"... As with other big government interventions, Hoover made the situation worse by attempting to control one part of the economic picture. When he froze wages, it amounted to across-the-board increases in buying power as deflation set in — and made their companies unable to pass along the costs of production to consumers. After two years, employment had dropped 35% and GDP by 27% as the American economy collapsed. Ohanian argues that two-thirds of that GDP decline can be directly attributable to this deal...."
In fact, as the historian David Southern has documented, the worst evils of the South's Jim Crow regime, including segregation, disfranchisement, mob violence, and lynching, all "went hand-in-hand with the most advanced forms of southern progressivism." Remember that progressives wanted an interventionist government with sweeping powers to regulate all walks of life, an approach that fit nicely with Jim Crow's bullying assault on economic liberty and freedom of association....
Have some ugly views cropped up at the recent health care protests? Sure. But to take that as evidence of a century-long battle between enlightened liberal reformers and knuckle-dragging laissez-faire racist goons is to believe in a self-serving fairy tale. It's time for any pundit who thinks that way to grow up.
I recently bought a pair of Vibram FiveFingers Sprint (pictured). They're minimal, lightweight shoes with "toes". They're designed to mimic barefoot walking as closely as possible, while protecting the feet from punctures and abrasion. The soles are thin, flexible and offer no padding whatsoever.
Lakes wilderness with a few friends last weekend. The Pacific Northwest has to be one of the most beautiful places in the world. I was expecting to use the shoes for a few miles and then swap them for my lightweight hiking shoes (Inov8 Flyroc trail runners). The beginning of the trail was really rocky and I thought I was going to have to take them off in the first few hundred yards. Surprisingly, my feet adapted, and although the trail stayed rocky, it became fairly comfortable by the time we had walked a mile.
rsome as well.
The Japanese had a very low rate of MI compared to both Caucasian-Americans and Japanese-Americans. The rate of MI in Caucasian-Americans and Japanese-Americans did not differ significantly. Thus, location but not race determined the susceptibility to MI. 
And for women: 
Again, location but not race largely determined the incidence of MI. MI was extremely rare in the African autopsies. Here's what they had to say: There was only 1 case of healed myocardial infarction among over 4,000 adult autopsies in the Uganda series, and only 2 cases of healed myocardial infarction among over 500 adult autopsies in the Nigerian series. In the New Orleans Negro series the occurrence rate was far greater in every sex and age group than in either one of the Negro series in East and West Africa.Over 4,500 autopsies and not a single fatal MI. If this isn't worth studying, what is? These data should be part of first-year training in medicine and health programs.
In the African Negro series no infarct was found in any age group [out of 244 hearts, 39 over 60 years old]. In the Korean series there were only 2 cases of myocardial infarction [out of 106 hearts] and they were both women... In the Japanese series there were 8 cases of myocardial infarction in 259 hearts. All were men...In the American sample, nearly 40% of the hearts of men and women over 60 showed signs of MI. The findings of the American pathologist confirmed the international autopsy data, showing that diagnostic bias did not contribute to the results significantly. They also took measurements of the thickness of the coronary artery wall, an index of atherosclerosis. They found that the Americans had the most atherosclerosis, but all cultures had some degree of it and there was overlap in the amount of atherosclerosis between samples. This led the investigators to state:
Myocardial infarction and coronary thrombosis are almost nonexistent in Uganda and Nigeria, and the amount of coronary arteriosclerosis is significantly less in Africans than in whites. However, in the two groups there was some overlapping in the degree of arteriosclerosis. No Africans had infarcts, but some had the same or a greater degree of coronary arteriosclerosis as a few whites who had myocardial infarctions. One explanation for this may be that some difference in clotting or clot-lysis mechanisms is present in the two groups. In a previous study, we showed that the incidence of thromboembolic phenomena in the pulmonary circulation [blood clots in the lungs] was low in East Africans as compared with Americans.Now, the authors' conclusions:
These data strongly suggest that among the Orientals the environmental factor is playing a major role in the etiology of myocardial infarction and coronary thrombosis. If the genetic factor is an important one, those Orientals who moved to this country many years ago or who were born in this country should still maintain their low occurrence rate of myocardial infarction at least to some extent, and one would not expect to see similar occurrence rates of myocardial infarction in Orientals and whites as old as 50 to 59 years... As with the Orientals, this suggests that for Negroes in the United States environmental factors are more important than genetic factors in the etiology of myocardial infarction.Africans in Africa and Japanese in Japan = low incidence of MI. Africans, Japanese and Caucasians in the US = high and similar incidence of MI. Genes only influence a person's susceptibility to MI when they live in an environment that promotes MI. Otherwise, genes are basically irrelevant.
