“What is needed is good policy. Good policy on GMO’s in Africa would consist of three elements. The first is public ownership and accountability. A major problem with GM crops is their corporate nature. The only way to ensure that GMO’s would be beneficial to Africa is to strip the profit motive from their research, design, testing and regulation. And the only way to do that is public ownership.
This brings us to the second element, accountability. There is a lot of mistrust around GMO’s, the motives behind them, their ecological and health impacts and their use. The only way to assuage these concerns is transparency. No for-profit corporation will be transparent about commercially sensitive information such as its own GMO’s, but public institutions can be transparent and can be designed to be so, by incorporating stakeholders and their concerns into their design and decision-making structures to ensure that those concerns are met.
The third element is collaboration. If GMO’s are truly going to be beneficial to Africa it will require collaboration on two levels. First between stakeholders within the agricultural industry, research scientists, farmers, environmentalists, doctors, consumers will all need to come together to guide the development of GM crops for the African context. A context in which small farmers are the vast majority of farmers, where climate change and changing weather patterns are making farming harder and where growing populations require more agricultural productivity to feed them. The second level is internationally. No single African country has the ability to set up and sustainably fund institutions that can design, develop, test and disseminate GM crops over the long term. However, together they could do so. The ability to pool funding, expertise, and facilities only makes sense, especially as many African countries face similar agricultural challenges and most staple and commercial crops are grown across multiple countries.”
The website catalogofbias.orgsummarises positive results bias as “the tendency to submit, accept and publish positive results rather than non-significant or negative results.</>”
It continues; “positive results bias occurs because a considerable amount of research evidence goes unpublished, which contains more negative or null results than positive ones. This leads to spurious claims and overestimation of the results of systematic reviews and can also be considered unethical. Non-publication of results can also lead to research wastage as researchers may unnecessarily repeat studies because the results are unpublished.”
This is an important point which we’ll return to. But the main findings of the study make for startling reading:
“Of 105 antidepressant trials, 53 (50%) trials were considered positive by the FDA and 52 (50%) were considered negative or questionable (Fig. 1a). While all but one of the positive trials (98%) were published, only 25 (48%) of the negative trials were published. Hence, 77 trials were published, of which 25 (32%) were negative (Fig. 1b). Ten negative trials, however, became ‘positive’ in the published literature, by omitting unfavorable outcomes or switching the status of the primary and secondary outcomes (Fig. 1c). Without access to the FDA reviews, it would not have been possible to conclude that these trials, when analyzed according to protocol, were not positive. Among the remaining 15 (19%) negative trials, five were published with spin in the abstract (i.e. concluding that the treatment was effective). For instance, one article reported non-significant results for the primary outcome (p = 0.10), yet concluded that the trial ‘demonstrates an antidepressant effect for fluoxetine that is significantly more marked than the effect produced by placebo’ (Rickels et al., 1986). Five additional articles contained mild spin (e.g. suggesting the treatment is at least numerically better than placebo). One article lacked an abstract, but the discussion section concluded that there was a ‘trend for efficacy’. Hence, only four (5%) of 77 published trials unambiguously reported that the treatment was not more effective than placebo in that particular trial (Fig. 1d). Compounding the problem, positive trials were cited three times as frequently as negative trials.”
A New York Times write-up of the study by Aaron E. Carroll (“congratulations, Your study went nowhere!)” points to several other studies that have revealed these kinds of distortions. It also makes the critical observation that because positive research tends to be cited much more frequently than negative research (citation bias), this distortion quickly proliferates through scientific literature:
“A modeling study published in BMJ Open in 2014 showed that if a publication bias caused positive findings to be published at four times the rate of negative ones for a particular treatment, 90 percent of large meta-analyses would later conclude that the treatment worked when it actually didn’t.”
Clearly this is a serious problem which calls the integrity of scientific research into question. In short, why should we accept ‘scientific evidence’ if that evidence is more the product of institutionalised bias rather than of open scientific enquiry.
Positive results bias is one of a number of problems in science that could be tackled by moving toward an open science approach. Open science can be defined as “the practice of carrying out scientific research in a completely transparent manner, and making the results of that research available to everyone” (Watson, 2015). The FDA require that all drug trials intended to help a treatment to gain FDA approval must be preregistered with them and the results published regardless of the outcome. This is a form of open science because it is opening up scientific research for anyone to access. It seems obvious that the more that science is moved out into the open, the less incentives there will be for things like positive results bias to distort it.
