[D] The burden of poverty & intergenerational racism.

While the media has reported ‘cases’ it has always been clear that healthier populations are likely to have little or even no symptoms, (to be asymptomatic) and be at very low risk of hospitalisation and death. Asymptomatic spreaders are more likely to be vaccinated.

The virus Sars-Cov-2 produces symptoms in certain individuals, and it is these symptoms (or pathologies), as a disease progression, that are known as COVID-19. COVID-19 is incredibly complex:

A September 2021 scoping review of the pathophysiology of COVID-19[i] noted that severe COVID-19 was ‘probably amongst the most complex of medical conditions known to medical science’. The review stated in the conclusion (page 10):

‘Severe COVID-19 infection is the consequence of the overlapping effects of macrophage activation with uncontrolled inflammation, a complement-mediated endothelialitis and a thrombotic microangiopathy with platelet activation and high circulating serotonin. In addition, mast cell activation, auto-antibodies, and an imbalanced RAAS contribute to the pathogenesis of severe COVID-19 disease. During the first 6 months of the pandemic, the World Health Organization (WHO) and almost all national guidelines recommended a “supportive care only” strategy for the management of severe COVID-19. Based on our increased understanding of this disease, such therapeutic nihilism is no longer acceptable. Patients’ transition through a number of different phases (clinical stages) and treatment must be tailored to each specific phase. Antiviral therapy is likely to be effective only during the viral replicative symptomatic phase. As patients progress into the pulmonary phase, they require treatment with multiple therapeutic agents that target the major pathogenetic mechanisms; these include anti-inflammatory agents (methylprednisolone, ivermectin, and fluvoxamine, etc), anticoagulants (heparin and ASA), and anti-serotonin agents (cyproheptadine). And finally, there is no one-size-fits-all protocol, and it is essential that the treatment strategy must be individualized according to the clinical phenotype of each patient.’ [ii]

Earlier, scientists described the principal cause of death as arising from an uncontrolled inflammatory cascade – a cytokine storm - which produces acute respiratory distress syndrome (ARDS), multiple organ dysfunction syndrome (MODS), and microvascular thrombosis.[iii] Cytokine storm syndrome involves uncontrolled immune activation, the result of ongoing - hyperinflammation and multiorgan disease.[iv]

Image: McCullough et al 2020.

From an early stage it was recognised that those at most risk – and most likely to be symptomatic would be the elderly and individuals with multiple chronic health conditions – particularly obesity related and heart-related conditions. [v] [vi] Diabetes, hypertension, stroke, and ischemic heart disease are risks, as well as the risk of blood clotting. Scientists recognised the importance of recognising and treating these conditions to prevent the inflammatory cytokine cascade and thrombotic events.[vii] [viii]

Thrombosis is such a significant problem[ix] that scientists have referred to COVID-19 as a thromboinflammatory disease.[x]

The disease progression is complex, and the severity of infection is closely connected to the health of the infected individual (some might say, the individual’s ‘terrain’). The different phases require treatment that is tailored to each phase. Antiviral therapy, is likely to be effective in during viral replication, then specific treatments for the pulmonary phase (such as anti-inflammatory agents, anticoagulants, and anti-serotonin agents). One-third of patients hospitalized with severe COVID-19 may develop macrovascular thrombotic complications, including venous thromboembolism, myocardial injury/infarction and stroke. [xi] Microthrombosis may play a role in the development of delayed cerebral ischemia, either following infection or vaccination.[xii] The different phases require treatment that is tailored to each phase. Antiviral therapy, is likely to be effective in during viral replication, then specific treatments for the pulmonary phase (such as anti-inflammatory agents, anticoagulants, and anti-serotonin agents).

From the Spanish flu onwards, it has been very clear that disadvantaged populations are most at risk of bad outcomes in viral pandemics. As a virus progresses through the population, healthier individuals with better nutrient levels from better quality diets are more likely to be asymptomatic, while less healthy individuals, often on low incomes, or who receive subsistence benefits, are more at risk. Not all people on low-incomes are obese, and some wealthy people are obese. However, obesity is strongly associated with poverty, racism and colonisation; and this intertwines with intergenerational and early life experiences. Obesity is the result of poor diets. The cheapest calorific foods in the supermarket are ultraprocessed high-energy, low (quality) fibre and low nutrition[xiii] [xiv]. State and media narratives have focussed on behaviour, often excluding discussion on the marginal income and time-poor status of groups who are structurally trapped by social factors, including inadequate incomes. The Commission on Social Determinants of Health has noted:

‘We believe that unless action also addresses the structural drivers of inequity in behaviour, it will not tackle the contribution of these behaviours to health inequities.’[xv]

Māori and Pacific communities face a much greater health burden from COVID-19[xvi]. A recent study revealed that:

‘an 80-year-old patient with COVID-19 in the NZ European/Other group without reported comorbidities has the same predicted risk of hospitalisation as a 59.3-year-old (95% CI 46.9–73.7 years old) patient in the Māori group without reported comorbidities.’[xvii]

Household income is a key determinant of food insecurity. Food insecurity is defined by ‘the absence of sufficient, nutritionally adequate, safe foods, as well as the inability to acquire such foods in socially acceptable ways.’[xviii] Discussion of COVID-19 risk[xix] can fail to recognise the relationship of undernutrition, obesity and COVID-19 risk. Food insecurity is a persistent problem[xx], and Māori and Pasifika populations are most vulnerable to food insecurity in New Zealand, while women experience food insecurity more than men.[xxi] Consequent stress is not only nutrition-related, but psychological, despite for example, Māori communities working hard to support community members.[xxii] The COVID-19 pandemic has exacerbated food insecurity.[xxiii]

The risk to Māori and Pasifika populations in the COVID-19 pandemic stems from unequal access to intergenerational resources, that has over time, resulted in a disproportionate disease burden across these populations. Institutional racism has contributed to the disease burden. Over time advantages and privileges accrue in one sector of the population while disadvantaging and enacting racism against another.[xxiv] Equity of health must be uppermost, and equity of medical care a sub-category. A person who has multiple conditions, and on multiple medications, can never achieve health and wellbeing, as a person lacking a multiple disease profile. The prescription of multiple medications (polypharmacy) in itself, is a driver of health risk. New Zealand health policy has historically been silent about Māori health, the fact that Māori are especially at risk and that the Crown, by not responding to health inequities has failed to uphold Treaty of Waitangi obligations. In failing to respond to the needs of Māori traditional knowledge, as mātauranga Māori has been marginalised.[xxv]

This is why it is important to not merely discuss equity of health care and access to medicine inside the health system. Such a policy, without addressing structural inequity and structural racism results in an implicit understanding that it is acceptable for Māori and Pasifika populations to tolerate a higher burden of disease, as long as they are medicated and treated properly. This is unjust, as quality of life, health and wellbeing are directly related to disease status, and the levels of multimorbidity in Māori and Pasifika populations are currently unacceptable.

Chronic disease is not only growing in Māori and Pasifika populations, but across the broader population, and so overarching policies to improve health status are important. Children currently have higher rates of non-communicable disease than previous generations, and differing levels of disease is associated with protective government policy. Scientists have found that it is very difficult to get the greater structural drivers of chronic disease into government policy. Governments have often targeted behaviour, rather than delivering policy directed to ensuring that low-income groups have sufficient incomes and non-working time to access and prepare nourishing food. [xxvi] Foodbanks do not assure adequate nutrition.[xxvii] [xxviii] Governments have been disinclined[xxix] to identify, regulate and tax ultraprocessed foods that drive disease including mental illness, metabolic syndrome, cancer and adverse COVID-19 outcome.[xxx] [xxxi]

Severe COVID-19 cases are connected to diabetes, heart problems and obesity, and often patients have all three conditions. These dismaying and debilitating diseases drive inflammation and impair lung function leading to much greater risk.[xxxii] [xxxiii] [xxxiv] Obesity and age may be the dominant variables for risk.[xxxv] Obesity is widely accepted as a disease of poverty, and in more affluent nations, the disease is commonly clustered in English speaking nations considered ‘market liberal’ who have greater levels of income insecurity, greater levels of inequality and are less likely to regulate fast food, as compared to many non-English speaking European nations.[xxxvi] In New Zealand it is increasingly likely that patients have multiple (multimorbid) conditions.[xxxvii] It is clear that social factors and inequality drives multimorbidity risk.[xxxviii] [xxxix] Undiagnosed, or newly diagnosed diabetes appears to place individuals more at risk.[xl]

It is important to draw attention to the drivers of increased risk from COVID-19, as when the Ministry records yet another ‘case’ it is highly likely the ‘case’ will be ‘someone’ from a disadvantaged household with a co-existing preventable disease. It is highly likely those who present as cases have sub-optimal nutrition. In this environment, it is disadvantaged populations who are more likely to be symptomatic, yet the cofactors that drive their risk have been left outside public discussion. It has been evident for decades, that health policy has failed to address the profound disparities in health in New Zealand, that are structural in origin – rather than a result of behavioural factors.[xli] [xlii] [xliii] Often when policy is developed, it concerns equity of access to medicine, as a ‘medical dominance’ paradigm, rather than policy which is structured to protect equity of access to a healthy life.[xliv] [xlv]