Those who incriminate animal fats in raising the blood lipids and causing coronary disease would have us stop eating the fats that we have been eating from immemorial time, such as the fat found in meat and in the butter and cream derived from milk, and eat instead a whole lot of new oils, mainly expressed from vegetable seeds, many of which oils are alien to us.From pages 100-101:
The keeping of flocks of sheep, herds of cattle, and other domestic animals, in order to provide a continuity of meat and milk, started with neolithic man many thousands of years before the Christian era... To these fats we are therefore well adapted, quite apart from man, as a hunter, being well acquainted with the fat of animals in evolutionary times far more remote than the neolithic ones.From page 101:
Contrast with these ancient fats the new oils, mainly expressed from vegetable seeds. Not only are many of these seeds not a natural food for man (e.g., cotton seed and sunflower seed-- and incidentally the sunflower does not even come from the Old World, as we do in the British isles, but from the New), but also the oils expressed from many of them never existed in any quantity before the invention of the modern hydraulic press or the new solvent procedures, and consequently were scarcely eaten in this country before the introduction of margarine, circa 1916, during the First World War. Evolutionarily these oils make us not so much men as the equivalent of a flock of greenfinches, and the evolutionary incongruity is heightened by the fact that the coronary explosion amongst us, as will be seen later, came in since the introduction of just these oils at the period stated, though in margarine they are often saturated by a stream of hydrogen.Now for a little John Yudkin. From "Dietary Factors in Arteriosclerosis: Sucrose" (Lipids 13(5):370. 1978):
In principle, it is very doubtful that one can in any way profoundly modify the diet of any species, including Homo sapiens, without introducing some hazard. The consumption of large quantities of PUFA [polyunsaturated fat] has been made possible only by the very recent development of sophisticated techniques of cultivating oilseeds, and extracting and refining vegetable oils. Before such techniques were available, these oils made only a small contribution to our diets, as they still do in the poorer countries. We cannot ignore the evidence that the large amounts widely recommended nowadays as a preventive of CHD can produce undesirable effects, such as increasing the risk of gallstones and possibly of carcinomatous changes in the skin. On the other hand, the reduction of the high amounts of sugar that we now consume is not known to be accompanied by any hazard.Drs. T. L. Cleave and John Yudkin: making sense since 1936.
"...But who would have thought that the sober, deliberative Barack Obama would have nothing to propose but vague and slippery promises -- or that he would so easily cede the leadership clout of the executive branch to a chaotic, rapacious, solipsistic Congress? House Speaker Nancy Pelosi, whom I used to admire for her smooth aplomb under pressure, has clearly gone off the deep end with her bizarre rants about legitimate town-hall protests by American citizens. She is doing grievous damage to the party and should immediately step down.
There is plenty of blame to go around. Obama's aggressive endorsement of a healthcare plan that does not even exist yet, except in five competing, fluctuating drafts, makes Washington seem like Cloud Cuckoo Land. The president is promoting the most colossal, brazen bait-and-switch operation since the Bush administration snookered the country into invading Iraq with apocalyptic visions of mushroom clouds over American cities."
LDL resistance to copper-induced oxidation, expressed as lag time, was highest during the MUFA-rich diet (55.1±7.3 minutes) and lowest during the PUFA(n-3)– (45.3±7 minutes) and SFA- (45.3±6.4 minutes) rich diets.This was published in a paper by P. Mata and colleagues in 1996. They fed 42 volunteers one of four different diets for 5 weeks each: one rich in saturated fat, one rich in monounsaturated fat, one rich in linoleic acid PUFA, and one rich in linoleic acid plus omega-3 PUFA. They emphasized the finding quoted above, as did the media. But there's an embarrassing piece of data buried in the paper that the authors, and the media, ignored (thanks to Chris Masterjohn for pointing this out). Here's what they saw when they looked directly at LDL oxidation in their volunteers:
Oops! LDL oxidation in the two PUFA groups was increased by more than 31%. The difference between the leftmost two groups and the rightmost two was statistically significant. As one would expect, oxidized LDL is proportional to the amount of PUFA in LDL, which is proportional to dietary PUFA. This somehow got left out of the abstract and media reports. The same investigators published a similar report a year later.The median plasma OxLDL-EO6 increased by 27% (P less than 0.01) in response to the low-fat, low-vegetable diet and 19% (P less than 0.01) in response to the low-fat, high-vegetable diet. Also, the Lp(a) concentration was increased by 7% (P less than 0.01) and 9% (P=0.01), respectively.This is the diet mainstream cardiologists have been prescribing to heart attack patients for 40 years. The trials I mentioned above are the only three I'm aware of in which fat quality was manipulated and oxLDL was directly measured (the first two were based on subsets of the same data). They all suggest that replacing saturated fat with PUFA increases oxLDL.