The most terrifying nine words in the English language, according to president Ronald Reagan, are ‘I’m from the Government, and I’m here to help’. Nowhere is this more true than in the whacky world of nutrition. Let’s start with the egg, and let the chicks fall where they may.
Many people still think that eggs are unhealthy, due to their high content of cholesterol. This misconception didn’t start with pure science but from an ugly collision of science, politics and money. At the fatty heart of it all stands Ancel Keys.
Although John Goffman blazed the cholesterol trail (1), Ancel Keys became better known because he was a better self-publicist and a more politically astute player. Ancel built his career on dietary fat and heart disease. It was known that atheroma in clogged arteries contained large amounts of cholesterol and Ancel’s key epidemiology papers, which linked saturated fat in the diet with serum cholesterol levels and heart disease, started to appear in 1966 (2).
US president Lyndon Johnson was struggling at the time to contain inflation. The price of eggs had risen dramatically that spring, so he decided to bring prices down by lowering demand. Johnson had the Surgeon General issue alerts as to the dangers of cholesterol in eggs (3), and a terrible meme was born.
The fact that Keys had been highly selective with his data (to put it mildly) was highlighted at the time (4), but ignored because it did not fit the Gadarene narrative – Keys was an earlier and less malignant version of Tony Fauci (5) – and it was not good for business.
Biochemists and pharmacologists everywhere rushed to develop cholesterol-lowering drugs. First-generation agents were not particularly successful because they were relatively ineffective (the fibrates), poorly tolerated (cholestyramine) or unprofitable (vitamin B3, aka niacin). Full disclosure – niacin lowers LDL-cholesterol and triglycerides, and raises HDL-cholesterol, but at pharmacological doses causes hot flushes and other potential problems.
More potent and better tolerated compounds soon emerged. Compactin aka mevastatin was the first to be identified (6) but another fungal derivate, the closely related molecule lovastatin, was the first to obtain FDA approval. It made Merck many billions of dollars (7).
There is an interesting back-story to this.
Compactin, which was developed by the Japanese company Sankyo, may have been deliberately sabotaged by forcing it through a safety screen designed to guarantee failure. Dogs received Compactin at 20 mg/kg/day (roughly 80 times the human dose) for two years without any problems. However, some animals which were given 100 and 200 mg/kg/day (400 and 800 times the human dose) for 2 years developed lymphoma. These results were published in 1980 (8).
Sankyo had made the strategic error of sharing their product and research portfolio with Merck from July of 1976 (9, 10). I was informed that Merck, who had immediately seen the financial potential of this new wonder-drug, pressured key Sankyo researchers ‘to test Compactin to obvious destruction’; leaving the field clear for them to exploit.
Sankyo were not going to be caught the same way twice and trialled pravastatin, their next compound, at a maximum dose of 25 mg/kg/day (8, 9), but they had lost the initiative. Merck gained FDA approval in 1987, with Sankyo coming in second almost two and a half years later.
I could be wrong about this. We are talking, after all, about the ethical industry.
After that, it was off to the races. Every drug company developed a statin analogue. Every doctor was taught (and increasingly instructed) to prescribe statins. Pharma-influenced working parties set lower and lower cholesterol levels for intervention, and statins became the plat du jour. They were everywhere.
Looking back, it was inevitable. Cholesterol is the most decorated molecule of all time, being the subject of no fewer than 10 Nobel awards and side-show to an 11th (11); and has been an object of morbid medical curiosity since 1913, when Nikolaj Anitschkow produced coronary artery disease in rabbits by force-feeding these notoriously carnivorous animals with cholesterol (12).
One award stands out in my memory. The unravelling of the cholesterol synthetic pathway garnered the 1964 Nobel prize for medicine for Konrad Bloch and Feodor Lynen. At the Nobel banquet Sten Friburg, rector of the Karolinska, announced that the discovery might not only provide weapons against some of mankind’s gravest maladies but would also, somehow, make mankind better (13).
