There was another phenomenally successful pseudoscientific fraud in the 70's and 80's.
A conglomeration of statin manufacturers, zero-population-growth nitwits, liberals, animal rights activists, grain-state lobbyists and politicians, vegetable oil pushers, and other monied interests successfully converted the world's official dogma to the belief that dietary fat was bad, and cholesterol was bad.
Now the truth, that excessive carbohydrates CAUSE deadly increases in small-dense-LDL, diabetes, metabolic syndrome, fatty liver disease, obesity, and more, is destroying our nation's health, right at the time when it is becoming the taxpayer's burden.
This from Dr. Mike Eades:
One of the major players in bringing cholesterol to the publics awareness was Time magazine. Its piece on cholesterol in the March 26, 1984 issue was a devastating hit piece on both dietary cholesterol and dietary fat. Both the article explained were a main driving force behind the development of heart disease.
Reading this article today, its amazing how it drips with misinformation. At the time, however, most people physicians included accepted it as gospel. Sadly, even today, many physicians who should know better believe in and act in accordance to the bountiful misinformation contained in this piece.
You Bet Your Life: An Epilogue to the Cholesterol Story
It has long been incorrectly assumed that saturated fat and cholesterol is unhealthy and leads to cardiovascular disease. Just the opposite is true. Saturated fat corrects cardiovascular disease. When after eating high saturated fat and low carbohydrate for 6 months and thereafter having a VAP blood level test performed, my blood levels were an astounding HDL 63 mg/dl, TRIG 63 mg/dl, and LDL 153 mg/dl, all large fluffy and buoyant. A 13- year follow-up Quebec Cardiovascular Study says CONCLUSIONS: These results indicated that estimated cholesterol levels in large LDL subfraction were not associated with an increased risk of (IHD) ischemic heart disease in men and that the cardiovascular risk attributable to variations in LI phenotype was largely related to markers of a preferential accumulation of small dense LDL particles.