Clapperton Chakanetsa Mavhungo is Associate Professor at the Massachusetts Institute of Technology. More pertinently to this post, he is a Zimbabwean and a Shona. He has just published a new book which delves into the ways in which the Shona and other African people’s dealt with the Tse Tse Fly prior to the arrival of Europeans and colonialism. This is a snippet of MIT’s overview of the book;
“Few animals are more problematic than the tiny African insect known to English speakers as the tsetse fly. This is the carrier of “sleeping sickness,” an often deadly neurological illness in humans, as well as a disease that has killed millions of cattle, reshaping the landscape and economy in some parts of the continent.
For generations, vedzimbahwe (the “Shona” people, builders of houses) and their African neighbors, assembled a significant store of ruzivo — knowledge — about mhesvi, their name for the tsetse fly. As MIT Associate Professor Clapperton Chakanetsa Mavhunga explains in a new book, this accumulation of local knowledge formed the basis for all subsequent efforts to control or destroy the tsetse fly and is an exemplary case of scientific knowledge being developed in Africa, by Africans.
“Ruzivo and practices based on it were the foundation of what became science and means and ways of tsetse control,” Mavhunga writes in “The Mobile Workshop: The Tsetse Fly and African Knowledge Production,” recently published by the MIT Press. However, he notes, Europeans nonetheless dismissed Africans as being “only good at creating and peddling myths and legends.”
In fact, Africans developed a diverse set of practices to combat mhesvi. For example, they used late-season forest burning to expose mhesvi to predators; moved herds through mhesvi-infested stretches at night while the insect was inactive; strategically located their settlements to neutralize the insect’s threat or turn it into a weapon against their human enemies; cleared bush and felled trees to create buffer zones between mhesvi-infested wildlife areas and human- and livestock-inhabited areas; and developed innoculations using live or dead mhesvi. Europeans appropriated many of these methods, or, at the very least, used their basic principles as starting points for what they then called “science.”
Nigerian Neuroscientist Mahmoud Bukar Maina discussed his research into the state of Neuroscience in Nigeria (“Putting Nigerian neuroscience research under the microscope” – The Conversation Africa). He outlines some of the key challenges Africans face in bringing our continent to the main table of state-of-the-art scientific resesrch. The following is an excerpt:
“Researchers are working hard to unravel the complex mysteries of the human brain and nervous system, as well as to find treatment for often incurable brain diseases. These neuroscientists are mostly based in Europe, the US, Japan and China. So most of our understanding of the brain comes from the global North, with only minor contributions from places like Africa.
That’s not to say neuroscience isn’t being researched across the continent. But there are huge barriers to innovation and productivity.
Most universities do not have equipmentfor scientific research. And where research is happening, it’s often being carried out using outdated equipment. The lack of reliable power across large stretches of the continent is another issue. This makes it difficult to acquire, use or store common materials used in biomedical research such as antibodies and tissue samples.
For neuroscience, a number of local and international programmes are trying to address these shortcomings. For example the International Brain Research Organisation and the International Society for Neurochemistry have invested in the training of many scientists across Africa. Not for profit bodies like Teaching and Research in Natural Sciences for Development in Africa and Seeding Labshave helped in setting up laboratories in some African countries. Such efforts have helped to boost the neuroscience skills of scientists in many African countries.
But this hasn’t yet levelled the difference in scientific output between researchers in Africa and those in the “global North”. Perhaps bridging this gap and identify methods that could boost the continent’s neuroscience capacity, requires more knowledge about scientists’ challenges and strengths in different countries.
With this in mind, my colleagues and I set out to examine the state of Nigerian neuroscience. By analysing more than 1,200 neuroscience extracted publications from PubMed, a free full-text archive of biomedical and life sciences journal literature, we found that Nigerian neuroscience research has its own strengths and shortcomings.”
Read full article at Conversation Africa here.
In early September 2018, the European Union helped to put Open Science into mainstream political and scientific consciousness with the launch of coalition S and Plan S. The following is from the launch statement.