Low-income groups have cascading trauma due to precarious work situations, increased rates of mental illness and cultural disparities that make accessing services and managing day to day stresses difficult.[xlvi] However other COVID-19 related issues can increase harm to these groups. The relatively common presence of associated (multimorbid) health conditions, result in these groups having less healthy immune systems. The immunosuppressed and older groups can have declining immunity (immunosenescence) which can impact vaccine efficacy.[xlvii] People with metabolic diseases have higher rates of inflammation and poorer immune systems. They have a reduced ability to fight infections and other diseases. All bodies respond differently to environmental stressors, including viruses. However, as diet related chronic disease rates increase so do immunosuppressed groups who are more at risk. These groups, unfortunately, are also more likely to have vaccine failure.[xlviii] This limits the protectiveness of vaccines. Critical work is required to improve understanding around when vaccine protection wanes.[xlix] Europe has recently authorised that a third vaccination (a booster) for those with severely weakened immune systems can be given at least 28 days after their second dose.[l] It is not known how long the third dose will remain effective.

NEXT: [E] Novel mRNA technologies – no silver bullet

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[ii] Marik et al. A scoping review of the pathophysiology of COVID-19. International Journal of Immunopathology and Pharmacology

[iii] Wang 2021. A potential association between immunosenescence and high COVID-19 related mortality among elderly patients with cardiovascular diseases. Immunity & Ageing 18:25

[iv] Henderson et al 2020. On the Alert for Cytokine Storm: Immunopathology in COVID-19

[v] Moore et al 2021 Modelling optimal vaccination strategy for SARS-CoV-2 in the UK

[vi] Malas 2020 Thromboembolism risk of COVID-19 is high and associated with a higher risk of mortality: A systematic review and meta-analysis. Arthritis & Rheumatology. Doi 10.1002/art.41285

[vii] Ruocco et al. Mortality Risk Assessment Using CHA(2)DS(2)-VASc Scores in Patients Hospitalized With Coronavirus

Disease 2019 Infection. The American Journal of Cardiology. (2020) https://doi.org/10.1016/j.amjcard.2020.09.029

[viii] Mahajan et al. COVID-19-Associated Systemic Thromboembolism: A Case Report and Review of the Literature. Cardiorenal Medicine (2020) 10:462-469

[ix] Chen W. & Pan J. Anatomical and Pathological Observation and Analysis of SARS and COVID-19: Microthrombosis Is the Main Cause of Death. Biological Procedures Online (2021) 23:4 https://doi.org/10.1186/s12575-021-00142-y

[x] Gasecka et al. Thrombotic Complications in Patients with COVID-19: Pathophysiological Mechanisms, Diagnosis, and Treatment. Cardiovascular Drugs and Therapy (2021) 35:215–229

[xi] Gasecka et al. Thrombotic Complications in Patients with COVID-19: Pathophysiological Mechanisms, Diagnosis, and Treatment. Cardiovascular Drugs and Therapy (2021) 35:215–229

[xii] Bhogal et al. COVID-19 and Delayed Cerebral Ischemia—More in Common Than First Meets the Eye. Clin. Med. 2021, 10, 2646. https://doi.org/10.3390/jcm10122646

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[xiv] Michalakis & Ilias 2020. SARS-CoV-2 infection and obesity: Common inflammatory and metabolic aspects. Diabetes & Metabolic Syndrome: Clinical Research & Reviews. 14:469-471

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[xvi] ESR https://nzcoviddashboard.esr.cri.nz/#!/

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[xxvii] Dey 2014 Recounting

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[xli] Ministry of Health 2018. Health and Independence Report 2017. The Director-General of Health's Annual Report on the State of Public Health. Ministry of Health.

[xlii] King, A. 2001. The New Zealand Health Strategy. Wellington: Ministry of Health

[xliii] Ajwani et al 2003. Decades of Disparity. Ethnic Mortality Trends in New Zealand 1980-1999. Wellington: Ministry of Health and University of Otago.

[xliv] Baum, F. (2019). Governing for Health: Advancing Health and Equity through Policy and Advocacy. Oxford University Press.

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[xlvi] Patel et al 2020. Poverty, inequality and COVID-19: the forgotten vulnerable. Public Health.183: 110–111.

[xlvii] Bajaj 2021 Aging, Immunity, and COVID-19: How Age Influences the Host Immune Response to Coronavirus Infections? https://doi.org/10.3389/fphys.2020.571416

[xlviii] Kimball et al 2021. Influenza Vaccine Failure Associated With Age and Immunosuppression. J Inf Dis 224:2;288-293

[xlix] Krammer 2021. A correlate of protection for SARS-CoV-2 vaccines is urgently needed. Nature Medicine 27:1145-1153

[l] European Medicines Agency. Comirnaty and Spikevax: EMA recommendations on extra doses and boosters. October 4 2021. https://www.ema.europa.eu/en/news/comirnaty-spikevax-ema-recommendations-extra-doses-boosters

[D] The burden of poverty & intergenerational racism.

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