36 replies to this topic

[Skötkonung]

Sorry all mighty Skotkonung, you sure the saturated fats haven't gone to your head to make you a little inflexible? just kidding around.

I was only referencing why I thought humans may not be suited to saturated fats -- and why how it might be possible to justify the title of this topic.

I will check out the other thread.

Almighty indeed! You know Olof Skotkonung was a viking king of Sweden?

Seriously though, I would be interested in your opinion of the other thread.

[yoyo]

Here is an interesting connection -- Barry groves gave us these stats for lowland gorillas'

Yeah, I don't know how accurate a dietary comparison between a gorilla and a human would be, seeing as we diverged evolutionarily several million years ago. They don't even share our genus.

For you to completely disconnect info from gorillas and or other primates would be a mistake -- of course we don't have multiple stomachs like they do -- but that was our trade off for a larger brain.

Most plant eating mammals would have similar patterns of nutrient intake -- because their gut flora would convert food sources to SCFAs. Humans have to get away with others sources of dense food to make up for that -- for some reason i bet we ate lots of bone marrow <---- high in MONOs right? And tubers -- they were an easy fuel source!

To say man is highly carnivorous would be a mistake -- we can't deal with the super high protein intake -- or the nutrients that would come from eating all of the insides of an animal -- and eating blood is dangerous unless it is treated as the Masai would. We don't even eat much of the connective issues -- which is consumed in large amounts by natural meat eaters.

Just because we can derive and use selective meat/liver tissues and cook them to increase bio-availability doesn't mean its optimal.

but much of the gain from that brain was in better utilizing certain dietary sources. at first meat, especially cooked, and later seeds especially grains, also milk

[Blue]

CLA also increases ceramide and insulin resistance

The effect of conjugated linoleic acid (CLA), a popular weight-loss supplement, on insulin sensitivity in humans is controversial and has not been extensively studied. To date no studies have examined the effects of CLA supplementation on human skeletal muscle metabolism or lipid content. It is also unknown whether CLA accumulates in human skeletal muscle with supplementation. In the present study, 9 overweight, non-diabetic individuals received 4 g/d of mixed CLA isomers in the form of 1 g supplements, for 12 weeks. CLA isomers significantly increased in both plasma and skeletal muscle following supplementation. Skeletal muscle ceramide content was also significantly increased, although there was no consistent change in muscle diacylglycerol or triacylglycerol content. Insulin sensitivity was significantly decreased (p<or=0.05) following CLA supplementation, with a significant increase in glucose and insulin area under the curve during an oral glucose tolerance test (p<or=0.005). The protein content of PPARalpha, for which CLA is a potent ligand, was unchanged following supplementation. Accordingly, there was no change in markers of muscle oxidative capacity. In conclusion, mixed-isomer CLA supplementation in overweight non-diabetic humans results in the accumulation of CLA and ceramide in skeletal muscle, and decreases insulin sensitivity.
http://www.ncbi.nlm....pubmed/17510671

[rabagley]

To say man is highly carnivorous would be a mistake -- we can't deal with the super high protein intake -- or the nutrients that would come from eating all of the insides of an animal -- and eating blood is dangerous unless it is treated as the Masai would. We don't even eat much of the connective issues -- which is consumed in large amounts by natural meat eaters.

Just because we can derive and use selective meat/liver tissues and cook them to increase bio-availability doesn't mean its optimal.

Actually, in societies that were largely carnivorous, they were very selective about the parts of the animals that they ate. They strongly preferred fat, and fatty cuts of meat, leaving lean meat for dogs in times of plenty. Among the internal organs, almost everything was eaten, though they did know when organs contained dangerous quantities of nutrients (too much Vitamin A in many animal livers) and ate those in moderation or avoided them.

Being a pure carnivore has been tested multiple times and we can do it quite well. Eat the fattiest cuts of meat and you can do it too. There are still a few mysteries like, "Why do we not get scurvy when the Vitamin C levels in meat are so low? It may be that carbs or other attributes of vegetable foods cause our bodies to lose or consume Vitamin C, turning it into a required nutrient. But it is known that sailors only got scurvy and had to bring along citrus when ships rations were changed from dried meat to hard tack to save money.

I suspect that humans are most properly classed as non-obligate carnivores instead of omnivores, but the categories clearly overlap, so who am I to say if someone else wants to have their own take on it?

