NU's Quest for Carnivory!

[NU_nutrition_TS]

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Wow, way to go on the rubuttal on those papers then.

I don't need to rebut them - they speak for themselves. Your interpretation of them is your own and does not necessarily follow on from the data.

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As for entropy, yes biological processes dissipate energy, big news story there. But is it sufficient enough to provide an advantage of low carb over other diets? The research I posted suggests not, as TEF goes Protein > Carbs > Fats, so again it's the protein content of a diet that matters when aruging metabolic advantage, not low carbs...

There are studies that still showed an advantage even when protein was held constant.

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As for your personal stash of bookmarks, how many of them are low carb / paleo blogs? I read both sides of the argument not just the one's that support my own.

They are varied - plus my former nutritional education was wholly based on the mainstream paradigm - so I have perspective from both sides of the debate.

[ATZ]

I think the conclusions are pretty clearly laid out by the authours of those studies. For you to just disregard them so readily shows a lack of impartiality on your behalf.

Feinman may have shown an advantage after lots of theoretical mastubation, and your reference to entropy no doubt refers to gluconeogensis (GNG) burning calories during low carb diets.

Fine and GNG does expend calories. Few things though:

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1. GNG goes down rapidly in the first 2-3 weeks of keto adaptation to spare protein. I don't see basing a metabolic advantage on 2-3 weeks very important
2. Any increase in GNG has to be weighed against a decrease in TEF from eating less carbs.
3. He never quantified the contribution of GNG

Yay for entropy!

[NU_nutrition_TS]

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I think the conclusions are pretty clearly laid out by the authours of those studies. For you to just disregard them so readily shows a lack of impartiality on your behalf.

Yawn! If you insist!

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Estimates of physical activity were stable in the dieters during the study and did not differ between groups. These results confirm that short-term weight loss is greater in obese women on a low-carbohydrate diet than in those on a low-fat diet even when reported food intake is similar. The differential weight loss is not explained by differences in REE, TEF, or physical activity and likely reflects underreporting of food consumption by the low-fat dieters.

Mmm! 'Likely' - not a fact then. And only in the low fat dieters? So dietary under-reporting is not a general human weakness then - just low fat dieters? COP OUT!

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Thermodynamics dictate that a calorie is a calorie regardless of the macronutrient composition of the diet. Further research on differences in the composition of weight loss and on the influence of satiety on compliance with energy-restricted diets is needed to explain the observed increase in weight loss with diets high in protein and/or low in carbohydrate.

This is not making any definitive point merely calling for more research to elucidate one!

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More studies of the efficacy of weight-loss and weight-maintenance diets that address protein content are needed. In addition, controlled studies of total energy expenditure or physical activity measured under free-living conditions that directly compare high-protein diets with those containing low and moderate carbohydrate content should also be performed.

Again, calling for more research - which is admitting this study does not, in itself, constitute definitive proof.

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Feinman may have shown an advantage after lots of theoretical mastubation, and your reference to entropy no doubt refers to gluconeogensis (GNG) burning calories during low carb diets.

Does it? I don't recall saying that!

Any 'metabolic advantage' is probably a multi-factoral phenomenon and cannot be pinned on any one thing. Hence why further research is needed.

Just to highlight that metabolic ward studies are not quite so sancrosanct:

From an article on metabolic ward nutritional study protocols in the American Journal of Clinical Nutrition.

[ATZ]

I've seen this kind of avoidance and changing of goalposts previosuly Nu. You want people to believe there's a metabolic advantage, yet you're unwilling to provide the evidence yourself, just take great pride in rebuking actual scientific studies I've posted rather than blog posts.

We all know low fat diets increase hunger, high carb, low fat and protein is not particulary satieting. You've pointed out how metabolic wards still leave roommfor diet cheating - that they do, but we know cheating on a low carb diet is less likely given it's effects on hunger, hence the conclusions.

