Hundred-Year-Old Sickle Cell Trait Accesses Genetic Services to Predict Risk of Hereditary Disease in Future Generations
CONGRATULATIONS FROM BUCKINGHAM PALACE!
Dr Emmanuel Evans-Anfom FGA MB ChB FRCS(Edinburgh) FWACS DSc (Salford Univ. Hon) FGCPS DTMH(Edinburgh) who was 100 years on October 7 2019  was congratulated from Buckingham Palace. The Duke of Edinburgh Prince Phillip, PATRON of Ghana Academy of Arts and Sciences [GAAS] and its First President 1959 to 1961 when he was succeeded by Dr Kwame Nkrumah 1961 to 1966 as the Academy’s Second President, sent a message of Congratulations to Dr Emmanuel Evans-Anfom who was himself once 8th of the 19 Presidents of GAAS.
“HISTORY SURPASSES SCIENCE” LECTURE FOR CENTENARIAN.
With Professor Henrietta Mensa-Bonsu FGA the present 19th President of GAAS chairing the Proceedings in a most competent manner, I considered myself greatly honoured and privileged to deliver a SPECIAL LECTURE not only preceded by introductory remarks of Professor Samuel Boakye FGA, Executive Secretary of the Ghana Academy of Arts and Sciences, but also by the impressive statement of Dr Emmanuel Evans-Anfom himself who can be seen and heard on Thursday 30th January 2020 here https://youtu.be/hV8NZJh1pg .
CENTENARIAN SERENDIPITOUSLY REQUESTS GENETIC MARKERS
Day after the Lecture dedicated to Dr Emmanuel Evans-Anfom I visited the great man at home at Leonora Lodge surrounded by his family [demure wife Elise, elegant daughter Rachel and confident husband Dr Henry Baddoo, impressive sons Charlie and Nii Teiko] when, out of the blue, he said to me “Felix will you confirm my genotype?” – meaning would I find out if he was/is one of the 1 in 3 Ghanaians (like my parents) with an abnormal beta haemoglobin gene “S” or “C”? [References 3 to 32].
I asked Dr Henry Baddoo, Consultant Anaesthetist son-in-law to draw blood for me to bring back to the UK for examination in the only laboratory I know in Central London that will quantify not only haemoglobin fractions but also the level of Glucose-6- Phosphate Dehydrogenase red cell enzyme whose deficiency in Ghana is high, 1 in 4 hemizygote males XminusY, 1 in 6 to 1 in 8 females (heterozygotes XminusX and homozygotes XminusXminus ) – Partial and Full Deficiency [18 19 23 24 27 to 42]
PERMISSION TO PUBLISH FINDINGS
I considered it serendipitous to be asked to confirm haemoglobin “genotype” just when BMJ was publishing such articles as “Promises and perils of using genetic tests to predict risk of disease”  and “Communities that prefer close blood marriages need more help to access genetic services”.  In the reliable Central London Lab I requested my “Konotey-Ahulu Profile Number 2” consisting of (a) Sickling Test, (b) Quantitative Haemoglobin Electrophoresis, (c) G6PD Quantitative value, (d) Haematological Values & ESR, and (e) Blood Group. I know of no other laboratory in the UK – Teaching Hospitals included – that can do these 5 tests for less than £100 (One Hundred Pounds Sterling).
RESULTS: (a) Sickling Test POSITIVE (b) Haemoglobin Electrophoresis “AS” with ‘S’ 38.1% (Hb S level being in the highest range of the 3 known Sickle Cell Trait ranges of ‘S’=20-28%, ‘S’=26-33%, ‘S’=34-39% [17 23 24 45 – 50]. Haemoglobin A2 3.0%, Haemoglobin F is 0.5% and the rest Normal Haemoglobin A. Red cell Glucose-6 Phosphate Dehydrogenase Enzyme level was 6.0 U/g [Normal Range 5.6 – 11.2].
VERDICT: Dr Emmanuel Evans-Anfom is therefore SICKLE CELL TRAIT “AS” with NORMAL G6PD. He readily gave me permission to publish the findings not only to help counter Misinformation, if not Disinformation, pervading the Internet based on flawed publications allowed in the best scientific and medical journals, but also to make this finding in a very alert Centenarian a MEDICAL MEMORANDUM.
MISINFORMATION MAKES NONSENSE OF GENETIC COUNSELLING
The very well-thought-out articles of Ian Scott, John Attia, Ray Moynihan  and Naz Khan and Sarah Salway  do not adequately explain the sheer size and varying details of genetic epidemiology for which people worldwide request guidance to prevent hereditary pathology in their offspring. The former concentrate on genetic disposition to malignant conditions of breast, ovary, and prostate  while the latter concern themselves with genetic consequences of marrying relatives . The genetic epidemiological burden discussed by these authors [43 44] amounts to a tiny-fractional-tip of the global genetic iceberg whose huge base is in the Mediterranean countries, Middle East, Asia, Canada, USA, South America, the West Indies and, notably, Africa where genetic red cell defects, namely Haemoglobinopathy (qualitatively ABNORMAL haemoglobin genes), Thalassaemias (abnormal quantities of NORMAL Haemoglobin genes) and genes for G6PD Deficiency abound world-wide. [18 19 24 27 – 42 51 52 53].
