July 19, 1897
Reply: THE VALUE OF AN EXCLUSIVE RED MEAT DIET IN CERTAIN CASES OF CHRONIC GOUT.
Dr Wainwright writes about the efficacy of an exclusive red meat diet for helping children who are passing uric acid crystals.
THE VALUE OF AN EXCLUSIVE RED MEAT DIET IN CERTAIN CASES OF CHRONIC GOUT."
To the -Editors of THE LANCET.
SIRS,-Mr. William Armstrong’s paper under this heading in The Lancet of July 3rd has shown the good that can be done by sometimes using what on the face of it appears to be a theoretically wrong diet. Reasoning as the writer does on the subject of auto-intoxication the diet has much in its favour; its results are good in his practice.
Speaking of children in whom the uric acid diathesis is sometimes very marked, I will give a case in my own practice which supports the assimilation theory. A child at two days old passed a quantity of red urine which alarmed the nurse, so much so that she saved me a specimen which on being tested was found to contain pure uric acid crystals. This urine was constantly being passed by the child, who screamed a great deal, had flatulence and sickness, and seemed very miserable altogether. The mother's milk was rich in cream, but turned acid rapidly. Careful dieting of the mother had no effect on the child for good. I found eventually that no milks would agree, so I abandoned milk and put the child on mutton juice. This agreed perfectly, the crying and sickness ceased, the general aspect of the child changed for the better, and the uric acid ceased to be marked after twenty-four hours of mutton-juice feeding. I gradually brought the feeding back to a sterilised cream mixture; the child is now well and taking food without difficulty. Curiously enough the family history of this infant reads like a list of Spa patients--viz., paternal grandmother has rheumatoid arthritis; the father has passed quantities of uric acid calculi; the mother has what Sir Willoughby Wade would call gouty neuritis accompanied by acid dyspepsia.
When Dr. Eustace Smith introduced meat-juice feeding he saw the wonderful way in which the albumin was assimilated, and I am quit econvinced that it is in cases of uric acid diathesis that milk-mixed carbohydrate-diets often disagree. Beef-tea I never give to children, as I only see harm from its use. In several other cases of children unable to digest milk well I have noted uric acid, but the family history is not so marked. When one considers that sugar, which is almost harmless in itself, can (as Sir Dyce Duckwork has pointed out) by setting up fermentation produce flatulence and acidity, it is obvious that carbohydrates may retard stomach digestion by acting as diluents alone, as well as by improperly fermenting and throwing the whole digestive tract out of gear by sending into the duedenum a fermenting mass, the toxins of which are absorbed--veritable taskmasters to an overworked system. Sir William Roberts has called attention to the value of mixed diets, and they certainly are more comfortable than the single red meat and water or vegetarian; but in the special cases mentioned by Mr. Armstrong the microbes must be mastered.
I am, Sirs, yours faithfully,
Lennox Wainwright, M.D. Brux., &c.
Folkestone, July 19th, 1897
January 1, 1957
High Fructose Corn Syrup is produced for the first time after a new enzyme is invented.
HFCS was first produced by Richard O. Marshall and Earl R. Kooi in 1957 after they created the enzyme glucose isomerase. The enzyme rearranged the composition of glucose in corn syrup and made it into fructose.
HFCS is produced from corn that was milled into corn starch. Which is then turned into corn syrup. The glucose isomerase enzymes are then added to turn the some of the glucose in the corn syrup into fructose. Then you've got HFCS.
September 1, 1968
Studies of muscle capillary basement membranes in normal subjects, diabetic, and prediabetic patients
A science paper is published that shows how to diagnose carbotoxicity with muscle cell biopsies, finding that "basement membrane thickening is a very constant finding among overtly diabetic patients, in that approximately 98% of individual diabetic subjects demonstrated this lesion."
