Gyroscopic Investing

Gumby wrote: Also, tossing modern people into that old-fashioned lifestyle for a week is a silly experiment in terms of analyzing one's response to it. Most people feel pretty run down after the first week of switching to a high-fat/high-protein diet — even without doing any labor. My guess is that those actors were doing terribly by the end of the one-week study. After a few months of living that lifestyle, they would have felt like they could have done anything.

It takes about two weeks for the body to adjust from burning solely carbs to burning fat for energy.  While it can burn both at any time, adaptions still have to take place.  Generally, carbs staying under 25% of total calories will keep the pump primed for fat burning and prevent insulin resistance and all that jazz.

smurff wrote: BTW, Southerners carry a lot of fat on their bodies because they consume lots of starches and sugary sweets--Coca Cola, Pepsi Cola and their ilk (RC Cola, etc....) were invented and perfected in the South as medicines and exported to the rest of the country as casual drinks.  Southerners also tend to put sugar in recipes that ordinarily don't contain sugar elsewhere in the country, like spaghetti sauce, mac and cheese, meat loaf, etc. And the Great Cornbread Debate--whether sweet-tasting cornbread or non-sweet cornbread is the best--still rages.

You forgot all the white breaded, deep fried chicken ala KFC!!!

MachineGhost wrote:Leaving aside my personal experience with saturated fat (which could as easily just be too much Omega-6 vs Omega-3 in factory farmed meat -- I'll have to try a grass fed meat self-test again, although I think I tried it before with negative results)

MG, I can't help but wonder if you need to give your self-tests two weeks to really see the results. Couldn't one eat something very beneficial that produces a short term detoxification reaction (rash, nausea, die-off, etc)?

MachineGhost wrote:the most I can find is that the cholesterol hypothesis is based on at least one flawed study with rabbits conducted way back in the 1930's and 1940's.

Yes. That study seems rather flawed. The book, Eat Fat, Lose Fat, explained some other problems with that study....

...The kind of plaque the rabbits developed was completely different from the kinds of plaque humans develop. Second, the rabbits were fed purified cholesterol that was oxidized (damaged by processing), not the kind contained in ordinary food.
Source: Eat Fat, Lose Fat, p. 35

The book also references some interesting scientific material for why you need to consume saturated fats for the proper operation of your brain chemistry, your cells, your bones, your liver, your heart, your lungs, your kidneys, your hormones, your cell communication.

And Gary Taubes' 2002 article, in the New York Times ("What if It's All Been a Big Fat Lie?"), explains that the the theory of a low-fat diet was promoted by politicians — with no scientific proof — and its effects have been a disaster by causing more obesity and related diseases.

http://nyti.ms/i9lQST

From the article:

It was Ancel Keys, paradoxically, who introduced the low-fat-is-good-health dogma in the 50's with his theory that dietary fat raises cholesterol levels and gives you heart disease. Over the next two decades, however, the scientific evidence supporting this theory remained stubbornly ambiguous. The case was eventually settled not by new science but by politics. It began in January 1977, when a Senate committee led by George McGovern published its ''Dietary Goals for the United States,'' advising that Americans significantly curb their fat intake to abate an epidemic of ''killer diseases'' supposedly sweeping the country. It peaked in late 1984, when the National Institutes of Health officially recommended that all Americans over the age of 2 eat less fat. By that time, fat had become ''this greasy killer'' in the memorable words of the Center for Science in the Public Interest, and the model American breakfast of eggs and bacon was well on its way to becoming a bowl of Special K with low-fat milk, a glass of orange juice and toast, hold the butter -- a dubious feast of refined carbohydrates.

In the intervening years, the N.I.H. spent several hundred million dollars trying to demonstrate a connection between eating fat and getting heart disease and, despite what we might think, it failed. Five major studies revealed no such link. A sixth, however, costing well over $100 million alone, concluded that reducing cholesterol by drug therapy could prevent heart disease. The N.I.H. administrators then made a leap of faith. Basil Rifkind, who oversaw the relevant trials for the N.I.H., described their logic this way: they had failed to demonstrate at great expense that eating less fat had any health benefits. But if a cholesterol-lowering drug could prevent heart attacks, then a low-fat, cholesterol-lowering diet should do the same. ''It's an imperfect world,'' Rifkind told me. ''The data that would be definitive is ungettable, so you do your best with what is available.''

Some of the best scientists disagreed with this low-fat logic, suggesting that good science was incompatible with such leaps of faith, but they were effectively ignored.

Source: What if It's All Been a Big Fat Lie?

MachineGhost wrote:

Gumby wrote: What seems like a very unhealthy diet (and maybe it is) has made me feel great and look younger. Hard to imagine this was a placebo effect when I was actually pretty nervous to give this all a try.

I'd say its only unhealthy if you eat unbalanced long-term.  By that, I mean if you ignore the vegetables and fruits necessary to balance off the acidity and toxic-byproducts of all the acid-forming meat and fats, and missing out on the antioxidants, phytonutrients, flavonoids, and all the other micro-nutrients that are in plants.  Assuming you do get enough fat soluble vitamins from the fatty meat, the bigger issue to me would be ingesting enough of the macro-nutrient minerals which have been deficient in our soils for at least 70 years.  That's essentially potassium and magnesium (since calcium and phosphorous would be taken care of by the dairy or meat), which can be dealt with by using top-shelf true chelated multiminerals (Albion) and using Himalayan pink salt or unrefined sea salt (grey color) instead of regular salt to get the trace minerals (i.e. gold).  Getting the RDA for potassium is notoriously difficult (the FDA limits a serving to 99mg because it threatens blood pressure drug profits) without consuming a lot of vegetables, so just fill your plate up with 'em.

The large ingestion of calcium Westerners ingest will promote organ and artery hardering over time, so unless you want to wind up suddenly dying like Jack LaLanne, you should make sure you are smarter than he was and marry all that Vitamin D3 with the two forms of Vitamin K2 so the calcium stays where it belongs.  K1 from veggies won't cut it but its typically provided along with the K2's.

