How is this different than anything else we eat? Except for the correction there that it passes into the portal circulation, where it passes through the liver before getting into the general circulation. And if this was truly a problem, why don't we see the inflammatory response in these other tissues like we do in the small intestine of people with Celiac?

It's very different. Gluten doesn't necessarily even make it to the liver. It can pass directly into the blood stream through the lining of the intenstines. As I mentioned in my previous post, I believe it does cause inflammation in other tissues. The idea is just now starting to be studied. Gluten is the only problem with grains. The relative low amounts of micronutrients, its affect on gut flora, and its impact on blood ph all contribute as well.

I'm confused...what context exactly is that?

That's the point. Context defines whether or not saturated fat is contributing to poor health. If your sendentary and insuline resistant, eat a ton of saturated fat may not be the best decision. However, if you're relatively lean and active, adequate saturated fat intake is essential to proper hormon and neurological function. I believe the amounts a healthy indnividual could/should consume is a good bit higher than the FDA recommends.

Explain to me, how:

1) making it to the blood stream through the lining of the intestines is different than other nutrients

2) how it doesn't necessarily even make it to the liver even though it is passing into the blood supply of the intestines

Some sort of link to these studies, or mention of the ideas of these studies, would be much appreciated.

What effect does it have on gut flora?

Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial.

Biesiekierski JR, Newnham ED, Irving PM, Barrett JS, Haines M, Doecke JD, Shepherd SJ, Muir JG, Gibson PR.

Am J Gastroenterol. 2011 Mar;106(3):508-14; quiz 515. Epub 2011 Jan 11.

J Physiol Biochem. 2010 Jun;66(2):153-9. Epub 2010 Jun 1.

Gliadins induce TNFalpha production through cAMP-dependent protein kinase A activation in intestinal cells (Caco-2).



Laparra Llopis JM, Sanz Herranz Y.



Microbial Ecophysiology and Nutrition Group, Instituto de Agroquímica y Tecnología de Alimentos (CSIC), Apartado 73, 46100 Burjassot, Valencia, Spain. mlaparra@iata.csic.es

Abstract



Celiac disease is an autoimmune enteropathy caused by a permanent intolerance to gliadins. In this study the effects of two gliadin-derived peptides (PA2, PQPQLPYPQPQLP and PA9, QLQPFPQPQLPY) on TNFalpha production by intestinal epithelial cells (Caco-2) and whether these effects were related to protein kinase A (PKA) and/or -C (PKC) activities have been evaluated. Caco-2 cell cultures were challenged with several sets of gliadin peptides solutions (0.25 mg/mL), with/without different activators of PKA or PKC, bradykinin (Brdkn) and pyrrolidine dithiocarbamate (PDTC). The gliadin-derived peptides assayed represent the two major immunodominant epitopes of the peptide 33-mer of alpha-gliadin (56-88) (LQLQPFPQPQLPYPQPQLPYPQPQLPYPQPQPF). Both peptides induced the TNFalpha production triggering the inflammatory cell responses, the PA2 being more effective. The addition of the peptides in the presence of dibutyril cyclic AMP (cAMP), Brdkn or PDTC, inhibited the TNFalpha production. The PKC-activator phorbol 12-myristate 13-diacetate additionally increased the PA2- and PA9-induced TNFalpha production. These results link the gliadin-derived peptides induced TNFalpha production through cAMP-dependent PKA activation, where ion channels controlling calcium influx into cells could play a protective role, and requires NF-kappaB activation.



PMID: 20514534

J Cell Biochem. 2010 Mar 1;109(4):801-7.

Bifidobacteria inhibit the inflammatory response induced by gliadins in intestinal epithelial cells via modifications of toxic peptide generation during digestion.



Laparra JM, Sanz Y.



Instituto de Agroquímica y Tecnología de Alimentos (CSIC), Burjassot (Valencia), Spain.

