The info sungam gave is correct, though one thing caught my mind: how does being a poor student stopping you from having a proper diet? I'm in the same boat

The info sungam gave is correct, though one thing caught my mind: how does being a poor student stopping you from having a proper diet? I'm in the same boat (poor student) and since I cant afford pizza/eating out I have to cook at home. This leads to having a more balanced diet than eating junk food in the city Of course you still need some nutrition basics for that, but eating white meat (chicken) with vegetables and rice is a good (though boring) diet. Throw some food supplement (I'm eating a multivitamin pill each day) and you can't go wrong.

Wow thanks man thats means a lot! I need to write this down. but that stuff sounds real good and cheap! lucky I got food shopping tonight,, time for a change in diet =) thank you heaps again.

Ps. sounds like you have a good girl friend that looks after you! ha

Thanks again

Hey man thats such a good idea, ear plugs are known to fall out though? but i will definitely get some of though's as soon as i can thanks a lot! you feed back is awesome =)

The only foods I really avoid are grains, most dairy (I only consume full-fat dairy).

my diet is pretty crap being a poor student so I was wondering if you guys have any tips on Nutrition?

I'm a big fan of the Paleo style diets (no grains, lots of veggies, fruits, meats, and nuts). I believe that diets high in grains and added sugars are inflammatory. High systemic inflammation increases recovery time, and brings on all sorts of problems. Hell, it even looks like wheat gluten might be responsible for all sorts of auto-immune related issues.

I find the diet to be very easily maintainable. I can eat as many veggies as I want. I eat lots of awesome meats (mostly free range and wild). I eat a healthy amount of fruit and nuts as well. If I want something starchy, I'll grab a potatoe or banana. The only foods I really avoid are grains, most dairy (I only consume full-fat dairy), and legumes (peanuts/beans). I am leaner than I've ever been and I feel like I haven't put much effort into maintaining this diet at all.

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.

I'm not trying to pick a fight here, but I think you have things backwards. While we don't know exactly what causes Celiac Sprue, evidence points to an auto-immune reaction due to proteins in gluten resembling proteins in our own bodies. This is different than gluten causing "all sorts of auto-immune related issues". It'll only happen in predisposed people, and as far as I understand, its only ONE auto-immune related issue caused by gluten. Yes, people with auto-immune issues tend to have a few different auto-immune diseases, but this is a base problem with their immune system, not with gluten per se. We see the same thing in people with auto-immune disease but no Celiac. And there are MANY fewer people with Celiac than people think. Much like with lactose, the number of people who don't digest wheat products well is much greater than the number of people with Celiac's, a true auto-immune disease requiring very specific anti-bodies causing very specific visible changes to the small intestines.

As far as I'm aware, there is no good evidence to show that, on the whole, grains and added sugars are inflammatory.

Out of curiosity, what dangers are you referring to?

Correlations with other diseases have been made and are now being studied. That being said, correlation does not necessarily equal cause and effect. The problem is as you mentioned. Gluten resembles proteins in our own bodies. It has the ability to pass through the gut directly into the bloodstream. There, it is easily transported to just about any tissue in the body due to the fact that it resembles certain proteins. When the body detects the foreign glycoprotein it may initiate an immune response.

It's actually a well established fact that grains specifically are pro-inflammatory. There are many glycoproteins within grains that were designed specifically to keep animals and humans from eating them. Grains have evolved to be scattered by the wind, not consumed such as the seeds from fruits.

Sorry, I was referring specifically to the supposed dangers of saturated fat. High saturated fat is only dangerous/unhealthy when taken in context.

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.

1) do you truely not have anything better to do than to start fights on the Internet?

2) who are you to say what works better for me?

3) do you ever provide any support for your attacks?

You're wrong. Humans have only been consuming grains for about 10,000 years.

(snip)

http://wholehealthsource.blogspot.com/2008/07/grains-and-human-evolution.html

The role of starchy plants in early hominin diets and when the culinary processing of starches began have been difficult to track archaeologically. Seed collecting is conventionally perceived to have been an irrelevant activity among the Pleistocene foragers of southern Africa, on the grounds of both technological difficulty in the processing of grains and the belief that roots, fruits, and nuts, not cereals, were the basis for subsistence for the past 100,000 years and further back in time. A large assemblage of starch granules has been retrieved from the surfaces of Middle Stone Age stone tools from Mozambique, showing that early Homo sapiens relied on grass seeds starting at least 105,000 years ago, including those of sorghum grasses.

She and her colleagues analyzed mortar and pestle-type stones that were found at three sites: Bilancino II in the Megello Valley of Italy, Kostenki 16 at Pokrovsky Valley, Russia; and Pavlov VI in southern Moravia, Czech Republic. Since modern humans as well as Neanderthals inhabited these regions, the researchers think it's possible that either or both groups had cooking know-how.

The food preparation tools were found to contain the remains of starch grains from various wild plants, including cattail rhizomes, cattail leaves, moonworts, the ternate grapefern, lady's mantle, burdock, lettuce roots, rye, burr chervil root, parts of edible grasses, edible seeds and more.

I won't spend much time on this, because it's a well accepted fact and not debated. The neolithic age began about 10,000 years ago. What seperated the paleolithic from the neolithic age? ...modern agriculture (primarily the milling of grains).

Humans have been around for about 250,000 years

So, as you can clearly see, we've only been consuming grains for about 1/25th of our existance. I don't believe that has given evolution enough time for us adapt to a diet high in grains. Compounding the fact is that we have consumed grains in the amounts we do today for only a couple of centuries.

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?