The other big risk with ingesting so much red meat is the iron which is the most potent free radical anyone can ingest.  Cruciferious vegetables along with the red meat is ideal to deal with this.  Horseradish too!

Thanks for the tips. I've been supplementing with the Fermented Cod Liver Oil/High Vitamin Butter Oil — which I believe is rich in K2 (the so-called Activator X?). I've also started to take trace mineral drops, but I will definitely consider incorporating your specific recommendations above. And, of course, I do enjoy at least one vegetable with every meal, so I plan to continue that habit.

MachineGhost wrote: The large ingestion of calcium Westerners ingest will promote organ and artery hardering over time, so unless you want to wind up suddenly dying like Jack LaLanne, you should make sure you are smarter than he was and marry all that Vitamin D3 with the two forms of Vitamin K2 so the calcium stays where it belongs.  K1 from veggies won't cut it but its typically provided along with the K2's.

But Jack LaLanne died at 97, still with great mobility and physical conditioning!  (Pneumonia did him in.)  Not bad at all!

Lone Wolf wrote:

MachineGhost wrote: The large ingestion of calcium Westerners ingest will promote organ and artery hardering over time, so unless you want to wind up suddenly dying like Jack LaLanne, you should make sure you are smarter than he was and marry all that Vitamin D3 with the two forms of Vitamin K2 so the calcium stays where it belongs.  K1 from veggies won't cut it but its typically provided along with the K2's.

But Jack LaLanne died at 97, still with great mobility and physical conditioning!  (Pneumonia did him in.)  Not bad at all!

Maybe MG was thinking of Jim Fixx, he died at 52, and was one of the original proponents for regular jogging.  But according to his wiki, his father died at the age of 43 from a heart attack, so I guess you cannot out run your genetics.

Also, Bill Hicks has a good bit comparing Jim Fixx to Keith Richards (1:30): http://youtu.be/awyiiK7JLHQ

MachineGhost wrote: You forgot all the white breaded, deep fried chicken ala KFC!!!

Yeah, that too, but not as much as the sweets.

BTW if you take vitamin D3, beware there is a genetic variation where the body stops producing all the different kinds of proteins for cartilage and tendons when the balance between vitamin D3 and vitamin K2 is disrupted. It can result in the body not producing enough of the kinds of stretchy proteins needed for tendons and substituting instead proteins that tear easily when subjected to stress.  A torn Achilles tendon or torn rotator cuff in someone who is not doing anything strenuous enough to tear anything is often the first indication something is wrong.

So if you take vitamin D3 you might want to consider adding vitamin K2. And don't overdose vitamin D3--in some people that can cause kidney stones.

Gumby wrote: MG, I can't help but wonder if you need to give your self-tests two weeks to really see the results. Couldn't one eat something very beneficial that produces a short term detoxification reaction (rash, nausea, die-off, etc)?

It's possible, but I've heard that claim ever since I started on a healthier lifestyle and it has never lived up to the hype of resolving when suffering through the agony for an extended period of time (a week or two).  It is far too easy to become an evangelist and excuse every negative symptom as a Herxheimer Reaction for a good cause, when it could be anything but.  For instance, if you feel like you've gotten food poisioning after drinking raw milk, is very unlikely to be a Herxheimer Reaction.  In the past, I have experienced cyclical vomiting for 12 hours straight (threw up flourescent-green listeria at the very end) necessitating an overpriced emergency room visit and more recently, naseua & fever chills for a day or so, each after drinking whole raw milk from two separate companies.  But, given your experience, I'll grit my teeth and try two weeks with something clean like extra virgin coconut oil.  (I don't have an issue with the fat in whole raw milk.)

demonstrate at great expense that eating less fat had any health benefits. But if a cholesterol-lowering drug could prevent heart attacks, then a low-fat, cholesterol-lowering diet should do the same. ''It's an imperfect world,'' Rifkind told me. ''The data that would be definitive is ungettable, so you do your best with what is available.''

If that was circa late 1980's, then today in 2012 the evidence that lowering cholesterol prevents heart attacks "beyond a reasonable doubt" is that it does not.

Lone Wolf wrote: But Jack LaLanne died at 97, still with great mobility and physical conditioning!  (Pneumonia did him in.)  Not bad at all!

He died about a year after an operation to replace a calcified coronary artery.  Pneumonia is the most common killer of the eldery, most especially after surgery (since it depresses the immune system big time) and being in a hospital (a giant petri dish).  The guy was in great shape up until the surgery, then it went all downhill.  He just didn't take Vitamin K2 seriously (or at least keep up with scientific evidence).  With all the calcium added to fority foods everywhere, organ calcification is not a trivial risk to ignore.

Gosso wrote: Maybe MG was thinking of Jim Fixx, he died at 52, and was one of the original proponents for regular jogging.  But according to his wiki, his father died at the age of 43 from a heart attack, so I guess you cannot out run your genetics.

Oh, so THAT's the guy responsible for starting the infamous aerobics trend, culiminating in this Perfect masterpiece of motion picture exotica:

[align=center][/align]

Gumby wrote: Arachidonic acid does still play a central role in inflammation related to injury and many diseased states. How it is metabolized in the body dictates its inflammatory or anti-inflammatory activity. Individuals suffering from joint pains or active inflammatory disease may find that increased arachidonic acid consumption exacerbates symptoms, presumably because it is being more readily converted to inflammatory compounds. Likewise, high arachidonic acid consumption is not advised for individuals with a history of inflammatory disease, or who are in compromised health. Of note, while ARA supplementation does not appear to have proinflammatory effects in healthy individuals, it may counter the anti-inflammatory effects of omega-3 fatty acid supplementation.[/font]

Ah, it turns out that when there is an overload of AA ingested from diet, the body increases the 5-LOX enzyme to clear the AA out.  So AA is not directly harmful per se.  5-LOX was the infamous enzyme that was killing hundreds of thousands of people a decade or so ago in response to Vioxx ingestion and other drug COX-2 blockers.  5-LOX increases the production of pro-inflammatory 5-HETE and excess accumulation of pro-inflammatory leukotrienes (B4) which are connected to cardiovascular disease, cancer, arthritis, asthma, COPD, Alzheimer's, bowel diseases, ostereoporosis, BPH, prostate cancer...  essentially 70% of the leading causes of death.