Abstract



Celiac disease (CD) is a chronic enteropathy triggered by intake of gliadin, the toxic component of gluten. This study aims at evaluating the capacity of different Bifidobacterium strains to counteract the inflammatory effects of gliadin-derived peptides in intestinal epithelial (Caco-2) cells. A commercial extract of several gliadin (Gld) types (alpha, beta, gamma, [symbol: see text] ) was subjected to in vitro gastrointestinal digestion (pepsin at pH 3, pancreatin-bile at pH 6), inoculated or not with cell suspensions (10(8) colony forming units/ml) of either B. animalis IATA-A2, B. longum IATA-ES1, or B. bifidum IATA-ES2, in a bicameral system. The generated gliadin-derived peptides were identified by reverse phase-HPLC-ESI-MS/MS. Caco-2 cell cultures were exposed to the different gliadin peptide digestions (0.25 mg protein/ml), and the mRNA expression of nuclear factor kappa-B (NF-kappaB), tumor necrosis factor alpha (TNF-alpha), and chemokine CXCR3 receptor were analyzed by semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) in stimulated cells. The production of the pro-inflammatory markers NF-kappaB p50, TNF-alpha, and IL-1beta (interleukine 1beta) by Caco-2 cells was also determined by ELISA. The peptides from gliadin digestions inoculated with bifidobacteria did not exhibit the toxic amino acid sequences identified in those noninoculated (alpha/beta-Gld [158-164] and alpha/beta-Gld [122-141]). The RT-PCR analysis evidenced a down-regulation in mRNA expression of pro-inflammatory biomarkers. Consistent with these results the production of NF-kappaB, TNF-alpha, and IL-1beta was reduced (18.2-22.4%, 28.0-64.8%, and abolished, respectively) in cell cultures exposed to gliadin digestions inoculated with bifidobacteria. Therefore, bifidobacteria change the gliadin-derived peptide pattern and, thereby, attenuate their pro-inflammatory effects on Caco-2 cells.

(c) 2009 Wiley-Liss, Inc.



PMID: 20052669

Int J Biol Macromol. 2010 Nov 1;47(4):458-64. Epub 2010 Jul 14.

Dietary glycosaminoglycans interfere in bacterial adhesion and gliadin-induced pro-inflammatory response in intestinal epithelial (Caco-2) cells.



Laparra JM, López-Rubio A, Lagaron JM, Sanz Y.



Institute of Agrochemistry and Food Technology, Spanish National Research Council (CSIC), PO Box 73, 46100 Burjassot, Valencia, Spain. mlaparra@iata.csic.es

Abstract



Dietary components may have an important role in maintaining a balanced gut microbiota composition. Celiac disease is an autoimmune enteropathy caused by gliadins, and has been associated with a reduced proportion of Bifidobacterium in gut microbiota. This study evaluates the influence of glycosaminoglycans (GAGs) on bacterial adhesion and their contribution in the gliadins-induced inflammatory response. The adhesion of potential probiotic (Bifidobacterium longum CECT 7347 and Bifidobacterium bifidum CECT 7365), commensal (Escherichia coli and Bacteroides fragilis) and pathogenic (Salmonella enterica CECT 443 and Listeria monocytogenes CECT 935) bacteria to mucin and Caco-2 cell cultures was determined. Gliadins were subjected to in vitro digestion (pepsin/pancreatin-bile), with/out GAGs, and the presence or not of cell suspensions of B. longum (10(8) CFU/ml). B. longum, E. coli, and L. monocytogenes, markedly interact with the high-sulphur-containing fraction of GAGs. The GAGs reduced the gliadins-mediated production of interleukin-1β, but not tumour necrosis factor-α. The results suggest that GAGs may ameliorate gliadin-induced inflammatory response, though they also slightly interfere with the action of B. longum.

Copyright © 2010 Elsevier B.V. All rights reserved.



PMID: 20637226

The literature is litered with papers demonstrating that atherosclerotic precursor lesions ("fatty streaks") start developing in the arteries of people between the ages of 10-15. This happens in people who are lean as well as not, active as well as sedentary, and the best correlations to fatty streak formation and progression is dietary saturated fats.