More studies are required, as (because I've already pointed out) most of the research out there compares high carb, low fat and low protein diets, with high fat and moderate protein diets. The diet with the highest amount of protein is most of the time going to come out on top.

[NU_nutrition_TS]

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I've seen this kind of avoidance and changing of goalposts previosuly Nu. You want people to believe there's a metabolic advantage, yet you're unwilling to provide the evidence yourself, just take great pride in rebuking actual scientific studies I've posted rather than blog posts.

It takes one to know one!

You were the one that quoted the Dr Eades' blog post about the MOUSE study and tried to twist the good doctors words to suit your agenda (I have already quoted the relevant section where he clearly says that MOUSE studies cannot be applied to HUMANS). On the other hand, the Dr Eades' blog post that I posted mentions the metabolic advantage in connection to a study done on HUMANS.

So I leave it up to the more discerning readers of this thread to decide for themselves which of the two of us is moving the goalposts and playing foul!

I don't want people to believe there is a metabolic advantage - that's up to them - it's people that automatically dismiss the possibility out-of-hand and/or use lame justifications like equilibrium thermodynamics on non-equilibrium systems to refute it that tick me off!

I didn't rebuke your studies - I just said they speak for themselves. In the one case the people on low carb diets lost more weight and more of that weight was fat. If the researchers - or you - want to interpret those results as the low fat dieters under-reported while the low carbers did not, then that is their - and your - opinion; it is not a proven fact. If I choose to interpret it as possible evidence for a metabolic advantage that's also my opinion and not a proven fact. People have to look at the evidence, the opinions and their own experience and decide for themselves which is more likely.

As to the others, they merely constituted literature overviews and called for more research rather than offering a definitive answer.

[NU_nutrition_TS]

Some more data for the arguments about whether a 'palaeolithic' diet was most often predominantly animal or plant based:

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FOCUS: Gough's Cave and Sun Hole Cave Human Stable Isotope Values Indicate a High Animal Protein Diet in the British Upper Palaeolithic

M. P. Richardsa, R. E. M. Hedgesa, R. Jacobib, A. Currentb and C. Stringerb
a Research Laboratory for Archaeology and the History of Art, University of Oxford, 6 Keble Road, Oxford, OX1 3QJ, U.K.
b Department of Palaeontology, Natural History Museum, Cromwell Road, London, SW7 5BD, U.K.

Available online 26 March 2002.

Abstract

We undertook stable isotope analysis of Upper Palaeolithic humans and fauna from the sites of Gough's Cave and Sun Hole Cave, Somerset, U.K., for palaeodietary reconstruction. We were testing the hypothesis that these humans had a mainly hunting economy, and therefore a diet high in animal protein. We found this to be the case, and by comparing the human δ15N values with those of contemporary fauna, we conclude that the protein sources in human diets at these sites came mainly from herbivores such as Bos sp. and Cervus elaphus. There are a large number ofEquus sp. faunal remains from this site, but this species was not a significant food resource in the diets of these Upper Palaeolithic humans.

ScienceDirect - Journal of Archaeological Science : FOCUS: Gough's Cave and Sun Hole Cave Human Stable Isotope Values Indicate a High Animal Protein Diet in the British Upper Palaeolithic

And, assuming the stable isotope evidence from palaeolithic fossils around the world shows a predominantly land mammal based diet was most prevalent, a letter to the AJCN which casts doubt on the oft-cited unhealthy PRAL of such a diet:

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Paleolithic diet, sweet potato eaters, and potential renal acid load

Thomas Remer and Friedrich Manz Department of Nutrition and Health Research Institute of Child Nutrition Heinstuck 11 Dortmund 44225 Germany E-mail: remer@fke-do.de


Dear Sir:
In a recent article in the Journal, Sebastian et al (1) provided a detailed analysis of the probable effect of ancestral preagricultural diets on systemic acid load (net endogenous acid production, or NEAP) and compared this with the average acid load of contemporary diets. The NEAP was calculated for retrojected preagricultural diets for which compositions were suggested by Eaton and Konner (2). Current food tables served to estimate the respective nutrient content. Final computation was based on an existing calculation model (3, 4) that was modified to more accurately estimate those food-dependent acid loads that lead to endogenous production (and renal excretion) of sulfate and organic acids (OAs).