AA is contained in egg yolks, red meat, poultry and organ meat as well as precursors in Omega-6 fats and carbohydrates.  No idea if it is in the fat or the meat, but if it is in the fat, that could explain associations between saturated fats and increased mortality.

At one time, I thought 5-LOX was the smoking gun for my inflammation sensitivity to everything in the above list short of chicken and lesser refined carbs, but 5-LOX blockers did absolutely nothing.  Since 5-LOX is such a silent and lethal killer, I think the only way anyone can know for sure if they are ingesting too much AA in relation to their body's ability to manage it safely (?), is to have their all of their fatty acid levels tested and see if anything/what is out of whack.  I am not aware of proven ways to block 5-LOX without using a supplement, even though lots of food-nutrients are claimed to have an influence on it.

MachineGhost wrote:Ah, it turns out that when there is an overload of AA ingested from diet, the body increases the 5-LOX enzyme to clear the AA out.

Animal meat contains a small amount of AA. A hamburger has about 35mg of AA, but organs contain higher levels — a 3oz serving of lamb liver has about 530mg of AA. I don't know anyone who eats lamb liver every single day. But, AA is necessary for life (for instance, you need it for sperm production, and to convert of omega-3s into resolvins...which helps reduce inflammation). Some people even have an AA deficiency. A deficiency of AA leads to low levels of sex hormones, hair loss, scaly skin and infertility. Without AA, your body can't induce, resolve, or suppress inflammation properly. MG... Did you take your AA pills this morning to get the Recommended Daily Allowance of AA?

MachineGhost wrote:AA is contained in egg yolks, red meat, poultry and organ meat as well as precursors in Omega-6 fats and carbohydrates.  No idea if it is in the fat or the meat, but if it is in the fat, that could explain associations between saturated fats and increased mortality.

There's never been any reliable associations between saturated fats and increased mortality. Perhaps you believe you can find a reliable association, but you haven't produced it yet. You'd think if the association were so easy to find, you would have found it by now. The only thing you'll find are flawed studies where they mix up Trans fats and Saturated Fats or studies that exclude conflicting data (as Ancel Keys did).

MachineGhost wrote:At one time, I thought 5-LOX was the smoking gun for my inflammation sensitivity to everything in the above list short of chicken and lesser refined carbs

You know, most people don't have inflammation sensitivity to those things — particularly if they come from pastured sources. For instance, there are many people who are allergic to supermarket eggs, but do fine with pastured eggs. And if you're cooking those things with modern cooking oils (canola oil, for instance), that's not going to help things either.

MG... in all seriousness, having an inflammation sensitivity is a sign that you might have an AA deficiency. Perhaps if you built up your AA stores, your body would have the proper amount of essential fatty acids it needs to resolve or suppress inflammation better. It might be worth considering.

MachineGhost wrote:I have experienced cyclical vomiting for 12 hours straight (threw up flourescent-green listeria at the very end) necessitating an overpriced emergency room visit and more recently, naseua & fever chills for a day or so, each after drinking whole raw milk from two separate companies.

Hmm... I'm not sure I would ever buy raw milk from "companies". I think it's better to find a local small-production farm (if possible) and make sure they are committed to safe practices before consuming raw milk.

The below is good overview of dietary fats from the WHO published way back in 2004.  The WHO tends to not be as corrupted by crony capitalism as U.S. institutions are.  I have highlighted key phrases.

Dietary fats
The relationship between dietary fats and CVD, especially CHD has been extensively investigated, with strong and consistent associations emerging from a wide body of evidence accrued from animal experiments, as well as observational studies, clinical trials and metabolic studies conducted in diverse human populations. This relationship was initially considered to be mediated mainly through the atherogenic effects of plasma lipids (total cholesterol, lipoprotein fractions and triglycerides). The effects of dietary fats on thrombosis and endothelial function as well as the relationship of plasma and tissue lipids to the pathways of inflammation have been more recently understood13. Similarly, the effects of dietary fats on blood pressure have also become more evident through observational and experimental research.

The association of plasma total cholesterol and its low-density lipoprotein sub fraction (LDL cholesterol) has been consistently demonstrated across several populations, with the Seven Countries Study offering strong evidence through within-population cohort experience and inter-population ecological comparisons14. The protective association of high-density lipoprotein (HDL) fraction of plasma cholesterol has also been well identified and the ratio of total to HDL cholesterol has emerged as a strong predictor of the risk of CHD. Plasma triglycerides too have been directly associated with the risk of atherosclerotic vascular disease and thrombotic events. The effect of various dietary fats on these plasma lipids has constituted the key link in the causal pathway that connects diet to CVD15.

Cholesterol in the blood and tissues is derived from two sources: diet and endogenous synthesis. Dairy fat and meat are major sources. Egg yolk is particularly rich in cholesterol but unlike dairy and meat does not provide saturated fatty acids (SFAs). Dietary cholesterol raises plasma cholesterol levels16. Although both HDL and LDL increase, the effect on the total/HDL ratio is still unfavourable17, but small. Observational evidence on an association of dietary cholesterol intake with CVD is contradictory10,11. The upper limit for dietary cholesterol intake has been prescribed, in most guidelines, to be 300 mg/d. However, there is no requirement for dietary cholesterol and it is advisable to keep the intake as low as possible. If intake of dairy fat and meat are controlled then there needs to be no severe restriction of egg yolk intake, although some limitation remains prudent.