Am J Clin Nutr. 2000 Mar;71(3):682-92.

Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets.

Cordain L, Miller JB, Eaton SB, Mann N, Holt SH, Speth JD.


Source

Department of Health and Exercise Science, Colorado State University, Fort Collins, CO 80523, USA. cordain@cahs.colostate.edu


Abstract

Both anthropologists and nutritionists have long recognized that the diets of modern-day hunter-gatherers may represent a reference standard for modern human nutrition and a model for defense against certain diseases of affluence. Because the hunter-gatherer way of life is now probably extinct in its purely un-Westernized form, nutritionists and anthropologists must rely on indirect procedures to reconstruct the traditional diet of preagricultural humans. In this analysis, we incorporate the most recent ethnographic compilation of plant-to-animal economic subsistence patterns of hunter-gatherers to estimate likely dietary macronutrient intakes (% of energy) for environmentally diverse hunter-gatherer populations. Furthermore, we show how differences in the percentage of body fat in prey animals would alter protein intakes in hunter-gatherers and how a maximal protein ceiling influences the selection of other macronutrients. Our analysis showed that whenever and wherever it was ecologically possible, hunter-gatherers consumed high amounts (45-65% of energy) of animal food. Most (73%) of the worldwide hunter-gatherer societies derived >50% (> or =56-65% of energy) of their subsistence from animal foods, whereas only 14% of these societies derived >50% (> or =56-65% of energy) of their subsistence from gathered plant foods. This high reliance on animal-based foods coupled with the relatively low carbohydrate content of wild plant foods produces universally characteristic macronutrient consumption ratios in which protein is elevated (19-35% of energy) at the expense of carbohydrates (22-40% of energy).

Is this what you learned from all those student loans I've been paying for?

I will say, patrickh, while I don't really agree with a lot of the conclusions you've drawn, I do appreciate that you have at least done some significant research into these things, and for the most part use good sources.

All he is doing is cherry-picking the literature for sources that support his belief. That's not doing valid research.

Jay

Saturated fat, vitamin C and smoking predict long-term population all-cause mortality rates in the Seven Countries Study
Daan Kromhouta, Bennie Bloemberga, Edith Feskensa, Alessandro Menottia,b, Aulikki Nissinenc and for the Seven Countries Study Group
+ Author Affiliations

aDivision of Public Health Research, National Institute of Public Health and the Environment, Bilthoven, The Netherlands.
bDivision of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, MN, USA.
cDepartment of Public Health and General Practice, University of Kuopio, Finland.
Reprint requests to: Prof. Daan Kromhout, National Institute of Public Health and the Environment, Division of Public Health Research, PO Box 1, 3720 BA Bilthoven, The Netherlands. E-mail: daan.kromhout@RIVM.nl
Accepted August 23, 1999.
Abstract

Background The Seven Countries Study has shown that population mortality rates for various chronic diseases are related to diet and smoking. This paper addresses the associations between diet, smoking and 25-year all-cause mortality.

Methods Baseline surveys were carried out between 1958 and 1964 on 12 763 middle-aged men constituting 16 cohorts in seven countries. In 1987/88 equivalent food composites representing the average food intake of each cohort at baseline were collected and chemically analysed in one central laboratory. During 25 years of follow-up 5973 men died and age-adjusted population mortality rates were calculated for each cohort.

Results Multivariate linear regression analyses showed that the population intake of saturated fat and the prevalence of smoking were positively associated with population all-cause mortality rates. Population vitamin C intake was inversely associated with all-cause mortality. It was calculated that a reduction in saturated fat intake of 5% of energy, a 20 mg/d increase in vitamin C and a 10% decrease in the prevalence of smokers may decrease the 25-year all-cause population mortality rate by 12.4% (95% CI : 5.6, 19.4%) at an average population all-cause mortality rate of 45%.

Conclusion At the population level saturated fat, vitamin C and cigarette smoking are important determinants of all-cause mortality.

No its not, and like I said, even given the cherry picking he is drawing some far out conclusions not supported by the articles.

Dietary fats aren't the primary factor associated w/ CVD; hypercholesterolemia is. You are, as far as I understand, correct there.

You are, however, forgetting that there are other deadly problems that are directly related to diets high in saturated fats.

to start...

If you go back and look at the logic of what you are trying to demonstrate with the hypertension studies, you'll see your conclusions really are far out.

And you'll see I just posted (probably while you were posting) that I agree, most studies show there isn't a clear link between dietary saturated fat and CVD. But there are strong links between saturated fats and morbidity and mortality. And I posted up a paper too...

No its not, and like I said, even given the cherry picking he is drawing some far out conclusions not supported by the articles.

But, even given all that, its better than most pissing matches on here.

I've heard of the Intelligence Squared debates, but must admit I really know nothing about them.

That sounds like a really interesting way to score a debate.

What did you think of the US News & World Report ranking of diets?

The grains mentioned in your paper differ greatly from the strains of wheat and barely we consume today. I can't read the full text of your first article and the second mentions dates only 30,000 years back. The seeds from cattails are not the same as the genetically engineered wheat that makes up a great portion of our cereals today.

Do you have any evidence to suggest what proportions of early human diet came from grain? The problem is that different cultures differ greatly in what is eaten even to this day. What people ate during the paleolithic era was based on calorie density and ease of access. I highly doubt that in most areas it was easy to gather a bunch a grains, grind them up, etc. than it was to slaughter one grazing animal that likely provided many more calories.

Posting a recipe for lecso, and this happens a few days later. Awesome. "Hungarian food is hot." has a new meaning.