• Sarah Hickson

Finding Personal Empowerment Through a Pandemic

Updated: Jan 28, 2021

When I was studying my post grad in counselling we learnt a formulation to help us make sense of someone's difficulties in their social relationships and circumstances, life events and the meaning that they applied to it all. The formulation was referred to as the 5 P's and comprised of the following:

  • The presenting problem

  • The predisposing factors (e.g. biological contributors, environmental factors, genetic vulnerabilities, and psychological factors - such as past trauma)

  • The precipitating factors (events preceding the onset of disorder)

  • The perpetuating factors (factors that maintain or drive the client's current set of difficulties)

  • The protective factors (strengths and the surrounding supports system that may help to mitigate the impact of the disorder)

The information gathered through this formulation process is a tool often used by therapists and practitioners to help conceptualise the client’s concerns while also identifying key areas that can be targeted, and strengths to be harnessed, to help their clients autonomously problem solve, move through their challenges and ultimately thrive (Macneil, Hasty, Conus & Berk, 2012).

As our current pandemic looms, our actions in response to it no doubt have far-reaching consequences that is impactive on the care and attention of other diseases, poverty, food security and economic growth (Nicola, Alsafi, Sohrabi, et al, 2020). Undoubtedly, decision-making is intensely pressurised as leaders try to navigate their way through so many unknowns, with the risks and impact of any decision so heavily weighted against each other. Conversely, fear and anxiety around personal vulnerability in contracting the virus, or that of a loved one, and uncertainty about when this will all end is also paramount, our collective mental health is being tested more than it ever had been in our lifetime. As the desperate search for a treatment continues with strong guidelines set in effort to control community spread, it is easy to feel as though one’s own sense of agency is blunted. However, feeling autonomous and in control of one’s own life are both innate human needs that are essential for our resilience, growth and psychological wellbeing – without them there is a greater risk of experiencing hopelessness, despair and dependency (Vansteenkiste & Ryan, 2013). During such challenging times, hope is the beacon of light that can help us to cope and propel forward. With knowledge and personal insight, perceived vulnerabilities can be minimised or even transcended through action and positive change. So where can you focus your energy that will give you the greatest sense of power? The answer will always be what is inside of your own control - your acceptance for how things are, your focus, your attitude and your actions.

In this series of blog posts, I'm keen to explore what you can do on a personal level to modify your risk factors to protect against serious infection in the long term, should you accidentally become infected. Are there any underlying mechanisms identified in the research that could predipose and then drive someone towards a serious and potentially long-standing illness? Are there any protective factors identified that could steer that pathway in a different direction? These questions, I hope, will help others to feel empowered as we journey through the trajectory of the COVID19 pandemic - which has been likened to "chasing a moving target" (Sahu, Michra & Lal, 2020).

COVID-19 - A Brief Overview

Late in 2019, a new disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in Wuhan, China, now classified as coronavirus 2019 (COVID-19) (Pirofski & Casadevall, 2020). Currently, almost seven million cases have been reported globally yet there is concern that that number could stretch into the billions (Pirofski & Casadevall, 2020). COVID-19 appears to be the most severe in older individuals and those with pre-existing health conditions, while in contrast, most children, COVID19 seems to be mild or without symptoms (Pirofski & Casadevall, 2020).

Coronaviruses are so named for their crown of spike proteins coating their outer surface, known as S proteins (Wiersinga, Rhodes, Chen, et al, 2020). While more research is needed to add further clarity, scientists have found that these spike proteins are the enabler, the keys that the virus utilises to bind with a particular receptor coating human cells, called angiotensin converting enzyme 2 (ACE2) receptors, so that it can enter the cell and self-replicate useing the cell's own machinary

(Wiersinga, Rhodes, Chen, et al, 2020). It is interesting to note that these ACE2 receptors perform an important functional role for our bodies in regulating blood pressure and fluid salt balance, they can be found throughout the lungs, cardiovascular system, oesophagus, kidneys, bladder, ileum (the latter part of the small intestine), the brain, and even on endothelial tissue that line the inner surface of blood vessel and lymphatic vessel walls (Ni,Yang, Yang, et al, 2020; Tortora & Derrickson, 2014).