I was only 14 at the time but I remember listening to Friberg on the radio with my parents, who were both life scientists. The Karolinska announcement, the earlier triumph of the Salk vaccine and the subsequent development of a series of blockbuster magic bullets in the clinical areas of pain, depression and hypertension seemed to herald a brave new world where the major causes of suffering and disease would inevitably be pushed back.
Bliss was it in that dawn to be alive, to be a scientist was very heaven. But it was a false dawn. Today’s appalling public health statistics show that Friberg’s ‘weapons’ have not made us better at all. We have become sicker. We have been worshipping the wrong gods.
By the turn of the century, significant gaps in the cholesterol theory were starting to appear.
- Statins reliably reduce plasma lipid levels, but their therapeutic impact is not commensurate (14-19). Death rates in early large trials such as the Heart Protection Study (20), PROSPER (21) and J-LIT (22) did not particularly favour statin intervention. In a recent (2019) meta-analysis, which included data from over 134,000 subjects in 28 clinical trials, statins reduced mortality by a mere tenth of 1% (23). This comes at a global cost of over $30 billion/year (24), so the statins are not cost-effective either. An even more recent meta-analysis found that the statins conferred no benefit at all (25).
- Niacin lowers LDL cholesterol by 10-20% and triglycerides by 20-50%, and raises HDL cholesterol by 15-35% (24). This matches or surpasses the effects of the widely used lovastatin (26), yet a recent meta-analysis found that niacin is not cardio-protective (27). Niacin has a different mechanism of action than the statins but if cholesterol-lowering is genuinely protective, that should not matter.
- A significant part of the paltry effects of statins is mediated via an anti-inflammatory mechanism (28-30), leading to improvements in endothelial function (30). Niacin has anti-inflammatory activity, and has also been shown to improve endothelial dysfunction (31, 32). The main difference between niacin and the statins therefore seems to be that niacin is available without a prescription, and is far cheaper.
- Although higher intakes of dietary fat increase cholesterol levels, recent studies show they do not increase the risk of cardiovascular disease (33-38). Historical data tell the same story. The mid-Victorians ate large amounts of organ meats and consumed three to four times more cholesterol and saturated fat than we do today (39) – yet were almost immune from heart disease (40). These findings alone demolish Keys’ shoddy case, and are reflected in the latest JACC position paper (41).
- The cholesterol in atheroma is not primarily derived from cholesterol fractions in the blood but from immune cells chasing and driving inflammatory and oxidative reactions in the vascular endothelium. Hypercholesterolaemia boosts the involvement of macrophages and monocytes in already formed atheroma (42), but does not itself initiate significant inflammatory changes unless oxidative stress (and therefore cholesterol and lipid oxidation products, aka COPS and LOPS) are present at significant levels (43).
There is a relationship between saturated fat, cholesterol and vascular disease but it must be set against the background of the whole diet (41, 44), in which sugar is a substantial risk factor and phytonutrients are highly protective (44).
So, for example, the vasotoxic effects of COPS are prevented by a pre-transitional diet low in sugar and rich in antioxidant and anti-inflammatory compounds which protect against endothelial dysfunction (45, 53-56).
Conversely, the more saturated fat and cholesterol you consume (almost exclusively in animal-derived foods), the less room there is left on your plate for plant-derived foods with their anti-inflammatory payload. The lower your intakes of plant-derived lipophile and amphiphile antioxidants, the more lipids and cholesterol in your blood will be oxidized to LOPS and COPS which are cytotoxic, angiotoxic and pro-inflammatory (42, 43, 46, 47).
COPS and LOPS occur in abundance in fast foods (48). Those same fast and/or ultra-processed foods contain large amounts of sugar, which works in parallel with the cholesterol and lipid oxidation products. Excess sugar triggers glycative and inflammatory stress, and endothelial dysfunction (49). It also damages liver function, producing a series of pathogenic changes which lead towards NAFLD and atherosclerosis, via shifts in lipoprotein production towards a more atherogenic phenotype (50, 51).