Fatty acids are grouped into three classes—SFAs, monounsaturated fatty acids (MUFAs) and polyunsaturated fatty acids (PUFAs). While such a classification is useful in providing a structural grouping, it tends to oversimplify the effects of dietary fats. Individual fatty acids, within each group, are now known to have differing effects on lipids, lipoproteins and platelet-vascular  homeostasis. SFA and MUFA can be synthesised in the body and hence are not dietary essentials. PUFA can be subdivided into n-6 and n-3 PUFA, derived from linoleic acid (LA) and a-linolenic acid (ALNA), respectively. These are essential fatty acids, since they cannot be synthesised in the body18,19.

Saturated fatty acids
SFAs as a group raise total and LDL cholesterol, but individual SFAs have different effects. Myristic and lauric acids have greater effect than palmitic acid, but the latter is more abundant in food supply. The plasma cholesterol raising effects of these three SFAs is higher when combined with high cholesterol diets. Stearic acid has not been shown to elevate blood cholesterol and is rapidly converted to oleic acid (OA) in vivo. Metabolic (feeding) studies demonstrate a marked elevation of both HDL and LDL cholesterol induced by SFA diets18–20. Replacement of saturated fatty acids by polyunsaturated fat reduces the total to HDL cholesterol ratio but replacement by carbohydrates does not. Also, tropical fats rich in lauric acid (C12) raise total cholesterol strongly, but because of their specific effect on HDL, the ratio of total to HDL cholesterol falls. Thus, effects on blood lipids can be variable, depending on which blood lipids are studied, and we need data on actual outcomes to determine the true effects of fats on CHD. The relationship of dietary saturated fat to plasma cholesterol levels and to CHD was graphically demonstrated by the Seven Countries Study involving 16 cohorts, in which saturated fat intake explained 73% of the total variance in CHD across these cohorts14. In the Nurses Health Study19, the effect of saturated fatty acids was much more modest, especially if saturates were replaced by carbohydrates. The most effective replacement for saturated fatty acids in terms of CHD outcome is by PUFAs, i.e. LA. This agrees with the outcome of large randomised clinical trials, in which replacement of saturated and trans fats by polyunsaturated vegetable oils effectively lowered CHD risk20–22.

Trans-fatty acids (t-FAs)
t-FAs are geometrical isomers of unsaturated fatty acids that assume a saturated fatty acid-like configuration. Partial hydrogenation, the process used to create t-FA, also removes essential fatty acids such as LA and ALNA. Metabolic studies have demonstrated that t-FAs render the plasma lipid profile even more atherogenic than SFA, by not only elevating LDL cholesterol to similar levels but also decreasing HDL cholesterol23,24. As a result, the ratio of LDL cholesterol to HDL cholesterol is significantly higher with a t-FA diet (2.58) than with a SFA diet (2.34) or an OA diet (2.02). This greatly enhances the risk of CHD (Fig. 2). Evidence that intake of t-FA increases the risk of CHD initially became available from large population based cohort studies in US25,26 and has recently been corroborated in an elderly Dutch population27. Levels of t-FA in a biochemical analysis of replicated baseline food composites correlated with the risk of coronary death in the cohorts of the Seven Countries Study. Most t-FAs are contributed by industrially hardened oils, but the dairy and meat fats of ruminants are also a source. Whether these two sources have the same effect on CHD risk is unclear, but reductions in ruminant fats are already advisable for other reasons. Eliminating t-FAs from the diet would be an important public health strategy to prevent CVD. Since these are commercially introduced agents into the diet, policy measures related to the food industry would be required along with public education. t-FAs have been eliminated from retail fats and spreads in a large part of the world, but deep-fat fried fast foods and baked goods are a major and increasing source28.

Monounsaturated fatty acids
The only nutritionally important MUFA is OA, which is abundant in olive and canola oils and also in nuts. The epidemiological evidence related to MUFA and CHD is derived from studies on the Mediterranean diet, as well as from the Nurses Health Study and other similar studies, which investigated the association and control of confounding factors29. MUFAs have been shown to lower blood glucose and triglycerides in type II diabetics and may decrease susceptibility of LDL to oxidative modification.

Polyunsaturated fatty acids
PUFAs are derived from Dietary LA (n-6 PUFAs) and dietary ALNA (n-3 PUFAs). The important n-6 PUFAs are arachidonic acid (AA) and dihomogammalinolenic acid (DHGLA), while the important n-3 PUFAs are eicosapentaenoic acid (EPA) and docasahexaenoic acid (DHA). Eicasanoids derived from AA have opposing metabolic properties to those derived from DHA. A balanced intake of n-6 and n-3 PUFAs is, therefore, essential for health.

The biological effects of n-3 PUFAs are wide ranging involving lipids and lipoproteins, blood pressure, cardiac function, arterial compliance, endothelial function, vascular reactivity and cardiac electrophysiology as well as potent anti-platelet and anti-inflammatory effects including reduced neutrophil and monocyte cytokine production13,30. Recent data have also shown that EPA and DHA have differential effects on many of these. DHA appears to be more responsible for the beneficial effects of fish and fish oils on lipids and lipoproteins, blood pressure, heart rate variability, glycaemic control, in comparison to EPA, while a mixture of DHA and EPA significantly reduced platelet aggregation in comparison to ALNA in vitro13,31. The very-long chain n-3 PUFAs powerfully lower serum triglycerides, but they raise LDL cholesterol32. Therefore, their effect on CHD is probably mediated through pathways other than cholesterol.

Much of the epidemiological evidence related to n-3 PUFAs is derived from the study of fish consumption in populations or interventions involving fish diets in clinical trials. Fish oils were, however, used in the GISSI study of 11,300 survivors of myocardial infarction33. In this factorial design, fish oil (1 g/d) and vitamin E (300 mg/d) were compared, alone and in combination, to placebo. After 3.5 years of follow-up, the fish oil group had a statistically significant 20% reduction in total mortality, 30% reduction in cardiovascular death and 45% decrease in sudden death. While most published studies do not indicate that dietary n-3 PUFA prevent restenosis after percutaneous coronary angioplasty or induce regression of coronary atherosclerosis, one study reported that occlusion of aortocoronary venous bypass grafts was reduced after 1 year by daily ingestion of 4 g fish oil concentrate34.