It is, in fact, this processes of fatty streak progression to atherosclerosis in lean men with high saturated fat intake that best explains frailty in the elderly. This is the very specific condition of an otherwise seemingly health older person (usually lean men) having a rapid decline in health. It is now understood that this is due to underlying atherosclerosis.

You may feel all you want, the evidence is not in your favor.

Low fat dairy never sits well with me. The high temperatures low fat dairy is exposed to denatures the lactose and proteins. My body handles things like heavy cream and full fat, plain yogurts much better. Besides, they taste better and the dangers are extremely exagerated. I use raw dairy whenever possible.

Boy, have you been sold a load of goods.

Jay

Clin Exp Pharmacol Physiol. 2005 Oct;32(10):825-31.
High-fat diet prevents cardiac hypertrophy and improves contractile function in the hypertensive dahl salt-sensitive rat.

Okere IC, Chess DJ, McElfresh TA, Johnson J, Rennison J, Ernsberger P, Hoit BD, Chandler MP, Stanley WC.

Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio, USA.

1. The role that dietary lipid and plasma fatty acid concentration play in the development of cardiac hypertrophy in response to hypertension is not clear. 2. In the present study, we treated Dahl salt-sensitive rats with either normal chow (NC), normal chow with salt added (NC + salt) or a diet high in long-chain saturated fatty acids with added salt (HFD + salt). Cardiac function was assessed by echocardiography and left ventricular (LV) catheterization. 3. The HFD + salt group had significantly higher plasma free fatty acid concentrations and myocardial triglyceride content compared with the NC + salt group, but did not upregulate the activity of the fatty acid oxidation enzyme medium chain acyl-coenzyme A dehydrogenase. Systolic blood pressure was elevated to a similar extent in the NC + salt and HFD + salt groups compared with the NC group. Although LV mass was increased in the NC + salt group compared with the NC group, LV mass in the HFD + salt group did not differ from that of the NC group and was significantly lower than that in the NC + salt group. 4. There was no evidence of cardiac dysfunction in the NC + salt group compared with the NC group; however, high fat feeding significantly increased LV contractile performance (e.g. increased cardiac output and peak dP/dt). 5. In conclusion, the HFD + salt diet prevented the hypertrophic response to hypertension and improved the contractile performance of the heart. It remains to be determined whether preventing cardiac hypertrophic adaptations would be deleterious to the heart if the hypertensive stress is maintained long term.

PMID: 16173943

Am J Hypertens. 2007 Apr;20(4):403-9.
High fructose diet increases mortality in hypertensive rats compared to a complex carbohydrate or high fat diet.

Sharma N, Okere IC, Duda MK, Johnson J, Yuan CL, Chandler MP, Ernsberger P, Hoit BD, Stanley WC.

Department of Nutrition, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106-4970, USA.

BACKGROUND: Chronic hypertension leads to cardiac hypertrophy, heart failure, and premature death. Little is known about the impact of dietary macronutrient composition on hypertension-induced cardiac hypertrophy and mortality. We investigated the effects of consuming either a high complex carbohydrate diet, a high simple sugar diet, or a high fat diet on cardiac hypertrophy and mortality in hypertensive Dahl salt-sensitive (DSS) rats. METHODS: Rats were assigned to four diets: complex carbohydrate (CC; 70% starch, 10% fat, 20% protein by energy), high fat (FAT; 20% carbohydrates, 60% fat, 20% protein), high fructose (FRU; 70% fructose, 10% fat, 20% protein), and "western" (WES; 35% fructose, 45% fat, 20% protein). Hypertension was initiated by adding 6% NaCl (+S) to the chow of half the animals within each diet (n = 10 to 13/group). Tail cuff blood pressure measurements were assessed after 5 and 11 weeks of treatment, and echocardiography were assessed after 12 weeks of treatment. RESULTS: All rats fed a high salt diet had similar levels of hypertension (CC+S 220 +/-2 mm Hg, FAT+S 221 +/- 3 mm Hg, FRU+S 221 +/- 1 mm Hg, WES+S 226 +/- 3 mm Hg). Echocardiography results show that the addition of salt to FRU resulted in increased regional wall thickness that was not observed in other dietary groups. All rats fed a low salt diet (CC, FAT, FRU, WES) and the FAT+S group survived 90 days. On the other hand, there was 90-day mortality in the WES+S group (18% mortality) and the CC+S group (30% mortality). In addition, FRU+S rats started dying after 45 days of salt feeding, and only 15% survived the full 90 days. CONCLUSIONS: These results demonstrate that a high fructose diet consumed during hypertension increases mortality and left ventricular (LV) wall thickness compared to either a high fat, high starch, or a "western" diet.