Cholesterol is a not an intrinsically causative / damaging variable unless levels are very high indeed, but it readily becomes one in the context of post-transitional dietary patterns which leave cholesterol vulnerable to oxidation. As you consume more ultra-processed and animal foods and less plant foods, your metabolism and your arterial linings therefore become more pro-inflammatory and your risk of cardiovascular disease increases (52).
Chronic inflammation drives ‘essential’ hypertension (which is not essential at all) and atheroma. These conditions are prevented and reversed in the majority of cases by omega 3 HUFA’s combined with amphiphile polyphenols (53-56) – both of which have largely disappeared from the post-transitional diet.
Critically, the omega 3 HUFA / amphiphilic polyphenol combination achieves these health benefits without lowering cholesterol levels. In fact, cardiologists know that fish oil can raise LDL cholesterol.
It’s not surprising that many doctors find our approach heretical, despite a rapidly increasing number of cases where atheromatous lesions vanish after initial screening, making subsequent angioplasty unnecessary. All of these patients had been using the same omega 3 HUFA / amphiphilic polyphenol combination.
Case histories have little value, however, which is why a series of prospective randomized, double-blind and placebo-controlled trials is underway with the first due to report later this year (57).
In the meantime, the fact that statins still dominate the market is largely due to financial and intellectual inertia, and the ability of Big Pharma to crush honest debate (58). The Keys papers and all those Nobel prizes still hold uncritically pharmaco-centric medics in thrall. Having had the opportunity to talk with some of the original researchers on the 7 countries project, I have learned to recognize an almost religious adherence to the cholesterol creed.
While I think their fixation on statins is preventing them from exploring more effective options, I profoundly empathise with them. The power and momentum of a seductively wrong idea, the history, the collegial chorus and the flood of pharmaceutical funding is more than enough to quench most doctors’ doubts. But …
The pharmaceutical industry learned from the Keys / statin scenario. Convince people there is a problem, use fear to quell their reason, sell them drugs to treat the ‘problem’. It’s a terrific business model, at least in the short term, and Big Pharma’s control of their media and political whores (59) is far greater today. They are aided and abetted by the useful idiots of wokedom, who in their excessive fear of minor risk (the ‘rona) have swallowed the greater risks of medical errors (60 – 65), vaxx damage (66-73) and burgeoning biofascism (74, 75).
Apostasy is not an easy option. But if we have our patients’ and our children’s hearts at heart, we must step outside the 20th century pharmaceutical model and adopt a more Bernardian approach.
We should also remain skeptical of governmental intrusions into our lives. Lyndon BJ’s anti-egg campaign and the band-wagon scientists who promoted it created wide-spread choline deficiency, a major contributory factor to the current pandemic of nonalcoholic fatty liver disease (76-78). As with Covid, the net effect of much public health propaganda appears to be overwhelmingly negative.
Next week: Nothing but a heartbreak every day (79); how to prevent atrial fibrillation from shaking your world.
- Gofman JW, Lindgren FT, Elliott H, Manz W, Hewitt J, Herring V. (1950) The role of lipids and lipoproteins in atherosclerosis.Science 111, 166–171
- Keys A, Aravanis C, Blackburn HW, Van Buchem FS, Buzina R, Djordjević BD, Dontas AS, Fidanza F, Karvonen MJ, Kimura N, Lekos D, Monti M, Puddu V, Taylor HL. Epidemiological studies related to coronary heart disease: characteristics of men aged 40-59 in seven countries. Acta Med Scand Suppl. 1966;460:1-392.
- Samuelson RJ. The Great Inflation and Its Aftermath: The Past and Future of American Affluence. Random House, 2008
- Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease; a methodologic note. N Y State J Med. 1957 Jul 15;57(14):2343-54.
- Endo A, Kuroda M, Tanzawa K. (1976) Competitive inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase by ML-236A and ML-236B fungal metabolites, having hypocholesterolemic activity. Federation of European Biochemical Societies Letters, 72, 323-326.