The Lyon Heart Study incorporated an n-3 fatty acid (ALNA) into a diet altered to develop a ‘Mediterranean diet’ intervention9. In the experimental group, plasma ALNA and EPA increased significantly and the trial reported a 70% reduction in cardiovascular mortality at 5 years in its initial report. Total and LDL cholesterol were identical in the experimental and control groups, suggesting that thrombotic and perhaps arrhythmic events may have been favourably influenced by n-3 PUFA. Since the diet altered many other variables, such as fibre and antioxidants (by increasing fruit and vegetable consumption), direct attribution of benefits to n-3 PUFA becomes difficult to establish.

The effect of different fatty acids on cardiac arrhythmias has been an area of great interest. Diets rich in saturated fatty acids increase the risk of ventricular fibrillation and sudden cardiac death in primates. A recent population based case–control study, using biomarkers, revealed a modest association of t-FAs in general and a strong association of trans isomers of LA in particular, with primary cardiac arrest in humans35. Several studies in different animal models, primate and rodent, have shown that n-3 PUFA are protective against cardiac arrhythmias, especially ventricular fibrillation36. It has been suggested that the fall in CHD mortality in USA and Australia, since 1967, is probably attributable to an increase in polyunsaturated fat consumption in both countries since 196037. The decline in CHD mortality in the Zutphen cohort has similarly been attributed to a decreased consumption, over time, of t-FAs27.

The proportions of SFA, MUFA and PFA as constituents of total fat intake and total energy consumption have engaged active attention, in view of the strong relationship of these fatty acids to the risk of CVD, especially CHD. The reduction of SFA in the diet has been widely recommended, but its replacement remains an area of debate as to whether the place of reduced SFAs should be taken by MUFA, PUFA or carbohydrate. Both MUFA and PUFA improve the lipoproteins profile, although PUFAs are somewhat more effective. In view of this, recent US dietary recommendations, suggested that SFA should be reduced to 7–8%, MUFA should be increased to 13–15% and PUFA raised to 7–10% of daily energy, with the total fat contributing to no more than 30% of all calories consumed29,38. These may need to be adjusted for populations who consume less quantities of total fat, so as to ensure an adequate intake of MUFA and PUFA even under those circumstances.

The total quantity of fat consumed, as a proportion of daily energy intake, has not shown a relation to CVD that is independent of the SFA content. It has now generally been agreed that the type of fats consumed in diet is more important than the total amount of fat consumed39. The compatibility of high-fat Mediterranean diets (with total fat contributing .30% of calories) with coronary protection has been cited as supportive evidence. While the emphasis on the type of fat is well placed, it must be recognised that high-fat diets are also high in energy. Whether this contributes substantially to overweight is a subject of much debate40. While the emphasis in dietary recommendations should be on using the healthier fats in preference to unhealthier fats, the total fat may be restricted to <30% of all energy in most populations and individuals. However, individuals who regularly undertake vigorous physical activity may consume higher levels of fat in their daily diets (up to 35%).

Enhancing the nutritional quality of dietary fat consumption, to provide greater cardiovascular protection, may be attempted by decreasing the sources of saturated fats and eliminating t-FAs in the diet, increasing the consumption of foods containing unsaturated fatty acids (both MUFA and PUFA) and decreasing dietary cholesterol consumption. Modification of cooking oils either through appropriate admixture of different oils41 or through genetic modification of oilseed crops42 may provide methods for improving the quality of dietary fat consumed through edible oils.

MachineGhost wrote:This agrees with the outcome of large randomised clinical trials, in which replacement of saturated and trans fats by polyunsaturated vegetable oils effectively lowered CHD risk20–22.

MG, do you believe that Polyunsaturated vegetable oils are the best cooking oils? I hope you know better than that. That statement was basically written by the edible oil lobby. As I've mentioned a number of times, above, most studies combine trans fats and saturated fats together when comparing risk. The statement you bolded did the exact same thing. This is intentionally done to make polyunsaturated oils look better than they are — to protect a multi-billion dollar industry.  

The key study referenced in that statement is the Seven Countries Study — which has been widely criticized for cherry picking data. Though, I guess it shouldn't surprise me — the entire diet-heart hypothesis was basically spawned from that flawed study.

"[Ancel] Keys hypothesized that a Mediterranean-style diet low in animal fat protected against heart disease and that a diet high in animal fats led to heart disease. In order to do this, Keys collected data on deaths from coronary heart disease and fat consumption from 22 countries, but chose to analyze the data from only 7 of these countries, a decision which has since, in recent years, resulted in criticism"
Source: http://en.wikipedia.org/wiki/Ancel_Keys ... ries_Study

If Keys had published the data from all 22 countries, his hypothesis would have been disproven by his own study. All he did was choose the seven countries that lined up with his diet-heart hypothesis. And yet, that study is considered one of the key arguments against animal fats and cited by WHO as fact. Amazing.

The fact of the matter is that the Diet-heart hypothesis and the Lipid hypothesis have never been proven. Only a handful of flawed studies have suggested it might be true (such as the Seven Countries Study). But, those studies are deeply flawed, and almost always combine or confuse saturated fats and trans fats into the same category.

If you want to prove the diet-heart/lipid hypothesis, you'll need to find some solid evidence that natural saturated fats — from animals — are harmful. This whole trans-fats and saturated fats being lumped together isn't going to cut it.

This thread has been going on for 10 pages now, and no one has produced any evidence that saturated fats, from animals, are harmful. You'd think a claim like that — which 99% of doctors and the population believes is true — would have lots of proof to back it up. You don't find it disturbing that our entire society is convinced of a major diet recommendation that has very little supporting evidence?

Here is the official document where the medical establishment formally recognized the association between high cholesterol and heart attacks:

http://consensus.nih.gov/1984/1984Chole ... 47html.htm

MachineGhost wrote: Here is the official document where the medical establishment formally recognized the association between high cholesterol and heart attacks:

http://consensus.nih.gov/1984/1984Chole ... 47html.htm

What a joke.