PMID: 17386347

What's interesting is that a quick glance at the articles you posted in response to me look like they are on point, and I'd like to take some time to read them more thouroughly.

However, the articles you posted in response to Jay are rediculous. The problem is not, as you point out, the rat models. The problem is that (I'm assuming) you are not a population that can be extrapolated to. You seem to be implying that diets high in saturated fats are healthier, and specifically for already healthy athletic people. But the studies were looking at the effects of diet on cardiac remodeling in the face of chronic hypertension. Unless you are using an extremely narrow and uncommon definition of healthy (namely, decreased cardiac hypertrophy in the setting of chronic hypertension), those studies are completely off topic.

I'll definitely grant you they are interesting. But you posted them in response to Jay, and in a way that implied you were using them to provide support to any one of your claims on saturated fats. Those studies, in no way, can be used to support any of your claims about saturated fats.

however, high fat feeding significantly increased LV contractile performance (e.g. increased cardiac output and peak dP/dt). 5. In conclusion, the HFD + salt diet prevented the hypertrophic response to hypertension and improved the contractile performance of the heart.

I just realized that the second one I posted was the wrong study. However, the first study definitely supports my beliefs..atleast for rats

[No, it very much doesn't. See the bolded part. Again, unless you are saying this diet is a healthier option for people with hypertension, it doesn't support your claim. And if you think its healthy in people without hypertension, you certainly haven't provided any reason to suppose those results are applicable to populations with normal blood pressures. And I'm doubtful this could be done, seeing that the benefit to the fats in the face of hypertension is that it prevents a detrimental response to a pathological condition. That has no real ramifications to the healthy state.

Red meat consumption and risk of stroke in Swedish men.
Larsson SC, Virtamo J, Wolk A.
SourceDivision of Nutritional Epidemiology, National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden and the Department of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland.

Abstract
BACKGROUND: Red and processed meat consumption has been implicated in several diseases. However, data on meat consumption in relation to stroke incidence are sparse.

OBJECTIVE: Our objective was to examine the associations of red meat and processed meat consumption with stroke incidence in men.

DESIGN: We prospectively followed 40,291 men aged 45-79 y who had no history of cardiovascular disease or cancer at baseline. Meat consumption was assessed with a self-administered questionnaire in 1997.

RESULTS: During a mean follow-up of 10.1 y, 2409 incident cases of stroke (1849 cerebral infarctions, 350 hemorrhagic strokes, and 210 unspecified strokes) were identified from the Swedish Hospital Discharge Registry. Consumption of processed meat, but not of fresh red meat, was positively associated with risk of stroke. The multivariable relative risks (RRs) of total stroke for the highest compared with the lowest quintiles of consumption were 1.23 (95% CI: 1.07, 1.40; P for trend = 0.004) for processed meat and 1.07 (95% CI: 0.93, 1.24; P for trend = 0.77) for fresh red meat. Processed meat consumption was also positively associated with risk of cerebral infarction in a comparison of the highest with the lowest quintile (RR: 1.18; 95% CI: 1.01, 1.38; P for trend = 0.03).

CONCLUSIONS: The findings from this prospective cohort of men indicate that processed meat consumption is positively associated with risk of stroke. The Cohort of Swedish Men is registered at clinicaltrials.gov as NCT01127711.

PMID:21653800[PubMed - as supplied by publisher

Conclusions: A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.