This modified approach, which considers individual dietary sulfur-containing amino acids (instead of average protein content) and dietary determinants of OA production, offers an important improvement to existing estimation models for net acid excretion. However, we do not fully agree with Sebastian et al, who argue that food-dependent endogenous OA production can be sufficiently predicted (with specific formulas) from the same nutrients (sodium, potassium, calcium, magnesium, chlorine, and phosphorus) that are needed to estimate the major food-dependent component (apart from sulfur-containing amino acids) of NEAP or of potential renal acid load (PRAL).


It is highly probable that the renal excretion of different OAs is dependent on diet. Aromatic organic acids are a dietary component, not mentioned by Sebastian et al, that may have a particularly strong effect. For example, phenolic and benzoic acids, which are found in considerable amounts especially in fruit (5, 6), are metabolically inactivated (detoxified) and excreted (mainly via the kidney) as acids, largely in the form of hippuric acid.


Interestingly, in the highlands of New Guinea, some Papuan tribes consume a low-protein vegetarian diet consisting predominantly of sweet potatoes. These sweet potato eaters excrete extremely high amounts of hippuric acid (31 mmol/d on average compared with 4 mmol/d in European control subjects), which adds substantially to their basal (not primarily food-dependent) urinary OA excretion (7). Basal OA excretion can be estimated from average anthropometric data as follows (3, 4):

(1)

As a result, 36 mEq/d is yielded for sweet potato eaters [young adult males weighing 53 kg, 1.55 cm tall, and with a body surface area of 1.5 m2; (7)], which together with their hippuric acid output amounts to 67 mEq total OA excretion/d.


The reported data (7) on average daily food intake and 24-h urinary excretion of sodium (7 mmol/d), chloride (4 mmol/d), potassium (180 mmol/d), and total nitrogen (2.6 g/d) allowed us to estimate the NEAP and PRAL of the sweet potato eaters. Urinary excretion rates not given in the original article (7) were calculated (3, 4) from the corresponding daily intakes of magnesium (443 mg/d), calcium (728 mg/d), and phosphorus (936 mg/d). They were obtained from the reported food consumption by using food tables (8) and yielded values of 12, 9, and 34 mEq/d, respectively. Urinary sulfate output (11 mEq/d) was estimated from protein degradation, ie, from total nitrogen excretion (see above), corresponding to an absorbed amount of 16.3 g protein/d. The nutrient-dependent PRAL (sulfate + phosphate + chloride - sodium - potassium - magnesium - calcium) was then calculated as -159 mEq/d. Because the NEAP corresponds to PRAL + OA, an average overall endogenous acid production of -92 mEq/d was finally yielded. This NEAP, directly calculated for "modern" stone age farmers by using measured (ie, hard) data for the intake and renal excretion of nutrients, is nearly identical to the average NEAP (-88 mEq/d) found by Sebastian et al for 159 retrojected preagricultural diets. However, the protein intake of the sweet potato eaters was very low (22 g protein/d, as estimated from urinary nitrogen output under the assumption of 75% net absorption), whereas protein intakes of 200 g are assumed for most ancestral diets (1, 9).

If the protein intake of sweet potato eaters was to isoenergetically increase by only 100 g/d (with protein replacing carbohydrates), the NEAP would increase (ie, net base production would fall) to -43 mEq/d. Therefore, it appears to us that the average net base production of -88 mEq/d (ie, the absolute figure) calculated by Sebastian et al may be too high for Stone Age persons with high protein intakes. This is also confirmed if the average PRAL and NEAP are calculated from the average nutrient intakes of Stone Age persons as recently published by Eaton and Eaton (9). Using their figures on daily nutrient intakes, we estimated a negative PRAL of -39 mEq/d, leading to an NEAP of 22 mEq/d, which is markedly lower than current net acid excretion (64 mEq) in the United States.