[oehaut]

The obvious explanation (well, maybe not obvious to paleos) is that saturated fat increases CVD which in turn decreases nutrition to the brain and casuses various problems.

Background. In the Seven Countries Study associations between intake of individual fatty acids and dietary cholesterol were studied in relation to serum cholesterol and 25-year mortality from coronary heart disease. All analyses concern only intercohort comparisons. Methods. In the baseline surveys carried out between 1958 and 1964, risk factors for coronary heart disease were measured among 12,763 middle-aged men constituting 16 cohorts in seven countries. In 1987 and 1988 equivalent food composites representing the average food intake of each cohort at baseline were collected locally and analyzed in a central laboratory. The vital status of all participants was verified at regular intervals during 25 years of follow-up. Results. Of the individual saturated fatty acids, the average population intake of lauric and myristic acid was most strongly related to the average serum cholesterol level (r > 0.8, P < 0.001). Strong positive associations were observed between 25-year death rates from coronary heart disease and average intake of the four major saturated fatty acids, lauric, myristic, palmitic, and stearic acid (r > 0.8, P < 0.001); the trans fatty acid elaidic acid (r = 0.78, P < 0.001); and dietary cholesterol (r = 0.55, P < 0.05). Conclusions. Interpreted in the light of experimental and clinical studies, the results of these cross-cultural analyses suggest that dietary saturated and trans fatty acids and dietary cholesterol are important determinants of differences in population rates of coronary heart disease death.
http://www.sciencedi...39d812fa5fb01dd

BACKGROUND: Metabolic studies suggest that saturated fatty acids differ in their effects on blood lipids. OBJECTIVE: The objective was to examine the associations between intakes of individual saturated fatty acids and their food sources in relation to the risk of coronary heart disease (CHD). DESIGN: This was a prospective cohort study of 80082 women in the Nurses' Health Study aged 34-59 y. Subjects had no known cardiovascular disease, cancer, hypercholesterolemia, or diabetes, and completed validated food-frequency questionnaires in 1980. RESULTS: During 14 y of follow-up, we documented 939 incident cases of major CHD events. In multivariate analyses in which age, smoking, and other covariates were controlled for, intakes of short- to medium-chain saturated fatty acids (4:0-10:0) were not significantly associated with the risk of CHD. In contrast, intakes of longer-chain saturated fatty acids (12:0-18:0) were each separately associated with a small increase in risk. The multivariate RR for a 1% energy increase from stearic acid was 1.19 (95% CI: 1.02, 1.37). The ratio of polyunsaturated to saturated fat was strongly and inversely associated with CHD risk (multivariate RR for a comparison of the highest with the lowest deciles: 0.58; 95% CI: 0.41, 0.83; P for trend < 0.0001). Conversely, higher ratios of red meat to poultry and fish consumption and of high-fat to low-fat dairy consumption were associated with significantly greater risk. CONCLUSION: A distinction between stearic acid and other saturated fats does not appear to be important in dietary advice to reduce CHD risk, in part because of the high correlation between stearic acid and other saturated fatty acids in typical diets.
http://www.ncbi.nlm....pubmed/10584044

Blue, this is a bit off topic, but I wanted to say something about this.

Using the Seven Country to make your point, like many others supporting the issu of saturated fatty acid with CVD, is really a big mistake. This study is a big joke. You should read this paper as to know why. I thought kind of everybody knew that Key's had totaly Cherry Picked his data to make up his result tho. He had data from 22 country and he chose only seven... god knows why.

Also, that study was a multivariate linear regression analysis. Keys himself, in page 263 of the study, admit that he did not look for the relation between Sugar and CVD. So he went to point sat fat without having taken the time to look at the relation with sugar.

That's a really, really bad study if you ask me (or any others concerned about methodology)

And, as for the Nurse Health Study, it's interesting to see that the Women Health Initiative, which was as big and CONTROLLED, not prospective, find no benefits of eating less sat fat. Actually, It found that in women with pre-existing CVD risk, eating more poly, vegetable and whole grains was associated with a 3.1 more chance of suffering from CVD.

[Blue]

And, as for the Nurse Health Study, it's interesting to see that the Women Health Initiative, which was as big and CONTROLLED, not prospective, find no benefits of eating less sat fat. Actually, It found that in women with pre-existing CVD risk, eating more poly, vegetable and whole grains was associated with a 3.1 more chance of suffering from CVD.