UK’s GENETIC BURDEN IS BUT A FRACTION OF GLOBAL BURDEN
Can we also tackle this world-wide problem efficiently? In the UK 1 in every 25 people carries the Cystic Fibrosis gene. In Ghana 1 in every 3 of us carries either Hb S gene or Hb C gene (like my parents – father AC, mother AS just like Dr Evans-Anfom) with the result that 4 of 100 consecutive children born in Ghana suffer from hereditary aching disease ACHEACHE “SS”, “SC”, or “CC”. We proved this at Korle Bu Teaching Hospital genotyping 13000 consecutive births in a single year. , confirming the Hardy-Weinberg Equation [23 24(page 15)]. Yes, 1 in 3 of us in the Diaspora is Sickle Cell Trait “AS” or Haemoglobin C Trait “AC” needing tracing. . Both Professor Graham Serjeant  in the West Indies and Professor Sir David Weatherall FRS  in Oxford acknowledge this global hereditary burden. For further emphasis, Cystic Fibrosis Carrier State is more than 8 times less than Sickle Cell Carrier State yet, as I  commented on Pascale Allotey’s excellent book-review  on “ethnicity and access to health care”, Lancet’s 7-part-series on Genetic Epidemiology came and went  “and not once was it mentioned that one in three west Africans in the UK has a β-globin variant gene whose unsuspecting owner needs to be identified and helped with genetic counselling and family size limitation. I am sure that Ian Scott and colleagues  do not intentionally set out to create “the impression in our minds that genetic epidemiology, which has been my chief concern for decades [24 57-61] had little to do with us non-whites” , but a passing reference in their article to the African Diaspora situation  would not have been out of place.
HINDRANCES TO REALISTIC GENETIC COUNSELLING AFTER TESTING
Hampering realistic counselling is a combination of factors such as Poor Definitions (eg referring to “Trait” as “Disease” or “Disorder” as do the UK Genetics Council , Noke et al , NIH  plus Laboratory Errors like confusing Sickle Cell Trait with Sickle Cell beta-plus Thalassaemia [24, 53].
But chief of all culprits is Misinformation which if deliberate becomes Disinformation. This very important Misinformation Culprit was scrutinised comprehensively by me  when responding to the very instructive article of Semsarian and Ingles “A clinical approach to genetic testing for non-specialists”  together with Allison Streetly’s helpful comments  and needs not delay us further except to mention the remarkable opportunity
Centenarian Sickle cell trait Dr Emmanuel Evans-Anfom, the international hockey player who has flown hundreds of thousands of miles , has given us to debunk once and for all the “scientific” publications on Sickle Cell Trait that lack probity.
SCIENTISTS PERSIST WITH SICKLE CELL TRAIT MISINFORMATION
It is not clear how many of the following examples constitute Disinformation, that is Deliberate Misinformation, but students, doctors, and Science Correspondents of major International Newspapers, Radio Outlets, and Television reporting for the Media, and even GOOGLE and WIKIPEDIA need to look up every single published reference in the following examples so as to be aware of what has happened:
1. Sickle Cell Trait blamed for dying suddenly while exercising 
2. Broken bones in child from baby bashing put to Sickle Cell Trait 
3. Aggressive renal cancer “seen almost exclusively in young patients with sickle cell trait” [71 Elliott Vichinsky et al.]
4. “Complications associated with sickle cell trait” Tsaras et al  Flawed article!
5. Fifteen-year-old black girl sterilized because of sickle cell trait 
6. Black prisoners beaten to death in jail – Autopsy verdict “Sickle Cell Trait” 
7. “Fatal pulmonary infarction in sickle cell trait”. No electrophoresis done. .
8. Sickle Cell Disease (2 beta-globin gene variants) described with Sickle Cell Trait mentioned in the title of article 
9. Beware of symptomatic Sickle Cell Traits 
10. Flight from Kumasi to Accra (45 minutes) produces intestinal infarction in Sickle Cell Trait [77 to 86]
11. Sickle Cell Traits have their insurance loaded 150% ]
12. Pilot with Rhabdomyolysis from Sickle Cell Trait – no laboratory test 
Well did I object “Dangerously flawed diagnosis of sickle cell trait in compartment syndrome rhabdomyolysis”  and “Blaming sudden death on Sickle Cell Trait”?  For other references on Sickle Cell Trait Misinformation see References 91 to 94.
IF LAW MAKERS GET IT WRONG, CAN GENETIC COUNSELLING BE DONE?
Who guides American Insurance Companies when a Massachusetts Law has such a statement as “the disease known as sickle cell trait?”.. There really is no excuse for such scientific obfuscation when there are established agreed definitions in Haemoglobinopathy [96 97]. And Sickle Cell Trait continues wrongly to be written “SCT” by Noke  and the NIH  where National Foundation/March of Dimes of the USA invited me twice to do Grand Rounds in the days of Professor Rudy Jackson.
The only correct phenotype designation for Sickle Cell Trait is “AS”, never “SCT” – a confusion that Insurance Companies use to defraud people because “SC” is the known designation for Sickle Cell Haemoglobin C Disease. The Martin Luther King Jr Foundation protected me with 4 bodyguards in Philadelphia for my Keynote Address “Vital Difference Between Sickle Cell Trait and Sickle Cell Disease”..
THE GREAT RESPONSIBILITY OF INTERNATIONAL MEDICAL AND SCIENTIFIC JOURNALS: A SERIOUS APPEAL TO THE LANCET!
