ডা. সিদ্ধার্থ মুখোপাধ্যায়
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স্টাটিন খাবেন না, খেতে দেবেন না
অর্থ ও স্বাস্থ্য দুইই নষ্ট।
কোম্পানি ও ওষুধের দোকানের লাভ শুধু।

আপনাদের বলি কিভাবে স্টাটিন এর আবিষ্কার হলো। এই লিংক টা পড়ুন।
https://academic.oup.com/qjmed/article/104/10/867/1591864?fbclid=IwAR2_HkmzsHIZbxDAAO2c5Ul8G943HWVs81yv4Omla62rplJSnwFGmqrIFt8
দেখবেন ফ্যামিলিয়াল জেনেটিক হাইপারলিপিডিমিয়া তে ব্যবহার হয়েছিল আগে এই স্টাটিন। তারপরে অমন রোগী তো মুষ্টিমেয়। সব্বাইকে খাওয়ানো হল, বহুজাতিক ওষুধ কোম্পানির অর্থবলে। এটি সাম্প্রতিক কালের সবচেয়ে বড় ড্রাগ স্ক্যাম। এমনকি FDA - USA ও নতি স্বীকার করলো, অর্থ ও প্রতিপত্তির কাছে।
যাদের ঐ জীনগত অসুখ আছে তাদের, আর সাধারণ মানুষের শরীরের কর্মকান্ড বা রোগের ধরণ পুরো আলাদা।।
লেখার লিঙ্ক :https://academic.oup.com/qjmed/article/104/10/867/1591864?fbclid=IwAR2_HkmzsHIZbxDAAO2c5Ul8G943HWVs81yv4Omla62rplJSnwFGmqrIFt8

এবার লেখার কিছু বিবরণ :

The great cholesterol myth; unfortunate consequences of Brown and Goldstein’s mistake
D. D. Adams
QJM: An International Journal of Medicine, Volume 104, Issue 10, October 2011, Pages 867–870, https://doi.org/10.1093/qjmed/hcr087
Published: 20 June 2011 Article history

Abstract
Following their Nobel Prize-winning discovery of the defective gene causing familial hypercholesterolaemia, Brown and Goldstein misunderstood the mechanism involved in the pathogenesis of the associated arterial disease. They ascribed this to an effect of the high levels of cholesterol circulating in the blood. In reality, the accelerated arterial damage is likely to be a consequence of more brittle arterial cell walls, as biochemists know cholesterol to be a component of them which modulates their fluidity, conferring flexibility and hence resistance to damage from the ordinary hydrodynamic blood forces. In the absence of efficient receptors for LDL cholesterol, cells will be unable to use this component adequately for the manufacture of normally resilient arterial cell walls, resulting in accelerated arteriosclerosis. Eating cholesterol is harmless, shown by its failure to produce vascular accidents in laboratory animals, but its avoidance causes human malnutrition from lack of fat-soluble vitamins, especially vitamin D.

Introduction
When post-mortem examinations are made of elderly people, opening of the aorta and smaller arteries often reveals atheroma, rough yellow plaques disfiguring the smooth pink lining of these blood vessels and impinging on the lumen. Often the extent of the atheroma formation makes one marvel at how long the patient has lived before succumbing to a vascular accident from obstruction or rupturing of an important artery.

Atheromatous plaques contain cholesterol. Accordingly, research workers have repeatedly fed laboratory animals large amounts of cholesterol in their diets,1 expecting this to produce vascular accidents. It never has, which shows that despite the presence of cholesterol in atheromatous plaques these lesions are not caused by eating cholesterol. Before describing the strong evidence that hydrodynamic stresses cause the arterial degeneration responsible for ischaemic heart disease and strokes, we shall recount description2 of the spectacular deviation from reality caused by a mistaken interpretation made by Goldstein and Brown after they had brilliantly discovered the defective gene that causes familial hypercholesterolaemia (FH).

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ডা. সিদ্ধার্থ মুখোপাধ্যায়
সুলেখক । কবি।
Diabetes & Endocrinology Consultant
M.D. at University of Madras । প্রাক্তন :
Calcutta National Medical College and Madras Medical College (MMC