forced to endure 1000 paper cuts on my private parts. I made the mistake of trying to make cogent, well thought out and well written article and all I got were replies that sounded like those patients who were in the Psychiatric Hospital I once worked in. Very quickly, droves of people went to my blog and picked me apart for posting a Paleo recipe that called for one giant whopping tsp of coconut sugar. Then, they said that my reduction in anxiety, depression and insomnia was because I'm now in recovery from alcohol and drugs. I calmly pointed out that I had been sober before for a much longer time, the only difference is that I was consuming 1000 calorie Cinnabons every morning along with my triple latte and that was just for breakfast. At lunch it was chicken salad and bread pudding. Dinner was KFC, Zaxbys, Burger King or Taco Bell and then more bread pudding at all hours of the night.
That's about the period of time I began seeing a psychiatrist for PTSD, OCD, Bipolar, BPD, ADD, and Panic Disorder. I was pumped full of Seroquel and other ugly drugs. I guess her followers don't understand that many AA's are miserable wrecks even at 20 and 30 years clean. That's because I watch them guzzle Big Gulp's and Donuts at every turn. I quit going to meetings because they were more toxic than the dysfunctional home I was raised in. People going from one addiction (alcohol) to straight sugar in the form of donuts and coffee. Ok, now I'm the one rambling, but Carbsane definitely irked me. When I asked her what SHE ate as part of a healthy diet, she balked and asked how dare I bring my entitled attitude to her forum and why should she have to answer to me? Well, because I'm not obese and I eat whole foods and walk 3-5 miles a day, every single day. Thank you for allowing me to vent here. Nice to meet you, I wouldn't have found your blog unless I went looking for people who agree that she's definitely not sane.
Sincerely,
Pepper Culpepper
Primal Zen Author
But no. Let's eat MOAR fat as it is healthy!! OK ... show me one culture. On a friend's FB wall yesterday, Neanderthin Ray Audette actually linked to Dana Carpender's Fat Fast page, and a paper on CVD in the Samburu who are milk drinkers like the Masai. Oh and I think some paper on ketosis in orangutans. I am NOT making this up!!!
http://www.youtube.com/watch?v=kOifkb4JlfY
Kudos to her for the exercise, though.
I've heard from several sources that Atkins softened his stance on carbs as he aged in terms of what was healthy, etc. The whole thing is a mess right now. Worse than 2009-10 in some ways and that is truly exasperating :(
they are beneficial, perhaps only for deficiencies.
The strategy has to be about lifestyle. I would base my diet around fruit, vegetables, animal protein, dairy, avoiding excessive intakes of omega-6, and getting sufficent omega-3. Similar strategies can be seen in Lyon, Oslo-2 (to some extent Oslo-1), and DART, where large benefits occured in short time, probably because they are actually targeting the real causes. Of course, keeping good weight, stress in check, and sufficient exercise would all be part of it. Since there is also quite a bit of evidence suggesting that oxidative stress may be a factor in numerous diseases, I would try to keep my iron levels low.
That's about it.
This was not aimed at diabetics, but for "those who are underweight or of normal weight. This one [the Meat and Millet Diet] can be suitable for a lifetime." But for those normal-weight people who found that these extra carbs still caused them to have difficulties controlling their blood sugars, they could "end up on a version of the ketogenic Atkins Diet"--[and by "end up" presumably is meant--a ketogenic level of carb restriction would BE their "maintenance diet" for life.]
Charles! Do you think that Lyle McDonald knows nothing???
"Since many diet books give the 30g/d value for a ketogenic diet, folks get a little anxious about carb intakes that are higher than that. However, strictly speaking, any diet with less than 100g/day of carbohydrate will cause ketosis to develop to some degree (more ketones will be generated as carbs are lowered). [Ketostix]...are misleading for a number of reasons, not the least of which is that while ketosis (as defined by blood concentrations of ketones) may develop, urinary ketones don't always show up, especially as carbs are raised to nearer the 100g/day high end." [Lyle McDonald @BodyRecomposition.com (How Many Carbohydrates Do You Need?)
[As NIGE remarked somewhere in one of his blogs: "what Lyle Mcdonald doesn't know about diet and physiology ain't worth knowing." Something like that--apologies to NIGE if I didn't get it 100% accurate]
This is about all I could find
http://www.bodybuilding.com/fun/irontamer6.htm
"Rules of the meat and millet diet. Unrestricted meat, fish, fowl, eggs, cheese.
The millet group includes all whole vegetables and whole grains . Emphasis should be on the most starch-containing group of vegetables. Therefore the best choices include millet, buckwheat, oats, groats, grits, bulgar,couscous,barley, brown rice, wheat and rice bran. Potatoes, yams and legumes are acceptable. Less starchy vegetables are also a part of the diet he says.
Foods in controlled quantities, fruits, milk and dairy, cheese and cream. Fats and oils permitted in moderate proportions. Best choices are cold pressed oils. Worst are margarine and
hydrogenated oils, coconut oil, shortening and lard. Butter and Mayo are permitted. Stone ground whole wheat breads and cereals are permitted.
He says--note that the total quantity of carbohydrate is unrestricted (page 278). On page 41 he has a chart group 1 of which contain the carbs you may eat without restriction on the meat and millet diet--all vegetables,all whole grains,all whole cereals,nuts, seeds, legumes and greens.
So, it seems to me that Atkin's diabetic patients didn't do so well on a diet which one might intuitively expect to be a good diet for diabetics (a ketogenic almost no carb diet), but on a diet more like the standard american diet without the refined and processed carbs--lots of meat, fish, eggs, cheese etc. Which looks like
for diabetics, even the SAD without any refined or processed foods
controls sugars in the long run better than the original atkins diet."