Following exposure to the virus, many people experience no symptoms, so here one could imply that the immune system was effective in eradicating the virus without causing any clinical manifestations (Pirofski & Casadevall, 2020). However, when damage by the infection exceeds a threshold that disturbs the homeostasis (normal balance) of the body, signs and symptoms start to present, ranging from mild upper respiratory symptoms to a life-threatening, acute respiratory syndrome, known as ARDS (Pirofski & Casadevall, 2020).

The Disease Process

The visionary of difficulty with breathing that we have become so familiar with in the media is reflective of the progression towards severe illness. Rather than being inflicted directly by COVID-19, this progression is actually caused by our own innate immunity, a system that seemed to have lost it way by ineffectively overreacting to viral infected cells through its weaponary of pro-inflammatory cytokines, releasing them excessively and in turn exerting gradiose levels of inflammation (known as the cytokine storm) that causes collateral destruction within respiratory tissue (Pirofski & Casadevall, 2020). Traumatised lung cells also release inflammatory chemicals as they die, further perpetuating the damage caused by the cytokine storm (Pirofski & Casadevall, 2020). Consequently, damaged alveoli (tiny air sacs found in the lungs) fill with fluid crippling their critical function role of gas exchange of blood (adding oxygen in, taking carbon dioxide out), creating a potentially annihilating pathway that can move towards viral pneumonia, acute respiratory distress syndrome (ARDS), pulmonary failure, cardiac injury, systemic inflammation and sepsis, resulting in a cascade of events that can lead towards multi organ failure and sadly death (Pirofski & Casadevall, 2020; Rothan & Byrareddy, 2020).

The Biological Risk Factors of COVID-19

Infection with COVID-19 seems to be the most severe in older individuals and in those with pre-existing health conditions, while most people seem to recover unscathed (Pirofski & Casadevall, 2020). Severe illness has been seen in all ages yet only rarely has this occured in children, with researchers presuming that this may be due to the smaller number of ACE-2 receptors expressed in children, and also because they seem to have a better adaptive immune response than observed in those with serious infection (Lingappan, Karmounty-Quintana, Davies, Akkanti, Harting, 2020). Scientists are still striving to understand the underlying mechanisms that drive the severity of COVID-19 so at this stage it is still too early to draw any firm clinical conclusions. However the following factors seem to be widely accepted as key players:

  • An impaired immune response by the individoual, characterised by an exaggerated innate response with a weak or failed adapative response (Velavan & Meyera, 2020; Chiappetta, Sharma, Bottino & Stier, 2020)

  • An exaggerated inflammatory response, likely because low grade inflammation was already pre-existing (Velavan & Meyera, 2020; Chiappetta, Sharma, Bottino & Stier, 2020)

  • Excessive oxidative stress that damages organ tissue (oxidative stress occurs when there is poor availability of antioxidants to combat the pro-oxidant effects of inflammatory chemicals released by our immune cells (Chiappetta, Sharma, Bottino & Stier, 2020)

  • Endothelial dysfunction (the inner surface tissue of our blood vessel walls) – leading to excessive blood clotting (Chiappetta, Sharma, Bottino & Stier, 2020; Varga, Flammer, Steiger, et al, 2020; Pons, Fodil, Azoulay, et al, 2020)

  • Uncontrolled blood glucose levels, which is characteristic of type 2 diabetes, but this can also occur in metabolic disorders such as insulin resistance (Velavan & Meyera, 2020; Ceriello, 2020; Chiappetta, Sharma, Bottino & Stier, 2020)

Interestingly, these same factors are also frequently observed in the chronic illnesses described below.

The Link Between Chronic Illness and COVID-19

According to the World Health Organisation (WHO), non-communicable (chronic) diseases are the leading cause of premature death (under 65y) worldwide, accounting for 71% of deaths, declaring them to be the biggest threat to human health (World Health Organization, 2018). Among them, cardiovascular disease is the leading cause of death (17.9 million people annually), followed by cancer (9 million), respiratory disease (3.9 million) and type 2 diabetes (1.6 million) (WHO, 2018). As WHO (2018) had stated, “tobacco use, physical inactivity, the harmful use of alcohol and unhealthy diets (characterised by the standard Westernised diet)" were all key factors that increased the risk of mortality from a non-communicable disease.