- Hajar R. Statins: past and present. Heart Views. 2011 Jul;12(3):121-7.
- Abstract Book of the VII International Symposium on Drugs Affecting Lipid Metabolism, held May 28–31, 1980 in Milan, Italy. pp. 224–234.
- Endo A. The discovery and development of HMG-CoA reductase inhibitors. J Lipid Res. 1992 Nov;33(11):1569-82.
- Endo A. Discovery and Development of Statins. MPC (2017). 12(8),1153-1156
- Heinrich Wieland (1928), Adolf Windaus (1928), Leopold Ruzicka (1939), Robert Robinson (1947), Otto Diels (1950): structure of cholesterol. Konrad Bloch & Feodor Lynen (1964): cholesterol biosynthetic pathway. Robert Woodward (1965): stereochemical synthesis of cholesterol. Derek Barton & Odd Hassel (1969): further elucidation of cholesterol molecular structure. John Cornforth (1975): cholesterol-related stereochemistry. Michael Brown and Joseph Goldstein (1985): regulation of cholesterol metabolism.
- Anitschkow N. (1913). Beitr. path. Anat. 56, 379.
- Ravnskov U. Statins as the new aspirin. Conclusions from the heart protection study were premature. BMJ 2002;324:789
- Kendrick M. PROVE IT- PROVE WHAT? http://www.redflagsweekly.com/applications/ui/login.php?Next=/kendrick/2004_mar10.php&e=4
- Jenkins AJ. Might money spent on statins be better spent? 2003 Oct 18;327(7420):933.
- Hecht HS, Harman SM. Relation of aggressiveness of lipid-lowering treatment to changes in calcified plaque burden by electron beam tomography. Am J Cardiol. 2003 Aug 1;92(3):334-6.
- Schatz IJ, Masaki K, Yano K, Chen R, Rodriguez BL, Curb JD. Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program: a cohort study. 2001 Aug 4;358(9279):351-5.
- The ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial. Major outcomes in moderately hypercholesterolemic, hypertensive patients randomized to pravastatin vs usual care: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT-LLT). JAMA 2002;288:2998-3007.
- Heart Protection Study Collaborative Group. Lancet 2002;360:7-22.
- Shepherd J, Blauw GJ, Murphy MB, Bollen EL, Buckley BM, Cobbe SM, Ford I, Gaw A, Hyland M, Jukema JW, Kamper AM, Macfarlane PW, Meinders AE, Norrie J, Packard CJ, Perry IJ, Stott DJ, Sweeney BJ, Twomey C, Westendorp RG; PROSPER study group. PROspective Study of Pravastatin in the Elderly at Risk. Pravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomised controlled trial. 2002 Nov 23;360(9346):1623-30.
- Matsuzaki M, Kita T, Mabuchi H, Matsuzawa Y, Nakaya N, Oikawa S, Saito Y, Sasaki J, Shimamoto K, Itakura H; J-LIT Study Group. Japan Lipid Intervention Trial. Large scale cohort study of the relationship between serum cholesterol concentration and coronary events with low-dose simvastatin therapy in Japanese patients with hypercholesterolemia. Circ J. 2002 Dec;66(12):1087-95.
- Cholesterol Treatment Trialists’ Collaboration. Efficacy and safety of statin therapy in older people: a meta-analysis of individual participant data from 28 randomised controlled trials. 2019 Feb 2;393(10170):407-415.
- IMS Institute for Healthcare Informatics. Top 20 global therapy areas 2014: England and Wales: IMS Health MIDAS, 2014.
- DuBroff R, Malhotra A, de Lorgeril M. Hit or miss: the new cholesterol targets. BMJ Evid Based Med. 2021 Dec;26(6):271-278.
- McKenney JM. Lovastatin: a new cholesterol-lowering agent. Clin Pharm. 1988 Jan;7(1):21-36.