MG...You really need to watch [url=http://]The Oiling of America[/url]. Among other things, it shows how the 1984 Consensus Conference was a total scam.

LRC [Lipid Research Clinics] researchers claimed that the group taking the cholesterol-lowering drug had a 17% reduction in the rate of CHD, with an average cholesterol reduction of 8.5%. This allowed LRC trials Director Basil Rifkind to claim that "for each 1% reduction in cholesterol, we can expect a 2% reduction in CHD events." The statement was widely circulated even though it represented a completely invalid representation of the data, especially in light of the fact that when the lipid group at the University of Maryland analyzed the LRC data, they found no difference in CHD events between the group taking the drug and those on the placebo.

A number of clinicians and statisticians participating in a 1984 Lipid Research Clinics Conference workshop, including Michael Oliver and Richard Krommel, were highly critical of the manner in which the LRC results had been tabulated and manipulated. The conference, in fact, went very badly for the NHLBI, with critics of the lipid hypothesis almost outnumbering supporters. One participant, Dr. Beverly Teter of the University of Maryland’s lipid group, was delighted with the state of affairs. "It’s wonderful’" she remarked to Basil Rifkind, study coordinator, "to finally hear both sides of the debate. We need more meetings like this" His reply was terse and sour: "No we don’t."

Dissenters were again invited to speak briefly at the NHLBI-sponsored National Cholesterol Consensus Conference held later that year, but their views were not included in the panel’s report, for the simple reason that the report was generated by NHLBI staff before the conference convened. [Dr.] Bev Teter [of the University of Maryland’s lipid group] discovered this when she picked up some papers by mistake just before the conference began, and found they contained the consensus report, already written, with just a few numbers left blank. Kritchevsky represented the lipid hypothesis camp with a humorous five-minute presentation, full of ditties. Edward Ahrens, a respected researcher, raised strenuous objections about the "consensus," only to be told that he had misinterpreted his own data, and that if he wanted a conference to come up with different conclusions, he should pay for it himself.

The 1984 Cholesterol Consensus Conference final report was a whitewash, containing no mention of the large body of evidence that conflicted with the lipid hypothesis. One of the blanks was filled with the number 200. The document defined all those with cholesterol levels above 200 mg/dL as "at risk" and called for mass cholesterol screening, even though the most ardent supporters of the lipid hypothesis had surmised in print that 240 should be the magic cutoff point. Such screening would, in fact, need to be carried out on a massive scale as the federal medical bureaucracy, by picking the number 200, had defined the vast majority of the American adult population as "at risk." The report resurrected the ghost of Norman Jolliffe and his Prudent Diet by suggesting the avoidance of saturated fat and cholesterol for all Americans now defined as "at risk," and specifically advised the replacement of butter with margarine.

The Consensus Conference also provided a launching pad for the nationwide National Cholesterol Education Program, which had the stated goal of "changing physicians’ attitudes." NHLBI-funded studies had determined that while the general population had bought into the lipid hypotheses, and was dutifully using margarine and buying low-cholesterol foods, the medical profession remained skeptical. A large "Physicians Kit" was sent to all doctors in America, compiled in part by the American Pharmaceutical Association, whose representatives served on the NCEP coordinating committee. Doctors were taught the importance of cholesterol screening, the advantages of cholesterol-lowering drugs and the unique benefits of the Prudent Diet. NCEP materials told every doctor in America to recommend the use of margarine rather than butter.

Source: http://www.drcranton.com/nutrition/oiling.htm

Let me repeat that if you didn't catch that. The so-called "Consensus" report was written before the conference even began — despite the fact that almost as many critics showed up to the conference as supporters. The people behind the Consensus Conference literally picked the number "200" at the end of the conference so that the average person would be put on cholesterol lowering drugs unnecessarily and told to eat margarine and avoid saturated fats. This was all done with an enormous budget to send cholesterol-monitoring kits to every doctor in America to "educate" them on the findings of this conference.

Sorry, MG. But, you're just showing the whitewashed conclusions of the edible oil lobby and statin/pharma lobby.

I realize that you're trying hard to prove the diet-heart and lipid hypothesis, but the fact is that neither of those theories have ever been proven to be true. If you spend the time to learn about the studies that tried to prove those theories, the more you'll be sickened by the realization that corporate interests have set out to demonize natural animal fats for no other reason than to make money by moving the entire population onto unnecessary medication and imitation oils/foods.


Sadly, in 1987, across-the-board recommendations for our entire population, including children, were formulated based on the findings of that deeply flawed conference.

From the New York Times, in 1987:

The most authoritative recommendations published in this country were developed by a 1984 conference of experts convened by the National Institutes of Health to seek a consensus on the issue. The consensus conference urged that all Americans whose high cholesterol levels put them in the top quarter of the population be treated with diet or with both diet and drugs...The consensus conference suggested that adults under the age of 30 try to reduce their levels to about 180 milligrams per deciliter, and that older adults aim for 200.
...
The 1984 panel recommended that even without such knowledge, all Americans 2 years old and older reduce fat in their diets to an average 30 percent of total calories, from the current 40 percent, with no more than 10 percent of total calories coming from saturated fats. The panel also recommended reducing dietary cholesterol to no more than 250 to 300 milligrams daily.
...
Some experts worry that a nationwide push to reduce cholesterol levels might actually cause more harm than good to many people, particularly children and adolescents who need fats, cholesterol and other essential nutrients for growth and development.
...
Dr. Marshall H. Becker, chairman of the department of health behavior and health education at the University of Michigan School of Public Health, asked: ''Why are we driving people nuts about cholesterol, why are we making such a big deal of it, when there are other things, like smoking, that are clearly phenomenally damaging?''