As stated by Lewin on the website for The Royal Australian College for General Practitioners (RACGP), older age, hypertension, type 2 diabetes, cardiovascular disease, insulin resistance, chronic respiratory disease and cancer are also factors that also predispose someone to developing severe infection from COVID19, the case fatality rate ranging between 5.6%-10.5%, in comparison to 0.9% for those with no (known) diagnosed comorbid conditions (Lewin, RACGP, 2020). At the time of writing, for people aged 80 and over, the fatality rate is higher at 15%, usually because immunity decreases with age, for a range of reasons, and there is also a greater prevalence of the above listed conditions (Lewin, RACGP, 2020). It is important here to recognise that chronic illness can predispose any individual to serious infection from influenza and other diseases due to a breakdown of their protective immunity, a deeper insight into why will be described below.

The Immune System and Inflammation

One of the most important medical discoveries over the last two decades has been the discovery that immune and inflammatory processes underlie not just a limited number of disorders, but rather a broad variety of physical and mental health problems that dominate disease and mortality globally (Furman, Campisi, Carrera-Bastos, et al, 2019). The presence of chronic inflammation has been traced back to early development and can persist across the lifespan, creating problems in adult physical health and mental wellbeing while also contributing to the risk of mortality (Furman, Campisi, Carrera-Bastos, et al, 2019). Chronic, uncontrolled inflammation is characteristic of the diseases listed above and is known to drive disease progression, but what is it exactly, and how can it get so out of hand? First, we need to understand the immune system.

An Overview of the Immune System

Our immune system is a highly complex yet fascinating network of cells and proteins that collectively protects us against infection. To give a very basic overview, it is comprised of two subsets - our innate immune system and our adaptive immune system.

The Innate Immune System

Our innate immunity refers to the non-specific defence system that comes into play immediately in response to any threatening pathogen and includes external physical and chemical barriers such as our skin, sebum, mucous, stomach acid, saliva, tears, vaginal secretions, cilia (tiny hairs that line mucous membranes in our respiratory system that propel dust and pathogenic material up towards the throat), internal defences such as the microbiome, antimicrobial substances, white blood cells (e.g. natural killer cells, neutrophils and phagocytes), inflammation and fever (Catanzaro, Fagiani, Racchi, et al, 2020; Tortora & Derrickson, 2014).

The Adaptive Immune System

Our adaptive immunity refers to the subset of our immune system that is made up of specialised white blood cells called lymphocytes (known as B and T cells) that work together to attack and destroy invaders (Catanzaro, Fagiani, Racchi, et al, 2020). Unlike our innate immune system, our adaptive immune system, while initially slower to respond, acts with specificity for foreign molecules (antigens) (Tortora & Derrickson, 2014). It also has the capacity for memory, keeping record of any pathogen it has ever been exposed to, so that it knows how to act more swiftly and effectively if ever exposed to that same pathogen again (Tortora & Derrickson, 2014). Our adaptive immunity is signalled into activation by our innate immunity while in turn it helps to regulate the innate immune response (Tortora & Derrickson, 2014).

Understanding the Role of Inflammation

Inflammation is a normal step of the innate immune response and refers to the process where our innate immune system recognises and removes harmful and foreign stimuli so that it can initiate the healing process, the reaction being either acute or chronic in nature (da Silva, Langer & Grat, 2019). Short bursts of inflammation, normal and frequent, are in fact essential for our survival, helping us to heal from physical injury, to recover from infection and to cope with environmental stresses (da Silva, Langer & Grat, 2019). In contrast, the presence of certain biological, environmental, psychological (trauma and loneliness) and even social factors can prevent the body’s ability to effectively heal following an episode of acute inflammation (Furman, Campsi, Verdin, et al, 2019). As such, the innate immune response fails to switch off and inflammation progresses into a slow yet persistent, chronic condition, lasting from several months to many years (da Silva, Langer & Grat, 2019). Generally, the impact and the effect of chronic inflammation varies depending on the cause of injury and the body’s ability to repair itself and heal (da Silva, Langer & Grat, 2019). Chronic inflammation is particularly characterised by a persistent elevation of pro-inflammatory cytokines (small immune system proteins). These cytokines create disturbances in healthy immune function and through a process called oxidative stress, cause collateral damage to surrounding tissue and organs over time, leading towards the development of disease (da Silva, Langer & Grat, 2019). Furthermore, persistent, chronic inflammation impairs normal, healthy adaptive immune function, increasing the susceptibility to infections, cancer and a poor response to vaccinations, which is what we are now observing as the risk factors in this pandemic (Furman, Campisi, Carrera-Bastos, et al, 2019).