I appeal to the Editors of Lancet to pursue the authors Rhida A, Khan A, Al-Abayechi S, Puthenveetil V who published this: “Acute compartment syndrome secondary to rhabdomyolysis in a sickle cell trait patient” Lancet 2014; 384:2172  without a shred of evidence for Sickle Cell Trait presented, and this resulted in the article going viral on the Internet, frightening people on Facebook when Whiskey Delta Charlie wrote this (QUOTE):
“Here is what’s possible if you are a carrier of Sickle Cell Trait Sept. 224:21pm2016 #sicklecellawarenessmonth #sicklecelltrait #exertion #Rhabdomyolysis http://dhmi.org/sickle-cell-trait-story/ September is Sickle Cell Awareness Month. Awareness to Sickle Cell Trait the gene responsible for creating Warriors who live with Sickle Cell” (UNQUOTE) plus illustrated ghastly pictures of rotting muscles of Rhabdomyolysis .
LOSS OF JOBS FROM SICKLE CELL TRAIT MISINFORMATION
How many pilots might have had their job threatened Corona Virus or no Corona Virus by this flawed Lancet article is not known, but what is known is that previous Editors of Lancet pursued authors of an article supposedly proving that homosexuals and some central Africans shared a common gene Gc1f  the flawed Science of which I was the first to criticize as “leaving a lot to be desired”  until the authors withdrew it from publication with the confession “Erroneous data”. .
So why can’t the present Editors of Lancet pursue the authors of the “Sickle Cell Trait Rhabdomyolysis Pilot” article , ask them to produce the alleged “Sickle Cell Trait” pilot so we know exactly what happened? Are we likely to expect another “Erroneous Data” confession in the Lancet? 
Researchers that need to read about Sickle Cell Trait Misinformation and Disinformation are referred to the huge number of references on the subject [91-95 103].
LORD SOLLY ZUCKERMAN AND PRIDE AND PREJUDICE IN SCIENCE
It was not Black People who dared to mention Prejudice in relation to Science. To imagine that Genome Sequencing, for example, has the answer to everything including Genetic Counselling fails to take into consideration the human element in Science. During my SPECIAL LECTURE dedicated to Centenarian Dr Emmanuel Evans-Anfom  I drew attention to the remarkable article of Professor Sir (later Lord) Solly Zuckerman where he proved conclusively that there was much Prejudice and Pride in Science., and I went on to mention the widespread declaration of Nobel Laureate Professor James Watson that the current Global Sequencing exercise would soon reveal that Africans had inferior intelligence.  He subjected himself to Genome Sequencing only to find that he himself was African , and I could hardly resist the observation on 4th December 2009 that “Watson, still alive today in USA was brutally reminded not only that there is but one human race, but also that African genes contributed to the Nobel Prize.in ‘Medicine or Physiology’ which he jointly won with Francis Crick and Maurice Wilkins on the DNA Double Helix in 1962”. His ancestor was in Africa same time as my great-grand father Konotey-Adade?  There is, indeed, but one human race. 
GENETIC COUNSELLING IN THE AFRICAN MILIEU
In the African milieu Genetic Counselling has been done more from laboratory tests, and we must not rely on Genome Sequencing results from experts like Professor James Watson who know what they will find before they do the examination. Simple Haemoglobin Electrophoresis methods (Alkaline and Acid media) plus clinical acumen have helped us quantify our 1 in 3 genetic incidence and to describe new haemoglobins like Haemoglobin Korle Bu , Haemoglobin Osu-Christiansborg , and discover an adult African, a Nungua fisherman, with only foetal haemoglobin in his body , and also tell the world of a No-Enzyme-at-all G6PD Deficient man in Ghana. [33 34]. The colour test is unable to distinguish Sickle Cell Disease “SC” Phenotype from Sickle Cell Trait “AS”. . Terms like “Up-to-date” [71 (Vichinsky)] and “Novel Clinical Significance” [69 (Key and Vimal)] regarding Sickle Cell Trait are more reflection of imperfect knowledge than, as we are urged to think, discovery of new knowledge. Like “SCT” written for Sickle Cell Trait, they are fraudulent Insurance Companies’ delight.
CORONA VIRUS: SIGNIFICANCE FOR WHITES WITH SICKLE CELL TRAIT AND G6PD DEFICIENCY
1. One often heard “Sickle Cell Disease – the hereditary disease of Blacks”. The past week found 1872 Turks POSITVE for Coronavirus. We must expect about 300 of them to be Sickle Cell Trait phenotype because Aksoy found 15% Turks to be Sickling POSITIVE. Indeed, 18% of Eti-Turks in southern Turkey have Sickle Cell Trait. , Choremis et al reported a high 30% Sickle Cell Trait incidence in Greece where Lake Kopais once was . With 650 reported cases of POSITIVE COVID-19 just as one island was flooded with Greeks returning home, would it surprise anyone if about 150 of these white-skinned Greeks were Sickle Cell Trait “AS”. Thousands of relatives worldwide are Sickle Cell Trait “AS”. Like Ghana , there is also a high incidence of G6PD Deficiency in Turks, Greeks, Italians in the Mediterranean Region as a whole [ 30 42].
2. Reports from China claim that Vitamin C in large doses intravenously has had a remarkably beneficial effect on patients. Linus Pauling who won Nobel Prize for discovering the molecular structure of Sickle Haemoglobin S  popularised taking large doses of Vitamin C  for the common cold, and for cancer 117], a recommendation that was criticized because he was “just a PhD, not an MD doctor”.
A medically qualified doctor, Physician Dr Abram Hoiffer MD PhD FRCP (C) has given Linus Pauling’s Vitamin C anti-cancer claim respectability.  Professor Linus Pauling himself was present and listened approvingly when I gave the Keynote Address “THE VITAL DIFFERENCE BETWEEN SICKLE CELL TRAIT AND SICKLE CELL DISEASE” at the Dr Martin Luther King Jr Foundation Award Dinner in Philadelphia  I shook hands with the only person who got two (un-shared-with-anybody-else) Nobel Prizes. He did not seem to be a person who would have talked about Vitamin C through his hat. And, indeed, Vitamin C has been proven to kill tumour cells with hard-to-treat mutation .
