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Author Archives: Glyn and Liz
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This is a new table that brings the rare earths in from the cold. In particular, it predicts a dramatic role for thulium (a hitherto obscure element) as between silver and gold in group I. The paper thus ended with a prediction and a hypothesis to test: that there exists monovalent thulium, either Tm[+1] analogous to aurous oxide or Tm[-1] analogous to caesium auride.
E. G. Marks and J. A. Marks
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“The Obesity Epidemic by Zoë Harcombe: What caused it? How can we stop it?” does what it says in the title – it answers those two critical questions. It takes you on the journey that the author, Zoë Harcombe went on to answer those 
questions and hopefully it will shock you as much as it shocked her.
ISBN: 978-1-907797-00-2
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The perfect storm for an obesity epidemic – Eat fat producing carbohydrates and pump our foods full of fructose and glucose. Fructose is 10 times more damaging than glucose. What do you put into ‘low fat’ foods to make them palatable – Fructose? Obesity and a range mature-onset medical-conditions accelerated after this combination of circumstances in the late 1970s. Eat sugar-generating foods and stop eating fats – and watch you belly expand!!!
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The wisdom of playwrights
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Healthy cell membranes contain an average of 20% molecular cholesterol. If the cell membranes cholesterol content is reduced the cell membrane becomes weak, leaky and deformed. Cholesterol lowering therapies have distressing consequences way beyond their intended outcomes. The real cause of raised LDL in blood plasma is the glycation (sugar-damage) of the LDL receptor mechanism. The sugar damage prevents organs from receiving fats, cholesterol and fat soluble nutrients. Sugar-damaged LDL is eventually scavenged by less discriminating fat storage cells.
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The metabolic syndrome (MetS) is manifested by a lipid triad which includes elevated serum triglycerides, small LDL particles, and low high-density lipoprotein (HDL) cholesterol, by central obesity (central adiposity), insulin resistance, glucose intolerance and elevated blood pressure, and it is associated with an increased risk of type 2 diabetes and coronary heart disease. We have developed a new hypothesis regarding MetS as a consequence of a high intake in carbohydrates and food with a high glycemic index, particularly fructose, and relatively low intake of cholesterol and saturated fat. We support our arguments through animal studies which have shown that exposure of the liver to increased quantities of fructose leads to rapid stimulation of lipogenesis and accumulation of triglycerides. The adipocytes store triglycerides in lipid droplets, leading to adipocyte hypertrophy. Adipocyte hypertrophy is associated with macrophage accumulation in adipose tissue. An important modulator of obesity-associated macrophage responses in white adipose tissue is the death of adipocytes. Excess exposure to fructose intake determines the liver to metabolize high doses of fructose, producing increased levels of fructose end products, like glyceraldehyde and dihydroxyacetone phosphate, that can converge with the glycolytic pathway.
Fructose also leads to increased levels of advanced glycation end products. The macrophages exposed to advanced glycation end products become dysfunctional and, on entry into the artery wall, contribute to plaque formation and thrombosis.
Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?
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Current guidelines encourage ambitious long term cholesterol lowering with statins, in order to decrease cardiovascular disease events. However, by regulating the biosynthesis of cholesterol we potentially change the form and function of every cell membrane from the head to the toe. As research into cell morphology and membrane function realises more dependencies upon cholesterol rich lipid membranes, our clinical understanding of long term inhibition of cholesterol biosynthesis is also changing. This review of noncardiovascular research concerning such membrane effects raises important new issues concerning the clinical advantages and disadvantages of the long term use, and broadening criteria, of cholesterol reductions.
Cholesterol-lowering therapy and cell membranes. Stable plaque at the expense of unstable membranes?
Liz & Glyn Wainwright 