Inflammation and COVID-19

There are currently over 30 000 peer-reviewed articles published investigating the relationship between inflammation, diet and health outcomes, recognising that low-grade, chronic systemic inflammation is associated with most chronic diseases, including the diseases listed above and also musculoskeletal disorders, developmental disorders (including autism spectrum disorders) and mental illnesses such as depression (da Silva, Langer & Grat, 2019). In particular, researchers have found that systemic inflammation, in addition to the metabolic disorder of poorly controlled blood glucose levels, insulin resistance and elevated blood pressure, were the biggest drivers of the progression of cardiovascular disease (Ahmad, Moorthy, Demler, et al, 2018).

In the case of COVID-19, researchers found that the progression towards critical illness reflected flawed mechanisms within within both our innate and adaptive immune systems, the former being overreactive, the latter ineffective (Catanzaro, Fagiani, Racchi, et al, 2020).

In infection with COVID19, researchers observed two potentially flawed mechanisms of the innate immune response, either being too hypervigilient and then aggressive, or that it was too slow to respond to the infection (permitting wide-spread viral infection of human cells), with a counterattack of an angry inflammatory response (excessively damaging tissue) (Catanzaro, Fagiani, Racchi, et al, 2020). To coincide with the innate hyperactivity, researchers also found an impaired response by cells of our adaptive immunity, being both ineffective in eradicating the virus and unable to smooth down the inflammatory innate immune response (Catanzaro, Fagiani, Racchi, et al, 2020).

Researchers have also found a multitude of inflammatory markers present in the blood samples of those with COVID19, including erythrocyte sedimentation rate (ESR) C-reactive protein (CRP), fibrinogen, tumour necrosis factor alpha (TNFa) and various other pro-inflammatory cytokines and chemokines (Velavan & Meyera, 2020). One marker in particular, a chemokine known as interleukin-6 (IL-6) - known to be one of the main mediators of our inflammatory and immune response to infections, was found to be positively correlated with severe infection in patients with COVID-19 and seemed to also be an important, independent predictor of disease prognosis, as such, this is a current target for drug threapy (Aziz, Fatima & Assaly, 2020). Interestingly, elevated levels of IL-6 can also be induced from diets high in processed foods and unhealthy lifestyle habits (e.g. little exercise and smoking), and is a also characteristic marker of metabolic inflammation and chronic disease (Sindhu, Thomas, Shihab, et al, 2020).

The Link Between Diet and Inflammation

Every stage of the immune response requires key nutrients for proper functioning. There is a substantial amount of evidence now available that suggests that food and nutrition, as environmental factors, are direct modulators of inflammation, both acutely and chronically (Minihane, Vinoy, Russell, et al, 2015). This is because the food we eat directly influence the way our cells behave and the chemical messengers that they produce. Furthermore, it shapes our microbiome in such a way that it will function as either a health promotor or a health demoter. Our modern, fast paced lifestyles created a demand for convenience where possible, and seeing opportunity, food industries evolved to create a breadth of products that fulfilled that need. Sadly, this created a dietary pattern so popular in our western culture that in the form of processed, pre-packaged foods that have now become so much of our norm, filled with nutrient poor foods such as refined carbohydrates (sugar and white breads/pastries), trans fatty acids (found in fried foods, pastry and margarines), red meat and industrialised oils such as canola oil instead of fresh, wholefoods. These processed foods have been consistently shown in the research to damage the immune system and contribute to immune dysfunction by causing over activity of our innate immunity, with a consequential release of inflammatory signalling resulting in systemic tissue damage (Yamashita, Belchior, Lira, et al, 2018). Furthermore, nutritional deficiencies can further contribute to immune dysfunction while offering little protection against uncontrolled oxidative stress.