But what has all this got to do with SICKLE CELL TRAIT in White people? ANSWER: Doctors in Europe who may follow Chinese intravenous Vitamin C therapy for Corona Virus must first find out which of their patients has G6PD Deficiency because such large doses of Vitamin C given intravenously can cause catastrophic intravenous haemolysis . Ghanaian doctors who may be adopting Vitamin C intravenous therapy are advised to check Glucose 6 phosphate Dehydrogenase enzyme level before proceeding. The New York Hospital that has started using i.v Vitamin C  will do well to take my advice because one undetected G6PD Deficient patient who collapses on Vitamin C drip will have the Food and Drug Administration come down on them heavily to stop what in my not-so-humble opinion promises to prove once again that Linus Pauling was far from being naïve. If the Chinese wondered why some who received intravenous Vitamin C recovered, while others on the same regime bled from every orifice, I suggest they henceforth do Quantitative G6PD estimation on every patient before treatment is commenced. Greek and Turkish Sickle Cell Traits with G6PD Deficiency, if given large doses of Vitamin C would be misdiagnosed as suffering from Sickle Cell Anaemia “SS” in haemolytic crisis when, in fact, they were Sickle Traits “AS” with anaemia.  The G6PD enzyme level of Dr Emmanuel Evans-Anfom is NORMAL.
I very much trust our British-trained Ghanaian Physicians to screen all admissions (as we used to do half century ago on Medical Floor Two Korle Bu Teaching Hospital) for G6PD Deficiency and administer to those found POSITIVE for COVID-19, immediately, 1,500 mg of intravenous Vitamin C. This is the advice of someone (myself) who shook hands with the Genius “Sickle Cell Linus Pauling” on Wednesday 31st May 1972 in Philadelphia. Take meticulous notes, and publish weekly progress promptly.
3. Africans receiving news from China that Blood Groups reacted differently regarding proneness/non-proneness to the present COVID-19 infection, namely that those with Blood Group A fared worse than O patients in their response to treatment, may confuse (as they have often done) “Blood Group A” with “Haemoglobin Type A” and draw wrong conclusions about how Haemoglobin variants (Hb “S” included) can dictate prognosis in COVID-19 illness We must be very careful about News Headlines when it comes to epidemiology.
SCIENCE NEWS HEADLINES CAN CAMOUFLAGE PREJUDICE
For example, after the “science” that homosexuals and some central Africans shared a common gene Gc1f had in Lancet on Saturday 2nd May 1987  the BBC broadcast the information in its “SCIENCE IN ACTION”  the very next day 3rd May GMT 09.15. My objections to Lancet followed just days later Lancet . But when the authors confessed their “Erroneous data”  some of us were waiting also for BBC to confess “ERRONEOUS SCIENCE IN ACTION.” We wondered why BBC WORLD SERVICE or the BBC HOME SERVICE Programmes did not carry Lancet’s withdrawal of the erroneous findings? Was this an example of BBC reflecting Lord Zuckerman’s diagnosis of “Pride and Prejudice”  in ‘Science In Action’? 
TWO FINAL CAUTIONARY PIECES OF ADVICE TO REMOVE CONFUSION
1. NEVER use SCT to stand for Sickle Cell Trait. It can be confused with “AS”; the “A” standing for normal Haemoglobin gene and “S” for abnormal sickle cell Haemoglobin, with “S” always less than 40% in the best laboratories. Facebook showed a man calling himself “Sickle Cell Trait” groaning from sickle cell crisis pain. When I commented “Ask your Doctor to do Haemoglobin Electrophoresis on you” he returned the next week to say he was “SC”, which is never Trait because “SC” is two Abnormal genes. Traits always have one normal beta-globin gene “A” plus one abnormal beta-globin gene. That is why I use the term “NORMACHE” for Traits, specifying what abnormal Haemoglobin gene the “ACHE” stands for. [See my “Competing Interest” below].
2. AVOID the term “Heterozygote” which just means 2 different genes. Sickle Cell Trait “AS” is Heterozygote, but so also is “SC” which, to avoid calling a disease “Trait”, is correctly designated as “Double Heterozygote”. [23 24]
THANK YOU VERY MUCH, CENTENARIAN DR EMMANUEL EVANS-ANFOM!
Let us thank Dr Emmanuel Evans-Anfom for enabling us to dismiss once and for all the fears of Professor James Bowman MD PhD, University of Illinois Professor of Medicine, Genetics, and Haematology when he lamented that “Persons with sickle cell trait will no longer be able to become ill or even die lest they find themselves subject of a case report” 
Competing Interest: I am the offspring of NORMACHE x NORMACHE Abnormal Haemoglobin parents (AS x AC) who had 11 children 3 of whom had sickle cell disease ACHEACHE (SC), 4 had Trait NORMACHE (2 AC & 2 AS) and 4 of us took no aching genes from our parents to be NORMNORM “AA” phenotype. Impossible it is to tell NORMACHE Traits from those of us who had no Hb gene variant except through blood test. Sickle cell disease phenotypes suffer hereditary cold-season Rheumatism – Tribal names Hemkom or Chwechweechwe – and are therefore physically identifiable. 