JAMA. 1997 Dec 24-31;278(24):2145-50.
Inverse association of dietary fat with development of ischemic stroke in men.
Gillman MW, Cupples LA, Millen BE, Ellison RC, Wolf PA.
Department of Ambulatory Care and Prevention, Harvard Medical School and Harvard Pilgrim Health Care, Boston, MA 02215, USA.

CONTEXT: A few ecological and cohort studies in Asian populations suggest an inverse association of the intake of both fat and saturated fat with risk of stroke. However, data among western populations are scant. OBJECTIVE: To examine the association of stroke incidence with intake of fat and type of fat among middle-aged US men during 20 years of follow-up. DESIGN AND SETTING: The Framingham Heart Study, a population-based cohort study. PARTICIPANTS: A total of 832 men, aged 45 through 65 years, who were free of cardiovascular disease at baseline (1966-1969). MEASUREMENTS AND DATA ANALYSIS: The diet of each subject was assessed at baseline by a single 24-hour dietary recall, from which intakes of energy and macronutrients were estimated. In Kaplan-Meier analyses, we calculated age-adjusted cumulative incidence rates of stroke. Using Cox regression, we estimated stroke incidence relative risks during 20 years of follow-up. MAIN OUTCOME MEASURE: Incidence of ischemic stroke, which occurred in 61 subjects during the follow-up period. RESULTS: Mean intakes were 10975 kJ for energy; 114 g (39% of energy) for total fat; 44 g (15%) for saturated fat; 46 g (16%) for monounsaturated fat; and 16 g (5%) for polyunsaturated fat. Risk of ischemic stroke declined across the increasing quintile of total fat (log-rank trend P=.008), saturated fat (P=.002), and monounsaturated fat (P=.008) but not polyunsaturated fat (P=.33). The age- and energy-adjusted relative risk for each increment of 3% of energy from total fat was 0.85 (95% confidence interval [CI], 0.78-0.94); for an increment of 1% from saturated fat, 0.91 (95% CI, 0.85-0.98); and for 1% from monounsaturated fat, 0.89 (95% CI, 0.83-0.96). Adjustment for cigarette smoking, glucose intolerance, body mass index, blood pressure, blood cholesterol level, physical activity, and intake of vegetables and fruits and alcohol did not materially change the results. Too few cases of hemorrhagic stroke (n=14) occurred to draw inferences. CONCLUSION: Intakes of fat, saturated fat, and monounsaturated fat were associated with reduced risk of ischemic stroke in men.

PMID: 9417007

BMJ. 2003 Oct 4;327(7418):777-82.
Dietary fat intake and risk of stroke in male US healthcare professionals: 14 year prospective cohort study.

He K, Merchant A, Rimm EB, Rosner BA, Stampfer MJ, Willett WC, Ascherio A.
Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA. hpkhe@channing.harvard.edu


OBJECTIVE: To examine the association between intake of total fat, specific types of fat, and cholesterol and risk of stroke in men. Design and setting Health professional follow up study with 14 year follow up. PARTICIPANTS: 43,732 men aged 40-75 years who were free from cardiovascular diseases and diabetes in 1986. MAIN OUTCOME MEASURE: Relative risk of ischaemic and haemorrhagic stroke according to intake of total fat, cholesterol, and specific types of fat. RESULTS: During the 14 year follow up 725 cases of stroke occurred, including 455 ischaemic strokes, 125 haemorrhagic stokes, and 145 strokes of unknown type. After adjustment for age, smoking, and other potential confounders, no evidence was found that the amount or type of dietary fat affects the risk of developing ischaemic or haemorrhagic stroke. Comparing the highest fifth of intake with the lowest fifth, the multivariate relative risk of ischaemic stroke was 0.91 (95% confidence interval 0.65 to 1.28; P for trend = 0.77) for total fat, 1.20 (0.84 to 1.70; P = 0.47) for animal fat, 1.07 (0.77 to 1.47; P = 0.66) for vegetable fat, 1.16 (0.81 to 1.65; P = 0.59) for saturated fat, 0.91 (0.65 to 1.28; P = 0.83) for monounsaturated fat, 0.88 (0.64 to 1.21; P = 0.25) for polyunsaturated fat, 0.87 (0.62 to 1.22; P = 0.42) for trans unsaturated fat, and 1.02 (0.75 to 1.39; P = 0.99) for dietary cholesterol. Intakes of red meats, high fat dairy products, nuts, and eggs were also not appreciably related to risk of stroke. CONCLUSIONS: These findings do not support associations between intake of total fat, cholesterol, or specific types of fat and risk of stroke in men.