Can a Mediterranean Dietary Pattern be Protective?

Understanding that there is a strong environmental link between diet and disease, where do we go from here in the case of this pandemic? I respectfully want to emphasize that there is currently little research available to support the use of dietary means to reduce individual risk factors of severe infection from COVID19. However, there is ample scientific evidence that widely recognises that a plant-based, whole food diet, as reflected in a particular dietary pattern known as the Mediterranean diet, has been consistenly shown to be effective in preventing or reducing the risk factors of many chronic diseases such as cardiovascular disease, type 2 diabetes and cognitive decline (Ahmad, Moorthy, Demier, et al, 2018). The Mediterranean diet refers to the traditional eating habits of European countries bordering the Mediterranean sea and is a highly palatable diet filled with vegetables, fruits, wholegrains, culinary herbs and spices, healthy fats, omega 3 rich oily fish, liberal use of extra virgin olive oil, low to moderate intakes of poultry, eggs and dairy, limited red meat and moderate alcohol intake in the form of a single glass of wine per day,

Over a 3 month period, the Mediterranean diet was shown to reduce inflammatory markers, modulate immune reactivity, improve blood cholesterol, improve blood pressure, strengthen endothelial (blood vessel wall) integrity, regulate blood glucose and promote weight loss (Casas, Sacanella & Estruch, (2016). Other studies have found those who had a high adherence to a Mediterranean diet were able to reduce the risk of all cause-mortality and chronic disease occurrence – including the diseases previously mentioned (Martinez-Gonzalez, Gea & Ruiz-Canela,2019). The large body of available literature strongly suggests that the health benefits of the Mediterranean diet are to attributed to the abundance of anti-inflammatory omega 3 fats, fibre, micronutrients and polyphenols offered in this diet (which are lacking in the typical Westernised diet), working together in synergy to protect against disease, while also supporting the health of our gut microbiome (Castro-Barquero, Lamuela-Raventos, Domenech & Estruch, 2018).


The best protection against COVID19 that we have available, of course, is to avoid getting infected in the first place. However, we need to also be looking long term and from a broader perspective, investigating the underlying factors that makes someone vulnerable, and what can be protective. At this stage it is sensible to assume that there will be no silver bullet in the treatment of COVID19. Instead, there will be a combination of treatments, and at an individual level, self care in the form of nourishing foods and healthy lifestyle practices are the most important things you can do to nurture your own resilience. From this preventative perspective, it seems wise for those who are over 60y to get a health check to explore potential risk factors that may increase their risk of severe disease (e.g. diabetes and cardiovascular disease biomarkers, high waist circumference, vitamin D and zinc deficiency and inflammatory markers) and to take the appropriate measures to improve poor baseline measures with a proper treatment plan and the support of a committed health care professional. If deemed high risk then extra precautions will need to be implemented to protect against exposure. A viable treatment may be a little way off yet, however creating delicious meals for yourself and members in your home using inspiration from the Mediterranean diet principles, regular movement, stress management, quality sleep and supporting a good nutritional status are all available to us to work on now. Science has demonstrated that these are collectively essential for immune resiliency. Empowering one’s own ability to improve their individual risk factors should be always be encouraged. This all is only temporary and there are lighter days ahead.


Ahmad, S., Moorthy, M.V., Demier, O.V., Hu, F.B., Ridker, P.M., Chasman, D.I., Mora, S. (2018) Assessment of Risk Factors & Biomarkers Associated with Risk of Cadiovascular Disease Among Women Consuming a Mediterranean Diet, Jama Network Open, Vol 1 (8), doi:10.1001/jamanetworkopen.2018.5708

Aziz, M., Fatima, R., Assaly, R. (2020) Elevated interleukin-6 & severe COVID-19: A meta-analysis, Journal of Medical Virology, Vol . DOI: 10.1002/jmv.25948