firstname.lastname@example.org Twitter @profkonoteyahul
Felix I D Konotey-Ahulu FGA MB BS MD(Lond) DSc(UCC) DSc (UH) FRCP(Lond) FRCP(Glasg) DTMH(L’pool) FGCP FWACP FTWAS ORDER OF THE VOLTA (OFFICER) Kwegyir Aggrey Distinguished Professor of Human Genetics University of Cape Coast, Ghana; Former Consultant Physician Genetic Counsellor in Sickle Cell and Other Haemoglobinopathies Korle Bu Teaching Hospital & Director Ghana Institute of Clinical Genetics, and 9 Harley Street, Phoenix Hospital Group, London W1G 9AL
Website www.sicklecell.md or www.konotey-ahulu.com
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50.. Konotey-Ahulu FID. Alpha-Thalassaemia nomenclature and abnormal Haemoglobins. Lancet 1984; 1: 1024-25. May 5 [“Of 82 consecutive Sickle Cell Traits seen in London in 24 months 36 (44%) had just one quarter of the total Haemoglobin as Sickle Haemoglobin (Mean 25%, Range 20-28”). The three known peaks od Haemoglobin S proportion in the West African Sickle Cell Trait are around 25%, around 30.
51.Lehmann H, Kynoch Pamela A M. Human Haemoglobin variants and their characteristics. North Holland Publication Company. Amsterdam – New York – Oxford 1976; [Elsevier North-Holland Biomedical Press] ISBN 07204 0585 8
52. Serjeant GR. Sickle Cell Disease. Oxford University Press, Oxford 1992. 53. Weatherall DJ, Clegg JB. The Thalassaemia Syndromes. Blackwell Scientific, Oxford 2008.
54. Konotey-Ahulu FID. Need for ethnic experts to tackle genetic public health. Lancet 2007; 370: 1826 [doi:10.1016/50140-6736(07)61771-1] www.thelancet.com/journals/lancet/article/PIIS0140-6736(07)61771-1/fulltext
55. Allotey P. Ethnicity and access to health care. Lancet 2007; 370: 475-476
56. Hooper JL, Bishop DT. Population based-based family studies in genetic epidemiology. Lancet 2005; 366: 1397-1406.
57.Konotey-Ahulu FID. Haenoglobinopathy: The Genetics that touches you and me. http://blog.sicklecell.md/sicklecell/sickle-cell-and-allied-haemoglobinopathy-the-genetics-that-touches-you-and-me/ University of Cape Coast Golden Jubilee Message 2012] Konotey-Ahulu FID. Maintenance of high sickling rate in Africa: Role of polygamy. J Trop Med Hyg 1970 Jan; 73(1): 19-21 (38 References). [Traits who voluntarily restrict number of children they produce do diminish burden of abnormal haemoglobin disease (SS SC CC Sbeta-Thalassaemia Cbeta-Thalassaemia Thalassaemia Major SF CF Fbeta-Thalassaemia SKorle Bu SOsu-Christiansborg in the Ghanaian population. My MPSI shows that Males need more to heed this message for Voluntary Family Size Limitation].
58. Konotey-Ahulu FID. The Sickle-cell Diseases: Clinical manifestations including the sickle crisis. Arch Intern Med 1974; 133(4): 611-619 http://archinte.ama.assn.org/cgi/reprint/133/4/611-pdf
59. Konotey-Ahulu FID. Maintenance of high sickling rate in Africa: Role of polygamy. J Trop Med Hyg 1970 Jan; 73(1): 19-21 (38 References). [Traits who voluntarily restrict number of children they produce do diminish burden of abnormal haemoglobin disease (SS SC CC Sbeta-Thalassaemia Cbeta-Thalassaemia Thalassaemia Major SF CF Fbeta-Thalassaemia SKorle Bu SOsu-Christiansborg in the Ghanaian population. My MPSI shows that Males need more to heed this message for Voluntary Family Size Limitation].
60.. Bonney GE, Konotey-Ahulu FID. Polygamy and genetic equilibrium. Nature 1977; 265: 46-47 doi:10.1038/265046a0..n5589/pdf/265046a0.pdf http://www.nature.com/nature/journal/v265/n5589/abs/265046a0.html
61. Konotey-Ahulu FID. Male procreative superiority index (MPSI): The missing co-efficient in African anthropogenetics. BMJ 1980; 291: 170
62. Konotey-Ahulu FID. Survey of sickle-cell disease in England and Wales. BMJ 1982; 284(6309): 112. doi:10.1136/bmj.284/6309/112-a (Jan. 9 1982) http://www.bmj.com/cgi/reprint/284/6309/112-a.pdf7.
63. Human Genetics Commission (HGC-UK) and direct consumer Genetic Tests, leading to Genetic Counselling. BMJ Rapid Response May 27 2009. http://www.bmj.com/cgi/eletters/338/may15_2/b1995#214r56
64. Noke Melissa, Peters Sarah, Uiph Fiona. A qualitative study to explore how professionals in the United Kingdom make decisions to test children for a sickle cell carrier state. Europ Journal of Human Gentics 2016, 24: 164-170. 74. Noke Melissa, Peters Sarah, Ulph Fiona. A qualitative study to explore how professionals in the United Kingdom make decisions to test children for a sickle cell carrier state. Europ. Journal of Human Genetics 2016; 24:164-170. doi:10.1038/ejhg.2015.104 [Terms like “SC prevalence” and “not so benign nature of ‘SCT’” reveal ignorance of approved Terminology.