What is cOAlition S? On 4 September 2018, 11 national research funding organisation, with the support of the European Commission and the European Research Council (ERC), announced the launch of cOAlition S, an initiative to make full and immediate Open Access to research publications a reality. It is built around Plan S, which consists of one target and 10 principles. cOAlition S signals the commitment to implement, by 1 January 2020, the necessary measures to fulfil its main principle: “By 2020 scientific publications that result from research funded by public grants provided by participating national and European research councils and funding bodies, must be published in compliant Open Access Journals or on compliant Open Access Platforms.” The 11 national research funding organisations that form cOAlition S have agreed to implement the 10 principles of Plan S in a coordinated way, together with the European Commission and the ERC. Other research funders from across the world, both public and private, are invited to join cOAlition S. The initiative was born from the cooperation between the Heads of the participating Research Funding Organisations, Marc Schiltz the President of Science Europe, and Robert-Jan Smits the Open Access Envoy of the European Commission. It also drew on significant input from the Scientific Council of the ERC. The research funders involved in cOAlition S will now collaborate with other stakeholders and work towards swift and practical implementation of these principles. The 10 Principles of Plan S The key principle is as follows: “After 1 January 2020 scientific publications on the results from research funded by public grants provided by national and European research councils and funding bodies, must be published in compliant Open Access Journals or on compliant Open Access Platforms.”
The British journalist George Monbiot has written a powerful article in the Guardian newspaper calling for an end to paywalls in scientific research. Below is a particularly enjoyable snippet on the origins of the paywall journal system:
“Everyone should be free to learn; knowledge should be disseminated as widely as possible. No one would publicly disagree with these sentiments. Yet governments and universities have allowed the big academic publishers to deny these rights. Academic publishing might sound like an obscure and fusty affair, but it uses one of the most ruthless and profitable business models of any industry.
The model was pioneered by the notorious conman Robert Maxwell. He realised that, because scientists need to be informed about all significant developments in their field, every journal that publishes academic papers can establish a monopoly and charge outrageous fees for the transmission of knowledge. He called his discovery “a perpetual financing machine”. He also realised that he could capture other people’s labour and resources for nothing. Governments funded the research published by his company, Pergamon, while scientists wrote the articles, reviewed them and edited the journalsfor free. His business model relied on the enclosure of common and public resources. Or, to use the technical term, daylight robbery.
As his other ventures ran into trouble, he sold his company to the Dutch publishing giant Elsevier. Like its major rivals, it has sustained the model to this day, and continues to make spectacular profits. Half the world’s research is published by five companies: Reed Elsevier, Springer, Taylor & Francis, Wiley-Blackwell and the American Chemical Society. Libraries must pay a fortune for their bundled journals, while those outside the university system are asked to pay $20, $30, sometimes $50 to read a single article.”
Sickle Cell Anaemia (SCA) is a disorder caused by a single gene mutation that affects haemoglobin, the oxygen-carrying molecule in red blood cells. If a person inherits one mutated gene, they carry the sickle cell trait but in the vast majority of cases will not develop SCA. But if a person inherits the mutated gene from both parents, then they will develop SCA.
The mutation causes haemoglobin to polymerise (stick together) which then deforms the red blood cell, causing it to take irregular shapes including a sickle shape. Consequently, these malformed blood cells can’t flow through the blood vessels properly which restricts blood supply to organs. This results in a vast array of problems, primarily hemolytic anemia (low blood caused by destruction of blood cells) and ischemic damage to tissues and organs resulting in frequent periods of severe pain and even organ failure. The acute chest syndrome is a typical example of organ failure in sickle cell disease and one of the leading causes of hospitalisation and death among patients (Piel et al 2017:1562-1565).
70% of babies born with SCA are born in sub-Saharan Africa, most notably in Nigeria and the Democratic Republic of Congo. Although infant mortality (death before 5) among children with SCA has fallen in developed countries, it is still extremely high in Africa. A 2010 estimate put it at between 50-90% though obtaining accurate statistics on sickle cell in Africa is difficult. Screening newborns for SCA is a vital component to being able to treat it as effectively as possible and this is normal practice in the UK, the US and other developed countries. To date no African country has implemented mass screening for the trait though some have conducted trial screenings (Kato et al 2018:2-3, 10).
The high prevalence of SCA in Africa is primarily explained by its connection with malaria. The so-called malaria hypothesis was first postulated by western scientists in the early twentieth century. The hypothesis begins by noting that malaria has been around for thousands of years and until recently has resulted in almost-certain death in infancy. These factors mean that it would have played a role in natural selection. Because malaria affects blood cells, any changes the structure of blood cells would also hinder the spread of malaria. Thus, it was hypothesised that genotypes associated with changes to the shape of blood cells should be more common in areas with high malaria prevalence (Luzzatto, 2012).
As discussed, SCA does indeed change the structure of blood cells. In the 1950s, a researcher working in Kenya demonstrated that SCA prevalence correlates closely with Malaria prevalence. He also showed that people with sickle cell trait seemed to contract malaria less frequently. Subsequent research has found that trait carriers can and do contract malaria but rarely the most severe form. In fact, they are 90% less likely than non trait carriers to get severe SCA (Kato et al 2018:2). If they do get SCA, they rarely die from it, even from the more severe kinds. It seems that red blood cells in sickle cell trait carriers do get sick, but they are then removed by white blood cells (Luzzatto, 2012).