Castro-Barquero, S., Lamuela-Raventos, R.M., Domenech, M., Estruch, R. (2018) Relationship between Mediterranean Dietary Polyphenol Intake & Obesity, Nutrients, Vol 10 (1523), Nutrients. doi: 10.3390/nu10101523

Ceriello, A. (2020) Hyperglycemia & the worse prognosis of COVID-19. Why a Fast Blood Glucose Control Should be Mandatory, Diabetes Research in Clinical Practice, Vol 163. doi: 10.1016/j.diabres.2020.108186

Chiappetta, S., Sharma, A.M., Bottino, V., Stier, C. (2020) COVID-19 & the Role of Chronic Inflammation in Patients with Obesity, Epidemiology & Population Health, International Journal of Obesity, Vol 44, p.1790-1792. Accessed 5th August, 2020 https://www.nature.com/articles/s41366-020-0597-4

da Silva, D.M., Langer, H., Graf, T. (2019) Inflammatory & Molecular Pathways in Heart Failure – Ischemia, HFpEF & Transthyretin Cardiac Amyloidosis, International Journal of Molecular Sciences, Vol 20 (9). doi: 10.3390/ijms20092322

Furman, D., Campisi, J., Verdin, E., Carrera-Bastos, P., Targ, S., Franceschi, C., Ferrucci, L., Gilroy, D. W., Fasano, A., Miller, G. W., Miller, A. H., Mantovani, A., Weyand, C. M., Barzilai, N., Goronzy, J. J., Rando, T. A., Effros, R. B., Lucia, A., Kleinstreuer, N., & Slavich, G. M. (2019). Chronic inflammation in the etiology of disease across the life span. Nature medicine, 25(12), 1822–1832. https://doi.org/10.1038/s41591-019-0675-0

Lewin, E. (2020) Examining the Factors that Worsen Coronavirus Severity, NewsGP, The Royal Australian College of General Practitioners. Accessed 5th August, 2020 from


Lingappan, K., Karmounty-Quintana, H., Davies, J., Akkanti, B., Harting, M.T. (2020) Understanding the age divide in COVID-19: Why are children overwhelmingly spared? Lung Cellular & Molecular Physiology, Vol 319 (1), p.L39-L44. https://doi.org/10.1152/ajplung.00183.2020

Macneil, C.A., Hasty, M.K., Conus, P., Berk, M. (2012) Is diagnosis enough to guide interventions in mental health? Using case formulation in clinical practice, BMC Medicine, Vol 10 (11). Accessed15th August from https://www.researchgate.net/publication/231222916_Is_diagnosis_enough_to_guide_interventions_in_mental_health_Using_case_formulation_in_clinical_practice

Martinez-Gonzalez, M.A., Bes-Rastrollo, M., Serra-Majem, L., Lairon, D., Estruch, R., Trichopoulou, A. (2009) Mediterranean Food Pattern & the Primary Prevention of Chronic Disease: Recent Developments, Nutrition Reviews, Vol 67 (s1), s111-s116. https://doi.org/10.1111/j.1753-4887.2009.00172.x

Non-Communicable Diseases Facts Page (2018) World Health O rganization. Accessed 5th August 2020 from https://www.who.int/news-room/fact-sheets/detail/noncommunicable-diseases

Minihane A.M, Vinoy S, Russell W.R, et al. (2015) Low-grade inflammation, diet composition and health: current research evidence and its translation, The British Journal of Nutrition, Vol 114 (7) p.999-1012. doi:10.1017/S0007114515002093

Nicola, M., Alsafi, Z., Sohrabi, C., Kerwan, A., Al-Jabir, A., Iosifidis, C., Agha, M., Agha, R. (2020) The socio-economic implications of the coronavirus pandemic (COVID-19): A review, International Journal of Surgery, Vol 78, p.185-193. https://doi.org/10.1016/j.ijsu.2020.04.018

Ni, W., Yang, X., Yang, D. et al. (2020). Role of angiotensin-converting enzyme 2 (ACE2) in COVID-19. Critical Care Vol 24 (422) https://doi.org/10.1186/s13054-020-03120-0