65. NIH (Bethesda) “ Sickle Cell Disease is the most common inherited blood disorder in the USA …” http://www.ghr.nlm.gov/condition/sickle-cell-disease [But as Sickle Cell Trait is written SCT when SC is known to be disease phenotype what interpretation do people in the USA put on the recently widely advertised NIH home-use-kit for checking for the gene? Especially when the commercial Haemoglobin S Test-Tube Colour-Test does not differentiate between Sickle Cell Trait “AS” (1 Normal gene + 1 Abnormal gene) and Sickle Cell Disease “SC” phenotype (2 Abnormal genes)?
66. Konotey-Ahulu FID. Genetic Testing and Counselling Towards Genetic Public Health http://www.bmj.com/contrent/358/bmj.j4101/rapid-responses BMJ Rapid Response 21 December 2017 to Semsarian C and Ingles J. PRACTICE [See below]
67. Semsarian C., Ingles J. A clinical approach to genetic testing for non-specialists. BMJ 2017; 358 doi: 10.1136/bmj.j4101. 28 Sept. 2017.
68. Streetly A. A common definition of genetic testing, can we agree on one? 18 October 2017 http://www.bmj.com/content/358/bmj.j4101/rapid-responses .
69. Key Nigel S, Derebail Vimal K. Sickle Cell Trait: Novel Clinical Significance. Hematology 2010: 418-422. “During exercise, Sickle Cell Trait appears to be a risk factor for sudden death and/rhabdomyolysis, particularly when the exercise is intense, and is performed at high altitude”
70. Kepron Charis, Somers Gino R, Pollamen Michael S. Sickle Cell Trait Mimicking Multiple Inflicted Injuries in a 5-Year-Old Boy. Journal of Forensic Sciences Volume 54, No.5, pp 1141 t0 1145 September 2009.
71.. Vichinsky Elliott P. Sickle cell trait. Literature Review UpToDate [Accessed 18 Feb 2011] http://www.uptodate.com/contents/sickle-cell-trait?view=print asserts falsely that “Renal medullary carcinoma is a rare and aggressive tumor that is seen almost exclusively in young patients with sickle cell trait.”
72. Tsaras, G, Owusu-Ansah A, Boateng FO, Amoateng-Adjepong, Y. Complications associated with sickle cell trait: a brief narrative review. American Journal of Medicine 2009; 122(6): 507-512. [The Ghanaian co-authors appear ignorant of what work had been done in Ghana (6 million Sickle Cell Traits) since 1953; See References 3 – 32]
73. Dyson Simon, Bosswell Gwyneth. Sickle Cell and Deaths in Custody. Whiting and Birch, London: June 2009; 230 pages “The misuse of Sickle Cell Trait to explain away sudden deaths”.
74. Malhotra Vinod, Ravi Prakash, Yeun Sook Choi, Bernard Chomet, Clifford G Pilz. Fatal Pulmonary Infarction in a Patient with Sickle Cell Trait. CHEST 1973; 64: 524-26. October 1973. “It is suggested that sickle cell trait should be considered in all Negro patients who present with suspected vaso-occlusive episode”. [Flaws in article: (a) How about the millions of white Greeks and Turks with Sickle Cell Trait? (b) Have the authors excluded Sickle Cell beta-Thalassaemia after quantitative electrophoresis? (c)
Is sickle cell haemoglobin C being referred to as Sickle Cell Trait. (d) Fatal pulmonary infarction occurs in Caucasian women on oral contraceptives. If a “Negro patient” was Sickle Cell Trait “AS”, and had been on contraceptives, why would she be prevented from having pulmonary infarction when white British women were also afflicted?]
75. Witkowska HE, Lubin BH, Beuzard Y et al. Sickle cell disease in a patient with sickle cell trait and compound heterozygosity for haemoglobin S and haemoglobin Quebec-Chori. New England Journal of Medicine 1991; 325: 1150-1154. [Note that the title of this article is incorrect: No human being can be said to have both Sickle cell trait and Sickle Cell Disease. The ‘AS’ pattern is sickle cell trait pattern, but this ‘A’ is not a true ‘A’ but the new haemoglobin called Quebec-Chori, producing a disease phenotype, not trait]
76. Konotey-Ahulu FID. World Sickle Cell Day 19h June 2014 http://bit.ly/1FuNXPi Beware of symptomatic sickle cell traits. Lancet, Feb 29, 1992, page 555. http://www.thelancet.com/journals/lancet/article/PII0140-6736(92)90377-F/fulltext
77. Green RL, Huntsman RG, Serjeant GR. Sickle cell trait and altitude. Br Med J 1971; 4: 593-595.
78. Addae R O. Sickle cell trait and altitude. BMJ 1972; 1: 53. [10 criteria (Addae’s Criteria) required to satisfy clinicians in regions where 1 in 5 people have the sickle cell trait that symptoms are due to the trait and nothing else.]
79. Djabanor F F T. Sickle cell trait and altitude. Brit Med J 1972; 1: 113
80. Konotey-Ahulu FID. Sickle cell trait and altitude. BMJ 1972; 1: 177-178.
81. Konotey-Ahulu FID. An international sickle cell crisis. [Editorial] Ghana Medical J; 1972; 11: 4-8 [A detailed account of how BMJ withdrew report]
82. Konotey-Ahulu FID. Sickle cell trait and altitude. BMJ 1972; 2: 231-32 April 22
83. Green RL, Huntsman RG, Serjeant GR. Sickle cell and altitude. Brit Med J 1972; 2: 294
84. Lehmann Hermann. Sickle cell and flying. The Times (London) 4 Jan 1972 That was when the “Science Editor” used false report on “Sickle Cell Trait and Flying” in BMJ to recommend grounding of all Black Air Crew.