- Schandelmaier S, Briel M, Saccilotto R, Olu KK, Arpagaus A, Hemkens LG, Nordmann AJ. Niacin for primary and secondary prevention of cardiovascular events. Cochrane Database Syst Rev. 2017 Jun 14;6(6):CD009744.
- Albert MA, Danielson E, Rifai N, Ridker PM; PRINCE Investigators. Effect of statin therapy on C-reactive protein levels: the pravastatin inflammation/CRP evaluation (PRINCE): a randomized trial and cohort study. 2001 Jul 4;286(1):64-70.
- Arsian F., Pasterkamp G., de Kleijn D.P. Unraveling pleiotropic effects of statins: bit by bit, a slow case with perspective. Circ Res. 2008;103(4):334–336.
- Martínez-González J, Badimon L. Influence of statin use on endothelial function: from bench to clinics. Curr Pharm Des. 2007;13(17):1771-86.
- Wu BJ, Yan L, Charlton F, Witting P, Barter PJ, Rye KA. Evidence that niacin inhibits acute vascular inflammation and improves endothelial dysfunction independent of changes in plasma lipids. Arterioscler Thromb Vasc Biol. 2010 May;30(5):968-75.
- Si Y, Zhang Y, Zhao J, Guo S, Zhai L, Yao S, Sang H, Yang N, Song G, Gu J, Qin S. Niacin inhibits vascular inflammation via downregulating nuclear transcription factor-κB signaling pathway. Mediators Inflamm. 2014;2014:263786.
- Hooper L, Martin N, Abdelhamid A, Davey Smith G. Reduction in saturated fat intake for cardiovascular disease. Cochrane Database Syst Rev. 2015 Jun 10;(6):CD011737. Update in: Cochrane Database Syst Rev. 2020 May 19;5:CD011737.
- de Souza RJ, Mente A, Maroleanu A, Cozma AI, Ha V, Kishibe T, Uleryk E, Budylowski P, Schünemann H, Beyene J, Anand SS. de Souza RJ, Mente A, Maroleanu A, Cozma AI, Ha V, Kishibe T, Uleryk E, Budylowski P, Schünemann H, Beyene J, Anand SS. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. 2015 Aug 11;351:h3978.
- Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010 Mar;91(3):535-46.
- Chowdhury R, Warnakula S, Kunutsor S, Crowe F, Ward HA, Johnson L, Franco OH, Butterworth AS, Forouhi NG, Thompson SG, Khaw KT, Mozaffarian D, Danesh J, Di Angelantonio E. Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis. Ann Intern Med. 2014 Mar 18;160(6):398-406.
- Schwab U, Lauritzen L, Tholstrup T, Haldorssoni T, Riserus U, Uusitupa M, Becker W. Effect of the amount and type of dietary fat on cardiometabolic risk factors and risk of developing type 2 diabetes, cardiovascular diseases, and cancer: a systematic review. Food Nutr Res. 2014 Jul 10;58.
- Ramsden CE, Zamora D, Majchrzak-Hong S, Faurot KR, Broste SK, Frantz RP, Davis JM, Ringel A, Suchindran CM, Hibbeln JR. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). 2016 Apr 12;353:i1246.
- Clayton P, Rowbotham J. An unsuitable and degraded diet? Part two: realities of the mid-Victorian diet. J R Soc Med. 2008 Jul;101(7):350-7.
- Rowbotham J, Clayton P. An unsuitable and degraded diet? Part three: Victorian consumption patterns and their health benefits. J R Soc Med. 2008 Sep;101(9):454-62.
- Astrup A, Magkos F, Bier DM, Brenna JT, de Oliveira Otto MC, Hill JO, King JC, Mente A, Ordovas JM, Volek JS, Yusuf S, Krauss RM. Saturated Fats and Health: A Reassessment and Proposal for Food-Based Recommendations: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020 Aug 18;76(7):844-857.