''Nobody knows,'' he said, ''what will happen to people in our society if you put them on severely restricted cholesterol diets. It's never been done for a lifetime. And the drugs you need to take have side effects.''
Source: http://nyti.ms/LEk7zz

In other words, that 1984 conference — which was clearly a scam — created millions of new patients for the pharmaceutical industry. Many of these new patients were/are healthy individuals who were now deemed to be "at risk". If your cholesterol is slightly above average, you are now a candidate for cholesterol lowering drugs because of that terribly flawed conference, for no other reason than to make pharmaceutical corporations more money.

The 1987 New York Times article goes on to quote doctors who believed that the '84 Consensus Conference was genuine and that people need to lower their cholesterol — even though, in reality, the theory has never been proven to be true.

Many critics of the lipid hypothesis believe that Cholesterol is the body's way of healing itself, and reducing Cholesterol interferes with the body's natural healing mechanism. Of course, few people now care to believe that because everyone thinks the "Consensus Conference" was genuine.

Gumby wrote:

MachineGhost wrote:Leaving aside my personal experience with saturated fat (which could as easily just be too much Omega-6 vs Omega-3 in factory farmed meat -- I'll have to try a grass fed meat self-test again, although I think I tried it before with negative results)

MG, I can't help but wonder if you need to give your self-tests two weeks to really see the results. Couldn't one eat something very beneficial that produces a short term detoxification reaction (rash, nausea, die-off, etc)?

MG/Gumby,
I convinced my family some time ago to use only olive oil and coconut oil (no vegetable oil at all).  About 3 months ago, my wife bought some vegetable oil so she could make some tempura shrimp.  Afterwards we all experienced very upset stomachs.  Same thing happened a month later so we gave away the rest of the vegetable oil.  From this I conclude either

1) people probably shouldn't be eating industrial lubricants like vegetable oil
2) perhaps it takes time for the body to adjust to a oil change (unlike a car)

I think Gumby is right.  Sudden changes in the oil one consumes probably does produce short term reactions.  If someone wants to change their diet as described above, you may want to ease into it rather than making an abrupt change. 

I thought all human cell membranes contain saturated fats..  so they are essential.  The question is how much of them do we need and how much is too much.

blackomen wrote:The question is how much of them do we need and how much is too much.

Many people consider breast milk to be the perfect food (at least for infants). Interestingly, human breast milk often has more fat than whole milk and contains about 6 times the cholesterol of a typical American diet.

Infants require fat and cholesterol to develop properly. Without fat and cholesterol, all sorts of development problems arise (mental, sensory, growth, etc). And without a diet that is rich in saturated fats and cholesterol, mothers (if they are lucky enough to get pregnant due to fertility issues) are unable to produce the milk they need to nourish their infants.

Furthermore, the idea that children above the age of 2 suddenly need to start drinking low-fat milk and eating a low fat diet wasn't based on any proven science. It was just an unproven theory — recommended by politicians — that has resulted in a significant increase in childhood obesity and development issues since it was enacted.

Gumby wrote: MG... in all seriousness, having an inflammation sensitivity is a sign that you might have an AA deficiency. Perhaps if you built up your AA stores, your body would have the proper amount of essential fatty acids it needs to resolve or suppress inflammation better. It might be worth considering.

Are you kidding me?  I point out evidence of what excess AA does to the body and you flip it on its head.  I've eaten just pastured egg yolks before -- which if they really don't have any saturated fat as claimed -- are loaded with AA and I get a burning and flushing face for hours afterwards.  I really doubt that is a AA defenciency when inflammation is a symptom of AA excess.  It's part of why high S.A.D. Omega-6 is so unhealthy.

I've started an experiment with pastured ghee (3T, then 2T, then 1T) with minor negative effects, but wow, I got a killer MSG-like headache on the third day and had to stop and recover for day or two.  I will retry with 1/8th teaspoon or less day by day and see how it goes.  This experience reminds me of the raw food "quack" book that claimed to have used raw butter and raw honey to heal a brain damaged patient.

But I think its now time I have all of my EFA levels checked.  Something has just got to be off.

Gumby wrote: Hmm... I'm not sure I would ever buy raw milk from "companies". I think it's better to find a local small-production farm (if possible) and make sure they are committed to safe practices before consuming raw milk.

That was actually the case.  The second farm consistently does pathogen testing and the levels always come in lower than general pastuerized milk.  So just be careful.  Groupies are like zombies and will ignore or censor contrary evidence to keep a harmony in their worldview (just think of straight-edge militant vegans).  That doesn't mean I believe the FDA when it says raw milk is "dangerous" or that I'm going to stop advocating for its abolishment or reform, but there usually is SOME truth as a basis of government supression for public health purposes.

Gumby wrote: MG, do you believe that Polyunsaturated vegetable oils are the best cooking oils? I hope you know better than that. That statement was basically written by the edible oil lobby. As I've mentioned a number of times, above, most studies combine trans fats and saturated fats together when comparing risk. The statement you bolded did the exact same thing. This is intentionally done to make polyunsaturated oils look better than they are — to protect a multi-billion dollar industry.  

Let me put it this way: do you believe unrefined, unprocessed vegetable oils are unhealthy (excluding tropicals)?  Because they do lower cholesterol scientifically.  Whether that effect is good or not, isn't the topic of debate here though, just saturated fats.

I bring this point up because you are taking a position that Omega-6 oils are "bad", but its really the processing that makes them so (whether cooking, refining or trans-fats), just as you are saying saturated fat is "good" when its really the pastured/grass feeding that makes it so.  Which implies there are other factors at work than just the type of fat itself.

If you want to prove the diet-heart/lipid hypothesis, you'll need to find some solid evidence that natural saturated fats — from animals — are harmful. This whole trans-fats and saturated fats being lumped together isn't going to cut it.

This thread has been going on for 10 pages now, and no one has produced any evidence that saturated fats, from animals, are harmful. You'd think a claim like that — which 99% of doctors and the population believes is true — would have lots of proof to back it up. You don't find it disturbing that our entire society is convinced of a major diet recommendation that has very little supporting evidence?