The Women Health Initiative looked at total fat primarily. Not saturated fat, although this was secondarily studied. Or cognitive decline. Source for the claim regarding 3.1 more chance please.

CONTEXT: Multiple epidemiologic studies and some trials have linked diet with cardiovascular disease (CVD) prevention, but long-term intervention data are needed. OBJECTIVE: To test the hypothesis that a dietary intervention, intended to be low in fat and high in vegetables, fruits, and grains to reduce cancer, would reduce CVD risk. DESIGN, SETTING, AND PARTICIPANTS: Randomized controlled trial of 48,835 postmenopausal women aged 50 to 79 years, of diverse backgrounds and ethnicities, who participated in the Women's Health Initiative Dietary Modification Trial. Women were randomly assigned to an intervention (19,541 [40%]) or comparison group (29,294 [60%]) in a free-living setting. Study enrollment occurred between 1993 and 1998 in 40 US clinical centers; mean follow-up in this analysis was 8.1 years. INTERVENTION: Intensive behavior modification in group and individual sessions designed to reduce total fat intake to 20% of calories and increase intakes of vegetables/fruits to 5 servings/d and grains to at least 6 servings/d. The comparison group received diet-related education materials. MAIN OUTCOME MEASURES: Fatal and nonfatal coronary heart disease (CHD), fatal and nonfatal stroke, and CVD (composite of CHD and stroke). RESULTS: By year 6, mean fat intake decreased by 8.2% of energy intake in the intervention vs the comparison group, with small decreases in saturated (2.9%), monounsaturated (3.3%), and polyunsaturated (1.5%) fat; increases occurred in intakes of vegetables/fruits (1.1 servings/d) and grains (0.5 serving/d). Low-density lipoprotein cholesterol levels, diastolic blood pressure, and factor VIIc levels were significantly reduced by 3.55 mg/dL, 0.31 mm Hg, and 4.29%, respectively; levels of high-density lipoprotein cholesterol, triglycerides, glucose, and insulin did not significantly differ in the intervention vs comparison groups. The numbers who developed CHD, stroke, and CVD (annualized incidence rates) were 1000 (0.63%), 434 (0.28%), and 1357 (0.86%) in the intervention and 1549 (0.65%), 642 (0.27%), and 2088 (0.88%) in the comparison group. The diet had no significant effects on incidence of CHD (hazard ratio  , 0.97; 95% confidence interval [CI], 0.90-1.06), stroke (HR, 1.02; 95% CI, 0.90-1.15), or CVD (HR, 0.98; 95% CI, 0.92-1.05). Excluding participants with baseline CVD (3.4%), the HRs (95% CIs) for CHD and stroke were 0.94 (0.86-1.02) and 1.02 (0.90-1.17), respectively. Trends toward greater reductions in CHD risk were observed in those with lower intakes of saturated fat or trans fat or higher intakes of vegetables/fruits. CONCLUSIONS: Over a mean of 8.1 years, a dietary intervention that reduced total fat intake and increased intakes of vegetables, fruits, and grains did not significantly reduce the risk of CHD, stroke, or CVD in postmenopausal women and achieved only modest effects on CVD risk factors, suggesting that more focused diet and lifestyle interventions may be needed to improve risk factors and reduce CVD risk. CLINICAL TRIALS REGISTRATION: ClinicalTrials.gov Identifier: NCT00000611.
http://www.ncbi.nlm....pubmed/16467234

Edited by Blue, 29 November 2009 - 05:40 PM.

[oehaut]

And, as for the Nurse Health Study, it's interesting to see that the Women Health Initiative, which was as big and CONTROLLED, not prospective, find no benefits of eating less sat fat. Actually, It found that in women with pre-existing CVD risk, eating more poly, vegetable and whole grains was associated with a 3.1 more chance of suffering from CVD.

Source for the claim regarding 3.1 more chance please.

I'm not sure here what you want but just look at the full paper in the comment section, the authors stated:

The intervention was associated with increased risk in the 3.4% of women with baseline CVD

You are right tho that it was about total fat and not saturated fat per se. i'll look for the data concerning the trend with SFA and CVD in just a moment after my homework are done.

I just realise reading the paper again to quote this that I was wrong tho. It's not a 3.1 more chance, it's increased risk in the 3.4% of the women with pre-existing risk. My bad. Sorry about that. I had read it long ago and had remembered what I wanted to remember it seems

Edited by oehaut, 29 November 2009 - 05:51 PM.