PMID: 14525873

The HFD was protective of the heart during hypertension. I think to most people, that would say a lot. It speaks volumes to the idea that HFD's are unhealthy. What you're asking for doesn't exist. If healthy individuals are studied and remained healthy afterwards, it's very hard to draw the conclusion that the HFD made them healthy. There are such studies, but you can only argue that the diet didn't contribute to poor health. Almost all of these sorts of studies are and will be done on unhealthy individuals.

And the types of studies I was referring to DO exist. They are case-control and cohort studies. Looking at 2 populations of subjects, both healthy, one with high saturated dietary fats and the other without. Pick your end-points (hypertension, CAD, stroke, all-cause morbidity...I don't care....), gather your data, and calculate the RR/OR/AR what-have-you.

In regards to the grain free diet I am currently using:

I know the Paleo diet is very trendy right now, and I'd suggest everyone be leary of such things. However, there is data to support it's use, and it makes sense from a biological/evolutionary stand point. I decided a few months ago, to give this sort of diet a 30 day trial. That's all I'd suggest anyone else do. This is purely anecdotal, but I feel better than ever, and I've been able to maintain a very low BF level almost without effort.

Since you have provided such good links on the biology, would you mind providing some support from an evolutionary stand point? By my quick check, we have had grains for 1/2 of our time as a species

Our species has been around for well over 100,000 years. We've only been consuming grains for the last 10,000 or so. Some cultures have been consuming them for less time. As an example, those with Irish ancestories have a very high incidence of celiacs. Coincidentally, they have followed the hunter gather diet for a deal longer than the rest of the world.

We've been consuming grains for 100,000 plus years. Like I said, got some good backup for the evolutionary evidence?

The first evidence of a calorically important domesticated crop I'm aware of was about 11,500 years ago in the fertile crescent. They were cultivating an early ancestor of wheat called emmer. Other grains popped up independently in what is now China (rice; ~10,000 years ago), and central America (corn; ~9,000 years ago). That's why people say humans have been eating grains for about 10,000 years.

H. sapiens

Main article: Archaic Homo sapiens

H. sapiens (the adjective sapiens is Latin for "wise" or "intelligent") have lived from about 250,000 years ago to the present. Between 400,000 years ago and the second interglacial period in the Middle Pleistocene, around 250,000 years ago, the trend in skull expansion and the elaboration of stone tool technologies developed, providing evidence for a transition from H. erectus to H. sapiens. The direct evidence suggests there was a migration of H. erectus out of Africa, then a further speciation of H. sapiens from H. erectus in Africa. A subsequent migration within and out of Africa eventually replaced the earlier dispersed H. erectus. This migration and origin theory is usually referred to as the recent single origin or Out of Africa theory. Current evidence does not preclude some multiregional evolution or some admixture of the migrant H. sapiens with existing Homo populations. This is a hotly debated area of paleoanthropology.

Current research has established that humans are genetically highly homogenous; that is, the DNA of individuals is more alike than usual for most species, which may have resulted from their relatively recent evolution or the possibility of a population bottleneck resulting from cataclysmic natural events such as the Toba catastrophe.[45][46][47] Distinctive genetic characteristics have arisen, however, primarily as the result of small groups of people moving into new environmental circumstances. These adapted traits are a very small component of the Homo sapiens genome, but include various characteristics such as skin color and nose form, in addition to internal characteristics such as the ability to breathe more efficiently at high altitudes.

H. sapiens idaltu, from Ethiopia, is an extinct sub-species who lived about 160,000 years ago.