85. Konotey-Ahulu FID. Aviation Safety, Ghanaians recall media disinformation deriving from scientific misinformation. BMJ Rapid Response March 1 2019; https://www.bmj.com/content/364/bmj.l735/rr-7 to Partha Kar: Applying aviation safety to healthcare – are we missing the fundamentals? Partha Kar 364:/doi10.1136/bmj.l735 :
86. Konotey-Ahulu FID. Lt-Col [Retd] Dr Frank F T Djabanor (1938 – 2019) Physician whose exposure of scientific falsehood saved Black People from humiliation. TRIBUTE. Accra & Odumase-Krobo 31st March 2019.
87. Konotey-Ahulu FID. Insurance and genetic testing. Lancet 1993, 341: 833. March 27 [See Reference 98 for when Dr Konotey-Ahulu was given 4 Body Guards in Philadelphia for stressing “Sickle Cell Disease is NOT Sickle Cell Trait and vice versa!” and thus upsetting Insurance Companies]
88. Rhida A, Khan A, Al-Abayechi S, Puthenveetil V. Acute compartment syndrome secondary to rhabdomyolysis in a sickle cell trait patient. Lancet 2014; 384:2172 [No evidence for Sickle Cell Trait was presented in this Lancet article].
89. Konotey-Ahulu FID. Dangerously flawed diagnosis of sickle cell trait in compartment syndrome rhabdomyolysis http://bit.ly/2d4t9Zd http://www.sicklecell.md/blog/index.php/2016/09/dangerously-flawed-diagnosis-of-sickle-cell-trait-in-compartment-syndrome-rhabdomyolysis-article/ [No evidence for Sickle Cell Trait was presented in the Lancet article (Reference 88)].
90.. Konotey-Ahulu FID. Blaming sudden death on Sickle Cell Trait? Flaws in article of Charis Kepron, Gino Somers and Michael Pollanen [Reference 37 above Exposed]. September 4 2011 www.sicklecell.md/blog/?p=105 or www.konotey-ahulu.com/blog/?p=105
91.Konotey-Ahulu FID. Sickle Cell Trait Misinformation and Disinformation. https://blog/sicklecell.md/sicklecell/sickle-cell-trait-misinformation-and-disinformation/ November 30 2011
92 Konotey-Ahulu FID. Further Communication on “Sickle Cell Trait Misinformation and Disinformation” and Sickle Cell Terminology: Disease or Disorder? April 6 2012 https://blog/sicklecell.md/sicklecell/further-communication-on-sickle-cell-trait-misinformation-and-disinformation-and-sickle-cell-terminology-disease-or-disorder/
93. Konotey-Ahulu FID. Sickle Cell Trait Confusion: Is it Deliberate? Or is this Ignorance? August 11 2017 https://blog.sicklecell.md/sicklecell/sickle-cell-trait-confusion-is-it-deliberate-or-is-this-ignorance/
94 Konotey-Ahulu FID. Sickle Cell Trait: As with statins when leading editors disagree please give principles same weight as details 20 September 2016 .http://bit.ly/2dy5fUJ/http://www.sicklecell.md/blog/index.php/2016/09/statins-when-leading-editors-disagree-please-give-principles-same-weight-as-details/
95. Beutler E, Boggs DR, Heller P, Maurer A, Motulsky AG, Sheehy TW. Hazards of indiscriminate screening for sickling. N Engl J Med. 1971 Dec 23;285(26):1485–1486 www.europepmc.org/articles/PMC178610 [Authors have commented on a Massachusetts Law which stated in part that “Every child, which the Commissioner of Public Health, by rule Law which stated in part that “Every child, which the Commissioner of Public Health, by rule or regulation, may determine is susceptible to the disease known as sickle cell trait or sickle cell anemia, shall be required to have a blood test”. [How on earth does one explain to the Americans that there is no such thing as “the disease known as sickle cell trait”? Making my African NORMACHE equal to ACHEACHE?]
96. Woodruff AW et al. Terminology of the Hereditary Haemoglobinopathies with haemoglobin variants. BMJ 1957; 1: 1235. .
97.. Boyo AE, Cabannes R, Conley CL, Lehmann H, Luzzatto L, Milner PF, Ringelhann B, Weatherall DJ, Barrai I, Konotey-Ahulu FID and Motulsky AG. Geneva WHO Scientific Group on Treatment of Haemoglobinopathies and Allied Disorders. (Technical Report) 1972; 509:83 pages. ]
98. Konotey-Ahulu FID. Four bodyguards and the perils of unmasking scientific truths. www.bmj.com/cgi/content/full/335/7612/210 doi:10.1136/bmj.39268.553021.47 BMJ 2007; 335: 210-211. [Day & Date: Wednesday 31st May 1972 – Philadelphia, Dr Martin Luther King Jr Foundation Award Ceremony for Outstanding Contributions in Sickle Cell Disease: Banquet – Dr Konotey-Ahulu’s Keynote Address was on ‘Difference between Sickle Cell Trait and Sickle Cell Disease’. Those also honoured present on the platform with me included Nobel Prize Winners Linus Pauling and Max Perutz, then Hermann Lehmann, Roland Scott, J V Neel, Bella Ringelhann, A C Allison, Bella Ringelhann, James Bowman, Helen Ranney, Charles Whitten, L Diggs, L Conley, Howard Pearson, Sam Charache, and Graham Serjeant.]