- Tall AR, Yvan-Charvet L. Cholesterol, inflammation and innate immunity. Nat Rev Immunol. 2015 Feb;15(2):104-16.
- Marchio P, Guerra-Ojeda S, Vila JM, Aldasoro M, Victor VM, Mauricio MD. Targeting Early Atherosclerosis: A Focus on Oxidative Stress and Inflammation. Oxid Med Cell Longev. 2019 Jul 1;2019:8563845.
- Kromhout D, Menotti A, Alberti-Fidanza A, Puddu PE, Hollman P, Kafatos A, Tolonen H, Adachi H, Jacobs DR Jr. Comparative ecologic relationships of saturated fat, sucrose, food groups, and a Mediterranean food pattern score to 50-year coronary heart disease mortality rates among 16 cohorts of the Seven Countries Study. Eur J Clin Nutr. 2018 Aug;72(8):1103-1110.
- Kaplan H, Thompson RC, Trumble BC, Wann LS, Allam AH, Beheim B, Frohlich B, Sutherland ML, Sutherland JD, Stieglitz J, Rodriguez DE, Michalik DE, Rowan CJ, Lombardi GP, Bedi R, Garcia AR, Min JK, Narula J, Finch CE, Gurven M, Thomas GS. Coronary atherosclerosis in indigenous South American Tsimane: a cross-sectional cohort study. 2017 Apr 29;389(10080):1730-1739.
- Sevanian A, Berliner J, Peterson H. Uptake, metabolism, and cytotoxicity of isomeric cholesterol-5,6-epoxides in rabbit aortic endothelial cells. J Lipid Res. 1991 Jan;32(1):147-55.
- Zhong S, Li L, Shen X, Li Q, Xu W, Wang X, Tao Y, Yin H. An update on lipid oxidation and inflammation in cardiovascular diseases. Free Radic Biol Med. 2019 Nov 20;144:266-278.
- Zhang WB, Addis PB, Krick TP. Quantification of 5-alpha-cholestane-3-beta,5,6-beta-triol and other cholesterol oxidation products in fast food french fried potatoes. J Food Sci 1991. 56(3)716-718
- Loader J, Meziat C, Watts R, Lorenzen C, Sigaudo-Roussel D, Stewart S, Reboul C, Meyer G, Walther G. Effects of Sugar-Sweetened Beverage Consumption on Microvascular and Macrovascular Function in a Healthy Population. Arterioscler Thromb Vasc Biol. 2017 Jun;37(6):1250-1260.
- Umpleby AM, Shojaee-Moradie F, Fielding B, Li X, Marino A, Alsini N, Isherwood C, Jackson N, Ahmad A, Stolinski M, Lovegrove JA, Johnsen S, Jeewaka R Mendis AS, Wright J, Wilinska ME, Hovorka R, Bell JD, Thomas EL, Frost GS, Griffin BA. Impact of liver fat on the differential partitioning of hepatic triacylglycerol into VLDL subclasses on high and low sugar diets. Clin Sci (Lond). 2017 Oct 17;131(21):2561-2573.
- Griffin BA, Freeman DJ, Tait GW, Thomson J, Caslake MJ, Packard CJ, Shepherd J. Role of plasma triglyceride in the regulation of plasma low density lipoprotein (LDL) subfractions: relative contribution of small, dense LDL to coronary heart disease risk. 1994 Apr;106(2):241-53.
- Srour B, Fezeu LK, Kesse-Guyot E, Allès B, Méjean C, Andrianasolo RM, Chazelas E, Deschasaux M, Hercberg S, Galan P, Monteiro CA, Julia C, Touvier M. Ultra-processed food intake and risk of cardiovascular disease: prospective cohort study (NutriNet-Santé). 2019 May 29;365:l1451.