Taken together, we also conclude that the average Paleolithic diet principally led to net base production (yielding a negative PRAL), but was possibly less alkaline than suggested by Sebastian et al. One of several uncertainties in this respect is obviously the intake of those OAs not metabolically combusted but renally excreted, eg, phenolic acid, which is excreted in the form of hippuric acid. Reasons for the historical shift from negative to positive PRAL are not only the displacement of alkali-rich plant foods in the ancestral diet by cereal grains and nutrient-poor foods in the temporary diet but also the modern processing and preparation of foods, which lead to considerable losses of base-forming nutrients such as potassium and magnesium.

Paleolithic diet, sweet potato eaters, and potential renal acid load -- Remer and Manz 78 (4): 802 -- American Journal of Clinical Nutrition

[NU_nutrition_TS]

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Q: Are there any negative effects associated with chia seeds which would make them inappropriate in The Paleo Diet?

Thank you.

A: Good question. I would imagine that many of our readers have never even heard of chia seeds much less eaten them. Chia seeds (Salvia hispanica L.) are a member of the Labiatae plant family and are native to southern Mexico and northern Guatemala. The seeds are small, oval shaped; either black or white colored and resemble sesame seeds1. These seeds were cultivated as a food crop for thousands of years in this region by the Aztecs and other native cultures. Chia seeds can be consumed in a variety of ways including roasting and grinding the seeds into a flour known as Chianpinolli which can then become incorporated into tortillas, tamales, and various beverages2. The roasted ground seeds were traditionally consumed as a semi-fluid mucilaginous gruel (Pinole) when water is added to the flour. In post-Columbian times the most popular use of chia flour was to make a refreshing beverage in which the ratio of seeds to water is decreased, thereby resulting in a less gelatinous consistency to which lemon, sugar or fruit juice are added2. The sticky consistency of chia seed Pinole or chia beverages comes from a clear mucilaginous, polysaccharide gel that remains tightly bound to the seeds3. This sticky gel forms a physical barrier which may impair digestion and absorption of fat from the seed4 while also causing a low protein digestibility5.

In the past 20 years a revival of interest in chia seeds has occurred primarily because of their high fat content of about 25-39% by weight, of which 50-57 % is the therapeutic omega 3 fatty acid and alpha linolenic acid (ALA)6, 7. In the past 10 years chia seeds have been used as a foodstuff for animals to enrich their eggs and meat with omega 3 fatty acids8-11. So I wholeheartedly approve of feeding chia seeds to animals and then eating the omega 3 fatty acid enriched meat or eggs of these animals.

How about feeding chia seeds to humans – should we consume chia seeds because of their high omega 3 fatty acid (ALA) content? The Table below shows the entire nutrient profile of chia seeds. At least on paper, it would appear that chia seeds are a nutritious food that is not only high in ALA, but also is a good source of protein, fiber, certain B vitamins, calcium, iron and manganese.

Unfortunately, the devil is always in the details, and as is the case with many other plant seeds (e.g. cereal grains, legumes) a frequent evolutionary strategy to prevent predation by animals and microorganisms is the natural selection by the plant for toxic compounds known as antinutrients. As I previously mentioned, the thick mucilaginous gel which is tightly bound to chia seeds may impair fat absorption in animals4 which, along with their high fiber content, causes the available protein to be poorly absorbed5. Another antinutrient found in chia seeds (~2,000 mg/100 g) is phytate or phytic acid, which impairs absorption of all divalent ions (calcium, iron, zinc, magnesium, manganese, etc) in a dose-dependent manner12, 13. Meaning that once in your body (in vivo), the available calcium, iron, zinc, magnesium and manganese from chia seeds are poorly absorbed, hence making chia seeds a poor dietary source for these minerals. Although Table 1 suggests that chia seeds may be good sources of vitamin B6, the bioavailability of B6 from plant foods tends to be low, whereas bioavailability of B6 from animal products is generally quite - high approaching 100%14.