This complex relationship between sickle cell and malaria is an example of so-called balanced polymorphism. The mutation can be beneficial or deleterious. It is beneficial in heterozygotes (people who carry only one mutated gene) because it gives them some protection against malaria. But the mutation is deleterious in homozygotes (people who carry two of these mutated genes) because it leads to malfunction and possible destruction of red blood cells which cause unpredictable episodes of intense pain and frequently death.
For African-descended people, getting screened for sickle cell trait is one way of preventing their future offspring from developing SCA. Those who carry the trait could employ assortative mating by avoiding having children with other trait carriers. This kind of preventative behaviour could be promoted in public health messaging in the same way that safe sex guidance is promoted.
“Background: Personal care products are a source of exposure to endocrine disrupting and asthma-associated chemicals. Because use of hair products diﬀers by race/ethnicity, these products may contribute to exposure and disease disparities.
Objective: This preliminary study investigates the endocrine disrupting and asthma-associated chemical content of hair products used by U.S. Black women.Methods: We used gas chromatography/mass spectrometry (GC/MS) to test 18 hair products in 6 categories used by Black women: hot oil treatment, anti-frizz/polish, leave-in conditioner, root stimulator, hair lotion, and re-laxer. We tested for 66 chemicals belonging to 10 chemical classes: ultraviolet (UV) ﬁlters, cyclosiloxanes, glycolethers, fragrances, alkylphenols, ethanolamines, antimicrobials, bisphenol A, phthalates, and parabens.
Results: The hair products tested contained 45 endocrine disrupting or asthma-associated chemicals, including every targeted chemical class. We found cyclosiloxanes, parabens, and the fragrance marker diethylphthalate(DEP) at the highest levels, and DEP most frequently. Root stimulators, hair lotions, and relaxers frequently contained nonylphenols, parabens, and fragrances; anti-frizz products contained cyclosiloxanes. Hair relaxers for children contained ﬁve chemicals regulated by California’s Proposition 65 or prohibited by EU cosmetics regulation. Targeted chemicals were generally not listed on the product label.Conclusions: Hair products used by Black women and children contained multiple chemicals associated with endocrine disruption and asthma. The prevalence of parabens and DEP is consistent with higher levels of these compounds in biomonitoring samples from Black women compared with White women. These results indicate the need for more information about the contribution of consumer products to exposure disparities. A precautionary approach would reduce the use of endocrine disrupting chemicals in personal care products and improve labeling so women can select products consistent with their values.” (Helm et al., 2018)
Helm, J. et al. (2018). Measurement of endocrine disrupting and asthma-associated chemicals inhair products used by Black women. Envionmental Research, 165, pp.448.458. [Full text link, accessed 24/08/18]
Eumelanin is essential for protection against UV radiation which causes skin cancer by damaging DNA. Black skin blocks out twice as much UV radiation as White skin. The melanocytes in black skin are more resistant to damage and also give more durable supplies of melanin.
“Dark skin, which contains more eumelanin than fair skin is better protected against UV-induced damage, and eumelanin is thought to be superior to pheomelanin in its photoprotective properties. As discussed by Gloster and Neal melanin in Black skin is twice as effective compared to White skin in inhibiting UVB radiation from penetrating. While Black epidermis allows only 7.4% of UVB and 17.5% of UVA to penetrate, 24% UVB and 55% UVA passes through White skin. Further, melanosomes in dark skin are resistant to degradation by lysosomal enzymes, remain intact throughout the epidermal layers and form supranuclear caps in keratinocytes and melanocytes which contribute considerably to photoprotection against UV-induced damage. In contrast, in lightly pigmented skin, melanosomes are degraded and only persist as “melanin dust” in the suprabasal layers. This reduction of melanosomes in the upper epidermis is considered to be an important factor in carcinogenesis, as it compromises the photoprotection of the skin. Other important properties of eumelanin are its functions as a free radical scavenger and superoxide dismutase that reduce ROS.” (Brenner and Hearing, 2008:541-542)
At the same time, the skin depends on UV light to synthesise vitamin D which is essential for healthy and strong bones. Vitamin D deficiency is associated with a number of problems, most notably weak bones. Because of this, a commonly-held belief is that people with darker skin struggle to get enough vitamin d from the minimal sunshine in the northern hemisphere. But this is problematic as the following demonstrates:
“Skin pigmentation influences the effectiveness of vitamin D3 synthesis in the skin as melanin absorbs UVB photons and competes for them with 7-dehydrocholesterol. However, available data about the relationship between solar UVR, skin pigmentation and vitamin D status show contradictory results. On the one hand, it was reported that skin pigmentation greatly reduces the UVR-mediated synthesis of vitamin D3 as those with Black skin require at least a 6-fold greater UVR dose to increase circulating levels of vitamin D3 than do those with White skin. It was also reported that many African Americans who live in northern parts of the US suffer severe vitamin D deficiencies in spite of supplementing foods with vitamin D. In contrast, Matsuoka found no difference in 1,25-(OH)2-vitamin D3 levels in the sera of different ethnic groups, although there was a significant association between skin color and vitamin D3 synthesis. This view was supported by Nelson et al. who reported that there is no difference in the disposition for calcium deficiency in dark-skinned compared to fair-skinned individuals and in that report they further emphasized that African women have the same bone mass as Caucasian women.” (Brenner and Hearing 2008:540-541)
In addition, studies show that black people have bones that have a stronger density and are at less of breaking (O’connor et al., 2003:263) which shouldn’t be the case if we are generally Vitamin D deficient.