- Eilertsen KE, Mæhre HK, Cludts K, Olsen JO, Hoylaerts MF. Dietary enrichment of apolipoprotein E-deficient mice with extra virgin olive oil in combination with seal oil inhibits atherogenesis. Lipids Health Dis. 2011 Mar 3;10:41
- Østerud B, Olvevoll EO. The combination of virgin olive oils and refined marine oils. Beneficial effects. Nutr. 2008, 10, 230-236
- Venturini D, Simão AN, Urbano MR, Dichi I. Effects of extra virgin olive oil and fish oil on lipid profile and oxidative stress in patients with metabolic syndrome. 2015 Jun;31(6):834-40.
- Clayton P. Personal experience
- Clayton P and 17 others, clinical trial in progress.
- Cameron HM, McGoogan E. A prospective study of 1152 hospital autopsies: I. Inaccuracies in death certification. J Pathol. 1981 Apr;133(4):273-83.
- Mercer J, Talbot IC. Clinical diagnosis: a post-mortem assessment of accuracy in the 1980s. Postgrad Med J. 1985 Aug;61(718):713-6.
- McKelvie PA. Medical certification of causes of death in an Australian metropolitan hospital. Comparison with autopsy findings and a critical review. Med J Aust. 1993 Jun 21;158(12):816-8, 820-1.
- Roulson J, Benbow EW, Hasleton PS. Discrepancies between clinical and autopsy diagnosis and the value of post mortem histology; a meta-analysis and review. 2005 Dec;47(6):551-9.
- Ong BB, Wong JJ, Hashim J. A retrospective study of the accuracy between clinical and autopsy cause of death in the University of Malaya Medical Centre. Malays J Pathol. 2004 Jun;26(1):35-41.
- Winters B, Custer J, Galvagno SM Jr, Colantuoni E, Kapoor SG, Lee H, Goode V, Robinson K, Nakhasi A, Pronovost P, Newman-Toker D. Diagnostic errors in the intensive care unit: a systematic review of autopsy studies. BMJ Qual Saf. 2012 Nov;21(11):894-902.
- Panou E, Nikolaou V, Kallambou S, Sidiropoulou P, Gerochristou M, Straigos A.Recurrence of cutaneous T-cell lymphoma post viral vector COVID-19 vaccination. JEADV Oct 2021: https://doi.org/10.1111/jdv.17736
- Goldman S, Bron D, Tousseyn T, Vierasu I, Dewispelaere L, Heimann P, Cogan E, Goldman M. Rapid Progression of Angioimmunoblastic T Cell Lymphoma Following BNT162b2 mRNA Vaccine Booster Shot: A Case Report. Front Med (Lausanne). 2021 Nov 25;8:798095.
- Brumfiel CM, Patel MH, DiCaudo DJ, Rosenthal AC, Pittelkow MR, Mangold AR. Recurrence of primary cutaneous CD30-positive lymphoproliferative disorder following COVID-19 vaccination. Leuk Lymphoma. 2021 Oct;62(10):2554-2555.
- Gundry SR. Abstract 10712: Mrna COVID Vaccines Dramatically Increase Endothelial Inflammatory Markers and ACS Risk as Measured by the PULS Cardiac Test: a Warning. 2021;144:A10712
- Appelbaum J, Arnold DM, Kelton JG, Gernsheimer TB, Jevtic SD, Ivetic N, Smith JW, Nazy I. SARS-CoV-2 spike-dependent platelet activation in COVID-19 vaccine-induced thrombocytopenia. Blood Adv. 2021 Nov 1:bloodadvances.2021005050.
- Yao ZM, Vance DE. The active synthesis of phosphatidylcholine is required for very low density lipoprotein secretion from rat hepatocytes. J Biol Chem. 1988 Feb 25;263(6):2998-3004.
- Zeisel SH, da Costa KA. Choline: an essential nutrient for public health. Nutr Rev. 2009 Nov;67(11):615-23.
- Huang DQ, El-Serag HB, Loomba R. Global epidemiology of NAFLD-related HCC: trends, predictions, risk factors and prevention.Nat Rev Gastroenterol Hepatol 18, 223–238 (2021).