99. Whiskey Delta Charlie on Facebook 24 September 2016 If you are a Carrier of Sickle Cell Trait Here is what’s possible: #sicklecellawarenessmonth#sicklecelltrait #exertion #Rhabdomyolysis http://dhmi.org/sickle-cell-trait-story/ September is Sickle Cell Awareness Month. Awareness to Sickle Cell Trait the gene responsible for creating Warriors who live with Sickle Cell” (UNQUOTE) plus illustrated ghastly pictures of rotting muscles of Rhabdomyolysis.
100. Eales L-J, Nye KE, Parkin JM, Weber JN, Forster SM, Harris JRW, Pinching AJ. Association of different allelic forms of group specific component with susceptibility to and clinical manifestation of human immunodeficiency virus infection. Lancet 1987; 1: 999-1002.
101. Konotey-Ahulu FID. Group specific component and HIV infection. Lancet; 1: 1267.
102. Eales NJ, Nye KE, Pinching AJ. Group specific component and AIDS: Erroneous data. Lancet 1988; 1: 936.
103. Konotey-Ahulu FID. The Sickle Cell Disease Patient Website www.sicklecell.md
104. Zuckerman Sir Solly. Pride and Prejudice in Science. Aerospace Medicine 1974; 45: 638-347 (Also re-published with permission in Ghana Medical Journal 1975; 14 (No.1).52-60.105.
105. Professor James Watson: Verkaik Robert. Scientist who sparked racism has black genes. The Independent, London. 10 December 2007. [Re: DNA Nobel Laureate Professor James Watson]
106.. Konotey-Ahulu FID. There is but one human race. New African, London. December 2009, page 4. [Great-grandfather of Nobel Laureate Professor James Watson would have been on the African Continent exactly the same time as my own great-grand father Konotey-Adade born in 1820 (Generation V going back to 1670) . Could the ancestor of James Watson have suffered enforced migration across The Atlantic? Born in 1928, if he is still alive at 92 years of age, would he kindly oblige to have his Haemoglobin Electrophoresis done to see whether he has a 1 in 3 chance of being (like my father and mother) phenotype NORMACHE “AS” or “AC”?
107. Konotey-Ahulu FID. Sickle Cell Disease in successive Ghanaian Generations for Three Centuries (Manya Krobo Tribe). References [23 and 24, pages 6 to 20]
108. Konotey-Ahulu FID., Gallo E, Lehmann H, Ringelhann B. Haemoglobin Korle Bu (alpha2 beta2 73 Aspartic Acid –> Asparagine), showing one of the two amino acid substitutions of Haemoglobin C Harlem. Konotey-Ahulu FID., Gallo E, Lehmann H, Ringelhann B. Haemoglobin Korle Bu (alpha2 beta2 73 Aspartic Acid –> Asparagine), showing one of the two amino acid substitutions of Haemoglobin C Harlem. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1468514 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1468514
109. Konotey-Ahulu FID, Kinderlerer, JL Lehmann H and Ringelhann B. Haemoglobin Osu-Christiansborg. A new chain variant of Haemoglobin A (beta 52 D3 Aspartic Acid to Asparagine) in combination with Haemoglobin ‘S’. J Med Genet 1971; 8(3): 302-305 http://lib.bioinfo.pl/pmid:5097135http://pubmedcentral.nih.gov/picrender.fcgi?artid=146917&blobtype=pdf
110. Kamazura H, Ringelhann B, Konotey-Ahulu FID, Lehmann H, Lorkin PA. The gamma chain in a Ghanaian adult homozygous for hereditary persistence of Fetal Haemoglobin. Acta Hematologica; 51: 197-184. .
111. Konotey-Ahulu FID. Detecting Sickle Haemoglobin. BMJ 1972; 2: 239 Nov 11; 4(5836) 376 See a Massachusetts law quoted below by Dr Beutler et al. Ref. 
112. Aksoy M. Sickle cell trait in Southern Turkey. Lancet 1955; 1: 589-90.
113. Choremis et al.. Blood Groups of a Greek community with a high sickling frequency. Lancet 1957; 2: 1333-1334.
114. 91. Konotey-Ahulu FID. The Sickle-cell Diseases: Clinical manifestations including the sickle crisis. Arch Intern Med 1974; 133(4): 611-619 http://archinte.ama.assn.org/cgi/reprint/133/4/611-pdf
115. Pauling Linus et al. Sickle Cell Anemia, a molecular disease. Science1949; 110: 543-8.
116.. Pauling Linus. Vitamin C and the Common Cold. Linus Pauling Institute Oregon State University. 1970.
117. Hoffer Abram, Pauling Linus. Vitamin C and Cancer: Discovery, Recovery, Controversy. 1979. [ISBN-10 1550820788 & ISBN-13 978-1550820782]
118. Mongelli Lorenn. New York Hospitals are treating coronavirus patients with Vitamin C. New York Post March 24 2020 https://nypost.com/2020/03/24/new-york-hospitalsreatingcoronaviruspatientswithvitaminc/?fbclid=IwAR0rO7trfM0j4GE53xuAnclKreZOtCp72X9qBpDT4fBpXb036t0qorg..
119. BBC SCIENCE IN ACTION Sunday 3rd May 1987 Dr Anthony Pinching interviewed about article in Lancet on Saturday 2nd May explaining why AIDS virus was spreading faster Central Africa than in the USA and how a gene Gc1f was common to homosexuals and Central Africans. The findings were found to be false, and withdrawn from publication, but BBC kept quiet about the “Erroneous Data”.
120. Bowman James. Ethical. Legal, and humanistic implications of sickle cell programs. INSERM 1975; 44: 353-378.