A number of chia seed supplementation studies in rats and experimental animals have demonstrated certain favorable health effects including improvements in blood lipids, and insulin metabolism9, 15, 16. However, these effects could not be replicated in a recent, well controlled study in humans, who consumed 50 grams of chia seeds per day for 12 weeks19. In fact, despite an increase in blood ALA concentrations, overweight men and women experienced no changes in body weight, blood pressure, blood lipids or inflammatory blood markers17. A recent review of all human chia supplementation studies concluded: "There is limited evidence supporting the efficacy of Salvia hispanica for any indication; thus far, only two clinical studies have examined the effects of Salvia hispanica on cardiovascular disease (CVD) risk factors (including body weight). One study showed some effects on some CVD risk factors, while the other did not. Neither study showed any effects of Salvia hispanica on weight loss."

One of the outcomes of the Nieman et al. study17 that will require further scrutiny suggests that chia seed consumption may contain one or more antinutrients which may promote chronic low level inflammation – not a good thing. If you look at the data carefully, both men and women experienced increases in a blood inflammatory marker called interleukin 6 (IL-6). After 12 weeks of eating chia seeds the men’s blood levels of IL-6 increased 10.2% and the women’s increased 10.1%. Additionally another inflammatory marker called monocyte chemotactic protein (MCP) increased 6.9% in men, and 6.1% in women. Although the authors deemed these increases to be statistically insignificant, the large standard deviations for the measurements suggest that confounding extraneous factors may have influenced the results. In support of the notion that chia seed consumption may adversely affect the immune system and promote inflammation is a rat study showing that a one-month high-chia seed diet increased blood levels of IgE by 112.8%18. IgE is an immunoglobulin that is a marker for allergenic food proteins that are processed through the gut19.

Just how chia seed consumption may promote chronic low-level systemic inflammation via their presence in the gastrointestinal tract is unclear. Although many species of Salvia have a high lectin content20, which may adversely affect the gut by increasing intestinal permeability21, Salvia hispanica or chia seeds do not contain any known lectins22. Consequently, it is possible that other antinutrients found in chia seeds may adversely affect gut tissue, including saponins, which are frequently found in Salvia species23, and which cause a "leaky gut"24-27. To date, the saponin content of chia has not been measured. The thick mucilaginous gel which is tightly bound to chia seeds is a complex polysaccharide, and these types of polysaccharide gums are known to adversely alter small intestinal cell function - including increased mucosal cell production28, which could increase intestinal permeability.

When the gut becomes "leaky" it is not a good thing, as the gut contents may then have access to the immune system, which in turn becomes activated, and thereby causes chronic low-level systemic inflammation. In particular, a component of the cell walls of gut gram negative bacteria called lipopolysaccharide (LPS) is highly inflammatory. Any LPS which gets past the gut barrier is immediately engulfed by two types of immune system cells (macrophages and dendritic cells). Once engulfed by these cells, LPS binds to Toll Like Receptor 4, which in turn causes an immediate immune system response including increases in blood levels of IL-6 as shown in the Nieman et al study17. Until further human studies are conducted, I would be cautious in recommending chia seeds for human consumption, particularly in people with food allergies or known autoimmune diseases.

From The Paleo Newsletter of Dr Loren Cordain.

Now why am I reminded of those technologically advanced but diseased of mind, spirit and body Mayan's in Mel Gibson's Apocalypto?