OH - KINKY!!
Betcha most will miss the mark?
OK, perhaps some of you may need a pair of "Keys" to unlock the mystery person!!!
We get it, Gary Taubes is wrong, low carbers are dumb and it's all hilarious, but what happened to Pepper here was a damn shame and the behavior displayed by all was not becoming of any mature adult, in my opinion. I'm sure you'll deny that you're naturally combative for no particular reason, but perhaps you would be able to have more reasonable conversations with people with whom you disagree if you stop acting like any sort of disagreement is a personal attack or a waste of your time.
By the way, because I know you're going to jump on it, no, I'm not asking you to stop everything just to give your take on the gluten study. Just pointing out that you seem to have endless free time to mock and demean people; I wonder how you find the time to discuss anything important.
http://synergyhw.blogspot.com/2013/08/a-lesson-in-what-we-truly-know.html
1) "Atherosclerosis may be readily produced in the rabbit and in the chicken by feeding a diet containing large amounts of cholesterol...while feeding cholesterol to man, or the monkey, has very little effect on the blood even when enormous doses of cholesterol are given."
2) "The cholesterol-fortified diet commonly used to produce
hypercholesterolemia and subsequent atherosclerosis in the
rabbit...corresponds to about 15 gm of cholesterol in a 3000 calorie diet for a man...Even when concentrating on foods of naturally high cholesterol content, it is difficult to devise a diet to provide, experimentally, as much as 2gm of cholesterol in the daily diet."
3) "That dietary cholesterol is not important for man would be predictedfrom the fact that the biliary output of cholesterol from the human liver is from 10 to 20 times as much as the daily amount of cholesterol in any diet of natural foods."
4) "Controlled experiments on men clearly show that serum cholesterol changes in direct relation to a change in the total amount of fat in the diet. Both animal and vegetable fats show this effect and the addition or removal of cholesterol from the diet does not change the result. The cholesterol level may fall, however, if the diet is almost exclusively pure fat and is free of carbohydrate."
5) "In the classification of the U.S. Department of Agriculture, by far
the largest proportion of the total fats, from 45 to 50 percent in
recent years, is "fats and oils as such, excluding butter." This means cooking and salad fats and oils- lard, corn oil, cottonseed oil, hydrogenated vegetable oil shortening, margarine, mayonnaise, etc."
Interview With Jerry Stamler, MD
DR. MOSER: Why does the public so readily accept very low-carb or Atkins diets when data suggest that that may not be the best way to lose weight and reduce the risk of heart disease?
DR. STAMLER: An essential fact about diet is: If you reduce calories, you reduce weight. So it is with Atkins-type diets that reduce carb intake. But long-term success, taking weight off and keeping it off? And long-term health effects? Unknown—likely adverse. No population in the world of any size, under any more or less ordinary circumstances (leaving out special limited and peculiar circumstances, e.g., small Inuit groups above the Arctic Circle) has ever subsisted for any length of time on a nutritional pattern such as recommended by Atkins originally or recently—under pressure from criticisms—with modifications. It is not possible to regard this diet as optimal in caloric density, ratio of nutrients to calories, or in key essential nutrients (minerals, vitamins, antioxidants, fiber) that—as we learn more and more—are protective. This diet also tends to be, unless you pick your fats very carefully and knowledgeably, excessive in saturated fats and cholesterol—dietary items that we have known for years are harmful. It's a bill of goods sold to the public without decent long-term scientific assessment.
I have a very lenient comment policy here. Always have, hope to always do. As a matter of fact, recently when the conversation strayed a bit too far for my liking on a book review, I did my best to save it and post a new post just so the meaningful discussion could continue.
Take a look at the post here. It is a serious topic. Do you have any comment on Ms. Teicholz views and/or how they clash with her friend and mentor's views on how science is supposed to work? Or are you just against grain?
I repeat for the listening impaired: This is not a personal blog, it is not a weight loss blog, it is not a diet advocacy blog. It is first and foremost a blog discussing what the science really says about low carb diets with some relevant other topics in the mix.
Pepper was given many opportunities to contribute here. She declined. She claimed she read lots of my posts, yet made absurd claims such as that my posts are full of foul language. She could have posted on another more relevant post. She did try one comment that was a direct insult. If you let people into your home simply to insult you, be my guest. I am not obliged to.
Now ... you can leave too.
But diabetic or not: Atkins said that for those normal weight people who found that they were unable to control their "blood sugar symptoms" while eating these added carbs, a ketogenic level of carbohydrate restriction was perfectly fine for them as a diet to "END UP ON"--so long as they took care to "prevent unwanted weight loss."
I was merely answering the question you had posed earlier to [the hapless, beleagured] Ms Pepper: "Please show me where Dr Atkins
EVER said to stay in the induction phase PERMANENTLY."
Well, it's on page 280 of the 1981 edition of Dr. Atkins' Nutrition Breakthrough.
I didn't go to this Pepper's blog and start "peppering" her with irrelevant questions after making ignorant and irrelevant claims. Then run off to another blog where she could get her psyche stroked and supported.
I don't have time to answer you. Correction, I won't spend much more time answering you. I will tell you that the chances of my diverting any of my precious time away from living my life to indulge your curiosity about gluten and leaky gut have gone from "low on my priority list because it's just not a topic I'm all that interested in in the larger scope of things" to "cold day in hades". Bye now.
> I missed her first comment. My mistake. Deleting comments. Or not. Can't figure out how.
This gluten thingie looms pretty large in his world though ...
It's basically a paean, an aria and ode to the ad hominem and the non-sequiter, basing a diet on being pissed off (because of allegations, not proven facts)
...
disheartening
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