I agree with everything you said.  There is plenty of evidence of an association between saturated fat and various diseases, but I don't think its the kind of evidence that controls for the confounding variables of pastured/grass-feeding, transfat, AA, hormones, antibiotics and iron intake.  Like I've said several times already, your OP is really that pastured/grass-feed fat and meat is healthy, not blanket saturated fats per se.

MachineGhost wrote:Are you kidding me?  I point out evidence of what excess AA does to the body and you flip it on its head.  I've eaten just pastured egg yolks before -- which if they really don't have any saturated fat as claimed -- are loaded with AA and I get a burning and flushing face for hours afterwards.  I really doubt that is a AA defenciency when inflammation is a symptom of AA excess.  It's part of why high S.A.D. Omega-6 is so unhealthy.

Hey. No need to get all inflamed .

AA is necessary for healthy skin. It's essential for hair growth, for libido, for sperm production, for fertility, and for creating inflammation when there is a response to injury. AA is necessary for your body to suppress inflammation. In a healthy human being, eating an egg yolk should not cause inflammation in the body.

AA is needed to respond to inflammation and suppress it. So, avoiding AA in your diet — in the hopes that it will prevent your body from creating an inflammation response — isn't going to work. If you're getting all inflamed from eating an egg yolk, it's highly likely that something else is wrong with your body, and it probably has nothing to do with AA.

MachineGhost wrote:Let me put it this way: do you believe unrefined, unprocessed vegetable oils are unhealthy (excluding tropicals)?

Once you heat many "unrefined" vegetable oils, they release free radicals. If you're going to heat an oil, it's far safer to use an a natural saturated fat that is solid at room temperature — which is more stable and can withstand heat better (generally below 400º).

MachineGhost wrote:Because they do lower cholesterol scientifically.

Who cares? Individuals with highest cholesterol tend to live the longest...

People with high cholesterol live the longest. This statement seems so incredible that it takes a long time to clear one's brainwashed mind to fully understand its importance. Yet the fact that people with high cholesterol live the longest emerges clearly from many scientific papers. Consider the finding of Dr. Harlan Krumholz of the Department of Cardiovascular Medicine at Yale University, who reported in 1994 that old people with low cholesterol died twice as often from a heart attack as did old people with a high cholesterol.1 Supporters of the cholesterol campaign consistently ignore his observation, or consider it as a rare exception, produced by chance among a huge number of studies finding the opposite.

But it is not an exception; there are now a large number of findings that contradict the lipid hypothesis. To be more specific, most studies of old people have shown that high cholesterol is not a risk factor for coronary heart disease. This was the result of my search in the Medline database for studies addressing that question.2 Eleven studies of old people came up with that result, and a further seven studies found that high cholesterol did not predict all-cause mortality either.

Now consider that more than 90 % of all cardiovascular disease is seen in people above age 60 also and that almost all studies have found that high cholesterol is not a risk factor for women.2 This means that high cholesterol is only a risk factor for less than 5 % of those who die from a heart attack.

But there is more comfort for those who have high cholesterol; six of the studies found that total mortality was inversely associated with either total or LDL-cholesterol, or both. This means that it is actually much better to have high than to have low cholesterol if you want to live to be very old.

Source: The Cholesterol Myths by Uffe Ravnvskov, MD, PhD
NewTrends Publishing, pp 64-65

1. Krumholz HM and others. Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years. Journal of the American Medical Association 272, 1335-1340, 1990.

2. Ravnskov U. High cholesterol may protect against infections and atherosclerosis. Quarterly Journal of Medicine 96, 927-934, 2003.

This is not to say that high cholesterol is always good. For instance...

Most studies of young and middle-aged men have found high cholesterol to be a risk factor for coronary heart disease, seemingly a contradiction to the idea that high cholesterol is protective. Why is high cholesterol a risk factor in young and middle-aged men? A likely explanation is that men of that age are often in the midst of their professional career. High cholesterol may therefore reflect mental stress, a well-known cause of high cholesterol and also a risk factor for heart disease. Again, high cholesterol is not necessarily the direct cause but may only be a marker. High cholesterol in young and middle-aged men could, for instance, reflect the body’s need for more cholesterol because cholesterol is the building material of many stress hormones. Any possible protective effect of high cholesterol may therefore be counteracted by the negative influence of a stressful life on the vascular system.
Source: The Cholesterol Myths by Uffe Ravnvskov, MD, PhD

MachineGhost wrote:Whether that effect is good or not, isn't the topic of debate here though, just saturated fats.

Well, if lowering cholesterol may or may not be beneficial, who cares with unrefined vegetable oils lower cholesterol? The second you heat unrefined vegetable oils, they start to become toxic. Saturated fats are more stable.

Gumby and others, one of my Facebook friends posted this seemingly ridiculous article and I was wondering if you could debunk it.  The idea that all fats are bad for you is frankly laughable, but I would be interested in where the holes are in their studies or logic:

http://engine2diet.com/the-daily-beet/t ... -giveaway/

Storm,

1. Every cell in your body is coated with a cell membrane made up of fat.

2. There are essential fats which the body needs and cannot live without.  You have to have them every day.   I would not recommend it, but one can live on a no/ultra low carb diet i.e. there are no essential carbohydrates (or close to it).

3. The web site is "engine2diet" i.e. the vegetarian/ultra low fat people.  A. these people ignore the established benefits of olive oil/omega 3 fatty acids/nuts/perhaps coconut oil should go here as well. B. These people are either clueless, or ignore the problems associated with eating shit loads of carbs (even good carbs) at one sitting e.g. their recipie for oatmeal.

As you may gather from my believing the TCM (traditional chinese medicine) diet approach, diet needs to be individualized, I do not think there is a one size fits all optimal approach that will  work for most people.  I will say that the ultra low fat approach is by itself silly (see 3A) and (if you are following the engine2diet vegetarian approach) problematic as there are a number of people who no matter what their wishes, their body would be better off eating some kind of animal protein.