[NU_nutrition_TS]

References (for the above):

1. Ixtainaa, VY, Nolascoa, SM, Tomás, MC. Physical properties of chia (Salvia hispanica L.) seeds. Industrial Crops and Products 2008;28:286-93.
2. Cahill, J.P. 2003. Ethnobotany of chia, Salvia hispanica L. (Lamiaceae). Economic Botany, 57(4):604-618.
3. Lin, K.Y., J.R. Daniel, and R.L. Whistler. 1994. Structure of chia seed polysaccharide exudate. Carbohydrate Polymers, 23:13-18.
4. Peiretti, P.B., G. Meineri. 2008. Effects on growth performance, carcass characteristics, and the fat and meat fatty acid profile of rabbits fed dietswith chia (Salvia hispanica L.) seed supplements. Meat Science, 80 (2008): 1116-1121.
5. Monroy-Torres, R., M.L. Mancilla-Escobar, J.C. Gallaga-Solorzano, S. Medina-Godoy, and E.J. Santiago-Garcia. 2008. Protein Digestibility of Chia Seed Salvia hispanica L. Revista Salud Publica y Nutricion, 9(1), Enero-Marzo 2008. Monterey, Mexico.
6. Ayerza, R. Oil content and fatty acid composition of Chia (Salvia hispanica L.) from five northwestern locations in Argentina. Journal of the American Oil Chemists Society 1995;72: 1079-1081.
7. Ting, I.P., J.H. Brown, H.H. Naqvi, J. Kumamoto, and M. Matsumura. 1990. Chia: a potential oil crop for arid zones. In: New Industrial Crops and Products, Proceedings of The First International Conference on New Industrial Crops and Products, edited by H.H. Naqvi, A. Estilai, and I.P. Ting. Association for the Advancement of Industrial Crops, Riverside, California, USA, pp. 197-202.
8. Ayerza R, Coates W. Dietary levels of chia: influence on hen weight, egg production and sensory quality, for two strains of hens.Br Poult Sci. 2002 May;43(2):283-90.
9. Ayerza R, Coates W, Lauria M. Chia seed (Salvia hispanica L.) as an omega-3 fatty acid source for broilers: influence on fatty acid composition, cholesterol and fat content of white and dark meats, growth performance, and sensory characteristics. Poult Sci. 2002 Jun;81(6):826-37.
10. Coates W, Ayerza R. Chia (Salvia hispanica L.) seed as an n-3 fatty acid source for finishing pigs: effects on fatty acid composition and fat stability of the meat and internal fat, growth performance, and meat sensory characteristics. J Anim Sci. 2009 Nov;87(11):3798-804.
11. Peiretti, P.B., G. Meineri. 2008. Effects on growth performance, carcass characteristics, and the fat and meat fatty acid profile of rabbits fed dietswith chia (Salvia hispanica L.) seed supplements. Meat Science, 80 (2008): 1116-1121.
12. Cordain L. Cereal grains: humanity’s double edged sword. World Rev Nutr Diet 1999; 84:19-73.
13. Torre M, Rodriguez AR, Saura-Calixto F: Effects of dietary fiber and phytic acid on mineral availability. Crit Rev Food Sci Nutr 1991;1:1-22.
14. Reynolds RD: Bioavailability of vitamin B-6 from plant foods. Am J Clin Nutr 1988;48:863-67.
15. Chicco, A.G., M. E. D'Alessandro, G.J. Hein, M.E. Oliva and Y.B. Lombardo. 2008. Dietary chia seed (Saliva hispanica L.) rich in α-linolenic acid improves adiposity and normalizes hypertriacylglycerolaemia and insulin resistance in dyslipaemic rats. British Journal of Nutrition, 101(2009): 41-50.
16. Ayerza R Jr, Coates W. Effect of dietary alpha-linolenic fatty acid derived from chia when fed as ground seed, whole seed and oil on lipid content and fatty acid composition of rat plasma. Ann Nutr Metab. 2007;51(1):27-34.
17. Nieman, D., C., E. J. Cayea, M. D. Austin, D. A. Henson, S. R. McAnulty, F. Jin. 2009. Chia seed does not promote weight loss or alter disease risk factors in overweight adults. Nutrition Research, 29(2009):414-418.
18. Fernandez, S., M. Vidueiros, R. Ayerza, W. Coates and A. Pallaro. 2008. Impact of chia (Salvia hispanica L) on the immune system: preliminary study. Proceedings of the Nutrition Soceity, Volume 67, Issue OCE, May 2008, E12.
19. Eigenmann PA. Mechanisms of food allergy. Pediatr Allergy Immuol 2009;20:5-11.
20. Perez G. Lectin prospecting in Colombian Labiatae. A systemic ecological approach – II. Caldasia 2006; 28(2):179-195.
21. Cordain L, Toohey L, Smith MJ, Hickey MS. Modulation of immune function by dietary lectins in rheumatoid arthritis. Br J Nutr. 2000 Mar;83(3):207-17.
22. Bird GW, Wingham J. More Salvia agglutinins. Vox Sang 1976;30:217-219.
23. Sabahi M, Ramezanian M, Jaffari GH, Heravi GH, Bahaeddini F. Survey of Iranian plants for saponins, alkaloids, flavonoids, and tannins. IV. The plants of Kerman Province. Int J Crude Drug Res 1985;23:165-175.
24. Keukens EA, de Vrije T, van den Boom C, de Waard P, Plasman HH, Thiel F, Chupin V, Jongen WM, de Kruijff B. Molecular basis of glycoalkaloid induced membrane disruption. Biochim Biophys Acta. 1995 Dec 13;1240(2):216-28.
25. Alvarez JR, Torres-Pinedo R. Interactions of soybean lectin, soyasaponins, and glycinin with rabbit jejunal mucosa in vitro. Pediatr Res. 1982 Sep;16(9):728-31.
26. Story JA, LePage SL, Petro MS, West LG, Cassidy MM, Lightfoot FG, Vahouny GV. Interactions of alfalfa plant and sprout saponins with cholesterol in vitro and in cholesterol-fed rats. Am J Clin Nutr. 1984 Jun;39(6):917-29.
27. Johnson IT, Gee JM, Price K, Curl C, Fenwick GR. Influence of saponins on gut permeability and active nutrient transport in vitro. J Nutr. 1986 Nov;116(11):2270-7.
28. Johnson IT, Gee JM. Gastrointestinal adaptation in response to soluble non-available polysaccharides in the rat. Br J Nutr. 1986 May;55(3):497-505.