A technique is described for the measurement of muscle capillary basement membranes by electron microscopic examination of needle biopsies of the quadriceps muscle. With this procedure it has been possible to obtain an objective evaluation of the significance of capillary basement membrane hypertrophy in diabetic microangiopathy. The results of such studies of muscle capillary basement membrane thickness in 50 normal, 51 diabetic, and 30 prediabetic patients have demonstrated the following. First, that the average capillary basement membrane width of diabetic patients is over twice that of normal subjects; moreover, such basement membrane thickening is a very constant finding among overtly diabetic patients, in that approximately 98% of individual diabetic subjects demonstrated this lesion. The degree of basement membrane thickening in diabetic patients is, however, unrelated to age, weight, severity, or duration of diabetes. Second, capillary basement membrane hypertrophy has been found in approximately 50% of patients who are genetically prediabetic but who have not yet demonstrated evidence of the manifest carbohydrate disturbances of diabetes mellitus. Third, in contrast to the results obtained in genetically diabetic patients, subjects with severe hyperglycemia due to causes other than genetic diabetes only infrequently show basement membrane hypertrophy.
These results indicate that thickening of the muscle capillary basement membranes is a characteristic of genetic diabetes mellitus, and further, that the hyperglycemia of diabetes is probably not the factor responsible for the microangiopathy characteristic of diabetes mellitus. Finally, the discovery of thickened capillary basement membranes in prediabetic patients suggests that basement membrane hypertrophy is a relatively early lesion of the diabetic syndrome and provides further support for the conclusion that this vascular defect is independent of carbohydrate derangements of diabetes mellitus.
January 1, 1978
High-fructose corn syrup enters the market
HFCS was rapidly introduced to many processed foods and soft drinks in the U.S. from about 1975 to 1985. Soft drink makers such as Coca-Cola and Pepsi still use sugar in other nations but switched to HFCS in the U.S. due to higher sugar costs.
HFCS is used in almost every packaged food and soft drink American consumers see today. HFCS has replaced more expensively priced sugar in a variety of uses including; the beverage industry (41%), processed food manufacturers (22%), cereal and bakery producers (14%), multiple-use food manufacturers (12%), the dairy industry (9%), and the confectionery industry (1%).
December 1, 2008
John White, consultant to the Big Sugar industry, publishes science article to refute high fructose corn syrup's role in chronic disease.
High-fructose corn syrup (HFCS) is a fructose-glucose liquid sweetener alternative to sucrose (common table sugar) first introduced to the food and beverage industry in the 1970s. It is not meaningfully different in composition or metabolism from other fructose-glucose sweeteners like sucrose, honey, and fruit juice concentrates. HFCS was widely embraced by food formulators, and its use grew between the mid-1970s and mid-1990s, principally as a replacement for sucrose. This was primarily because of its sweetness comparable with that of sucrose, improved stability and functionality, and ease of use. Although HFCS use today is nearly equivalent to sucrose use in the United States, we live in a decidedly sucrose-sweetened world: >90% of the nutritive sweetener used worldwide is sucrose. Here I review the history, composition, availability, and characteristics of HFCS in a factual manner to clarify common misunderstandings that have been a source of confusion to health professionals and the general public alike. In particular, I evaluate the strength of the popular hypothesis that HFCS is uniquely responsible for obesity. Although examples of pure fructose causing metabolic upset at high concentrations abound, especially when fed as the sole carbohydrate source, there is no evidence that the common fructose-glucose sweeteners do the same. Thus, studies using extreme carbohydrate diets may be useful for probing biochemical pathways, but they have no relevance to the human diet or to current consumption. I conclude that the HFCS-obesity hypothesis is supported neither in the United States nor worldwide.
The author is a consultant to the food and beverage industry in nutritive sweeteners, including HFCS and sucrose. His professional associations, past and present, include individual food industry companies as well as such organizations as the American Chemical Society, American Council on Science and Health, Calorie Control Council, Corn Refiners Association, Institute of Food Technologists, and International Life Sciences Institute.