re: Man’s hands fill with cholesterol after eating 6-9lbs of cheese and butter.

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The snark in that "news" article is unbelievable

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Cholesterol levels can be lowered through exercise, medication, and eating more vegetables and fruits, and fewer fatty foods. You know, like how your body is meant to consume nutrition.

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I asked you first

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Marshall Elam, PhD, MD | Professor, Pharmacology and Medicine University of Tennessee HSC, Memphis TN1
I would like to thank the authors for bringing this striking case to the attention of readers of the Journal. The dramatic increase in plasma cholesterol along with palmar and elbow xanthomas in response to high dietary saturated fat intake suggest an underlying genetic predisposition. The baseline cholesterol and presumed absence of tendinous xanthomas makes heterozygous familial hypercholesterolemia less likely. A more likely diagnosis is familial dysbetalipoproteinemia, a genetic disorder of lipoprotein metabolism in which mutation of the ApoE gene results in impaired clearance of VLDL and Chylomicron remnants. familial dysbetalipoproteinemia most commonly occurs in patients who are homozygous for the apoE2 (p.Arg176Cys) allele. The disorder manifests as mixed lipemia, often with a 1:1 ratio of cholesterol to triglyceride or markedly elevated triglyceride if hyperchylomicronemia is present. The presence of palmar xanthomas such as those seen in this case are considered pathognomonic. Defective apoE alone is not sufficient to manifest the disorder, additional factors such as obesity, hypothyroidism, diabetes and high dietary intake of saturated fats and carbohydrates are required. This disorder should be suspected in cases of mixed lipemia where there is a discrepancy between LDL-C calculated using the Friedewald formula versus directly measured LDL-C and/or the ratio of apoB/Total Cholesterol (mgl/dl) is low (<0.33) and Non-HDLC/ApoB (mg/dl) is high (>2.6). Definitive diagnosis requires genetic analysis of the apoE gene, preferably with Next-Generation sequencing as autosomal dominant ApoE variants have been identified. Other genetic disorders to be considered in this case are familial combined hyperlipidemia and familial hypertriglyceridemia. It is important to consider the diagnosis of familial dysbetalipoproteinemia in patients with mixed hyperlipidemia as the disorder is associated with greatly increased risk of atherosclerotic vascular disease and requires combined therapy with statin and a fibrate (fenofibrate) for control.

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