The key to understanding this apparently contradictory picture is to firstly recognise that the body needs to convert vitamin d into a different form before it can use it:
“In the liver D2 and D3 become hydroxlyated at the 25-carbon position leading to the formation of the biochemically stable compound, 25-hydroxyvitamin D (25(OH)D). Even though 25(OH)D is used clinically as a marker of vitamin D sufficiency, it is not biologically active. To become biologically active, 25(OH)D must undergo a second hydrox-ylation by 1α-hydroxylase to form 1,25-dihydroxyvitamin D (1,25(OH)2D)” (O’connor et al 2013:262)
“Because levels of total 25-hydroxyvitamin D are consistently lower in black Americans than in white Americans, blacks are frequently classified as being vitamin D–deficient. In our study involving community-dwelling adults, we found that levels of vitamin D–binding protein are also lower in blacks, probably because of the high prevalence of a common genetic variant. Lower levels of vitamin D–binding protein in blacks appear to result in levels of bioavailable 25-hydroxyvitamin D that are equivalent to those in whites. These data, combined with previous data from our group, suggest that low total 25- hydroxyvitamin D levels do not uniformly indicate vitamin D deficiency and call into question routine supplementation in persons with low levels of both total 25-hydroxyvitamin D and vitamin D– binding protein who lack other traditional manifestations of this condition.” (Powe et al 2013:7)
This is a great example of why it is important to factor in race and ethnicity into the study of the human body and medicine. If you simply take a ‘race-blind’ approach which assume that everybody is the same, you will inevitably come up with erroneous concepts and practices. The same biological indicator (in this case, circulating levels of 25(OH)D) can mean different things depending on the race/ethnicity of the person in question.
O’Connor, M. et al (2013). The Uncertain Significance of Low Vitamin D Levels in African Descent Populations: A Review of the Bone and Cardiometabolic Literature. Prog Cardiovasc Dis, Volume 56(3), pp.261–269 [Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3894250/ accessed 22/08/18]
Studies have consistently shown that African Americans have a higher risk of lung cancer even after controlling for a range of risk factors such as smoking behaviour. For example, a 2006 study found that African American men and women who smoked less than 30 cigarettes a day had higher rates of lung cancer than all other groups. The findings could not be explained by differences between populations in known or suspected risk factors, including diet, occupation and socio-economic status (Haiman et al, 2006).
One of the possible causes of this disparity is the relationship between nicotine and melanin. Beginning in the 1970s, research has demonstrated that several drugs including nicotine have an affinity to melanin. These include amphetamines, cocaine, codeine and methadone.
A 2006 literature review by Yerger and Malone reports that various drugs accumulate most intensely in the black pigment in eyes, hair and skin. Several drugs accumulated in these areas for months and in some cases, years. And the most abundant carcinogens in tobacco smoke have been shown to accumulate in melanin-containing tissues.” (Yerger and Malone, 2006)
Similarly, in the case of nicotine, “Investigators have reported that, compared with other racial/ethnic groups, Blacks have a higher intake of nicotine per cigarette and increased nicotine absorption… and have suggested that this higher nicotine absorption could help explain their lower quitting rates (Yerger and Malone, 2006:493).
The correlation suggests that the nicotine-melanin binding increases the toxic effect of nicotine on Africans.