Phillips, C.M., Chen, L.W., Heude, B., Bernard, J.Y., Harvey, N.C., Duijts, L., Mensink-Bout, S.M., Polanska, K., Mancano, G., Suderman, M., Shivappa, N., Herbert, J.R. (2019) Dietary Inflammatory Index & Non-Communicable Disease Risk: A Narrative Review, Nutrients, Vol 11 (8) doi: 10.3390/nu11081873

Pirofski L. A., Casadevall A. (2020) Pathogenesis of COVID-19 from the perspective of the damage-response framework, American Society for Microbiology, Vol 11 (4). https://doi.org/ 10.1128/mBio.01175-20.

Pons, S., Fodil, S., Azoulay, E., Zafrani, L. (2020) The vascular endothelium: The cornerstone of organ dysfunction in severe SARS-CoV-2 infection, Critical Care, Vol 24 (353). Accessed 15th August 2020 from https://ccforum.biomedcentral.com/articles/10.1186/s13054-020-03062-7

Rothan, H.A., Byrareddy, S.N. (2020) The epidemiology & pathogenesis of coronavirus disease (COVID-19) outbreak, Journal of Autoimmunity, Vol 109. doi: 10.1016/j.jaut.2020.102433

Sahu, K.K., Mishra, A.K., Lal, A. (2020) Trajectory of the COVID-19 pandemic: Chasing a moving target, Annals of Translational Medicine, Vol 8 (11) http://atm.amegroups.com/article/view/43684/html

Sindhu, S.,Thomas, R., Shihab, P., Sriraman, D., Behhehani, K., Ahmad, R. (2020) Obesity is a positive modulator of IL-6R & IL-6 expression in the subcutaneous adipose tissue: Significance for metabolic inflammation, PLoS One, Vol 10 (7). https://doi.org/10.1371/journal.pone.0133494

Tortora, G. T., Derrickson, B. (2014) Principles of Anatomy & Physiology 14th Edition, John Wiley & Sons, USA

Wang, S., Ma, P., Zhang, S., Song, S., Wang, Z., Ma, Y., Xu, J., Wu, F., Duan, L., Zhengrong, Y., Luo, H., Xiong, N., Xu, M., Zeng, T., Jin, Y. (2020) Fasting Blood Glucose at Admission is an Independent Predictor for 28-day Mortality in Patients with COVID-19 Without Previous Diagnosis of Diabetes: A Multi-Centre Retrospective Study, Diabetologia. Accessed 5th August, 2020 from https://link.springer.com/article/10.1007%2Fs00125-020-05209-1

Vansteenkiste, M., Ryan, R.M. (2013) On psychological growth & vulnerability: Basic Psychological need satisfaction & need frustration as a unifying principle, Journal of Psychotherapy Integration, Vol 23 (3), p.263-280. Accessed 15th August from https://biblio.ugent.be/publication/4303500/file/6810420.pdf

Velavan, T.P., Meyera, C.G. (2020) Mild versus severe COVID-19: Laboratory markers, International Journal of Infectious Diseases, Vol 95, p.304-307. DOI:https://doi.org/10.1016/j.ijid.2020.04.061

Wiersinga, W.J., Rhodes, A., Cheng, A.C., Peacock, S.J., Prescott, H.C. (2020) Pathophysiology, diagnosis, & treatment of coronavirus disease 2019 (COVID-19) A review, JAMA, Vol 324 (8), p.782-793. JAMA. 2020;324(8):782-793. doi:10.1001/jama.2020.12839

Varga, Z., Flammer, A.J., Steiger, P., Haberecker, M., Andermatt, R., Zinkernagel, A.S., et al (2020) Endothelial cell infection & endothelitis in COVID-19, The Lancet, Vol 395 (10234). DOI:https://doi.org/10.1016/S0140-6736(20)30937-5DOI:https://doi.org/10.1016/S0140-6736(20)30937-5

Yamashita AS, Belchior T, Lira FS, et al (2020) Regulation of Metabolic Disease-Associated Inflammation by Nutrient Sensors. Mediators of Inflammation, Vol 2018. doi:10.1155/2018/8261432

70 views0 comments

Recent Posts

See All