[Supadude]

Does Cordain hold the same view with regards to flaxseeds? I did a search on his site but found nothing conclusive?

[Wotan]

Quite franky SD I wouldn't bother with flaxseeds at all.

Three (possibly four) problems, really.

The omega 3 rich oil it contains is not well-used by the human body. Its a different length to that found in fish oils (one is 18 carbon atoms long and the other 22 carbon atoms long). It is possible for the body to convert them into a useable form but this conversion rate is fairly poor (in the region of about a 5% yield and is both enzyme and energy hungry). Best to stick to fish oils, basically.

On the other hand if you are thinking of eating them for their fibre content etc be warned - they are high in estrogenic lignans. Go for something else less likely to clash with your testosterone levels I'd say.

Third problem - the testa (seed coating) is tough, has sharp edges and was designed to withstand the rigours of an animals intestines. The plant didn't grow them to be eaten - they were supposed to turn into new flax plants. So you either need to grind them up yourself (which, quite frankly, is a fag) or buy them ready-dehulled. This latter option makes them pretty expensive though - especially if you plan to eat them in any quantity!

One last problem, which may or may not be of any significance depending upon the rest of your diet, is that they are not as good in amino acid ratios as things from animal sources (meat, cheese, eggs etc).

However if you just like them for the taste go ahead!!