How Artificial Intelligence is Transforming Cancer Immunotherapy


Immunotherapy has enormous potential to provide cancer patients with a treatment which is more personalised, more precise, and more effective than current therapies, but evidently its promises will only come to fruition with the assistance of improved predictive algorithms and bioinformatics tools. Recent explosions in publicly available cancer genomic data, coupled with advancements in machine learning methods is ensuring that the marriage of computation and biology will help to address challenges facing immunotherapy in the coming decade.


Quite deservingly, there has been great excitement in recent years surrounding the use of artificial intelligence and machine learning algorithms for immunotherapeutic discovery, as well as a wide range of other biological and medical applications. One area which has profited greatly from these computational tools is the discovery of neoantigens for cancer vaccine development.

Cancer Neoantigens and Vaccine Development

Underlying all immune responses is the ability of the immune system to distinguish self from non-self – to discern whether any protein it encounters is part of its own human body, or has come from some invading entity. In the context of cancer, tumour cells are recognised as ‘mutated self’ – a signal for the immune destruction. Based on this principle, there has recently been an enormous interest in developing immunotherapies capable of selectively eliminating cancer cells by amplifying the patient’s own immune response against his/her tumour. Cancer neoepitopes or neoantigens are protein products of the mutated cancer genome which serve to trigger an antitumour immune response upon presentation to immune cells called CD8+ T cells.


This places neoepitopes at the forefront of cancer immunotherapy. The challenge now for cancer biologists is to identify which neoepitopes are iliciting potent immune responses against tumours, and which ones might hold promise in developing anti-cancer vaccines. Similarly to vaccines used to immunise against viral infections, these immunotherapies would introduce some tumour-specific antigen into the body so that the immune system mounts a response against it, selectively killing tumour cells while leaving healthy cells unharmed.


To achieve tumour-specific killing, the vaccine should target MHC-1-restricted epitopes which then activate CD8+ T-cells to specifically kill cancer cells, binding to MHC-peptide complexes via their T-cell receptor.  Neoantigens are presented to T-cells by Antigen Presenting Cells – usually Dendritic Cells or tumour cells themselves. Antigen presentation is preceded by a train of intracellular events including proteasomal processing and transport of the resulting peptide to the cell surface.

Designing Neoepitope Prediction Algorithms with Artificial Intelligence 

As cancer cells progressively acquire somatic mutations, so too does the array of potential neoepitopes expand. The task at hand then is to predict which of these neoepitopes are likely to be presented on the tumour cell surface, to bind MHC-1 and be recognised by the T-Cell Receptor in vivo to trigger an immune response. Predicting clinically relevant neoantigens is a challenging task. Immunogenic mutations are highly specific to each individual patient, being restricted by the unique type of MHC molecules expressed on their cells. Moreover, a cancer’s mutational fingerprint is extremely heterogeneous between patients, as are cancer cells within one single tumour. The ideal neoantigen would need to be expressed homogeneously and in sufficient concentrations such that an immune response designed against it would destroy the entire tumour.

Because so few mutations are immunogenic, high throughput  computational methods to predict these neoepitopes are being employed to identify promising candidates for cancer vaccine development. Artificial Neural Networks (ANNs) – a branch of artificial intelligence – have been designed to determine how likely is a given 3D structure or 2D amino acid sequence to become an epitope. Such algorithms are largely focused on predicting peptide interactions with MHC-1. As the majority of peptides presented by MHC-1 are 9 amino acids in length, the algorithms usually look at peptides of length 8-11aas. One such algorithm is NetMHC, developed by scientists at the Technical University of Denmark. which has been trained using data from a large number of different MHC alleles. The server produces as output a predicted IC50 value representing the binding affinity of a peptide with MHC-1.


A further consideration which is critical here is predicting cross-reactivity of the neoantigen with non-tumour antigens in the body. If they are targeted therapeutically, shared epitopes could result in off-target toxicity, threatening patient safety. This can also be addressed using computational methods. German researchers have developed a tool called Expitope to assess crossreactivity of immunotherapeutic antigens against naturally expressed proteins in human tissues .


What’s Next  On the Horizon?

There remains a long road to travel towards the ideal predictive algorithm for cancer vaccine development. It is important to realise that the accuracy of the algorithm depends on the training data used as input. These predictive tools are typically constructed based on IC50 values obtained from binding affinity experiments in vitro. This means that the quality of in silico predictions is influenced by data gained previously from in vitro affinity studies. Basing predictions on binding affinity alone is problematic as it fails to fully reflect the complex peptide loading pathway which takes place in vivo. Only a small percentage of predicted high affinity binders are in reality recognised by the patient’s T-Cells, making them potential candidates for immunotherapy.  As a result, current strategies have scientists wading through a sea of false positives in the search for neoantigens.


There remains a major need to develop reliable methods of accurately verifying that neoepitopes found in silico can actually elicit  a tumor-specific immune response and ultimately achieve tumor regression. In in vitro experiments, a binding affinity threshold of < 500nM is used to determine a peptide’s potential to be a neoepitope, but this simplification may cause putative neoepitopes with lower affinity to be overlooked. It must be emphasised that many factors other than binding affinity can also play a fundamental role in presentation of neoepitopes and  immune activation. Rather than solely relying on binding affinity, improved computational methods will need to be developed which consider all aspects of antigen processing and presentation in order to successfully predict neoepitopes. Indeed similar sequence-based ANN algorithms are also in development which predict other informative steps in peptide processing such as  proteasome cleavage and Transporter Associated with Antigen Binding (TAP) protein binding. An even more daunting challenge which scientists hope to soon tackle is to predict interaction of the antigen-MHC complex with the T-Cell Receptor, whose binding mechanism is considerably more complex




Yarchoan, M., Johnson III, B. A., Lutz, E. R., Laheru, D. A., & Jaffee, E. M. (2017). Targeting neoantigens to augment antitumour immunity. Nature Reviews Cancer, 17(4), 209.


Brennick, C. A., George, M. M., Corwin, W. L., Srivastava, P. K., & Ebrahimi-Nik, H. (2017). Neoepitopes as cancer immunotherapy targets: key challenges and opportunities. Immunotherapy, 9(4), 361-371.


Jiang, T., Shi, T., Zhang, H., Hu, J., Song, Y., Wei, J., … & Zhou, C. (2019). Tumor neoantigens: from basic research to clinical applications. Journal of hematology & oncology, 12(1), 93.

Lab Rats Lost in Translation: Why We Use Animals in Research, and Why We Really Shouldn’t


This is a story of mice and men. It is not a happy story – not for us, and not for them. It is estimated that about 115 million animals are used annually in biomedical research and drug testing around the world, costing hundreds of thousands of dollars for every substance tested. Most of these millions are rodents – rats and mice. Rabbits and guinea pigs are also commonly used, and smaller amounts of dogs (mostly beagles) and non-human primates.

Medical research is often considered to be somewhat of a grey area when it comes to animal ethics. If a few animals have to die, but we end up finding a wonder drug that saves millions of human lives, then surely the benefit outweighs the cost, right?

The problem is it is more than just a few animals – it is millions of them – and the number of effective drugs actually being approved each year to treat human diseases is slim compared to the numbers of drug candidates initially tested in animals. The chances of animal experiments actually benefiting humans of often wildly overestimated.

In 2018, 59 new drugs were approved by the Food and Drug Administration (FDA), but scientists say the commercial potential of these new drugs is “lacklustre” (1). Although hundreds of drug candidates progress through animal studies to enter clinical trials in humans each year, only about 10% ever penetrate the market, and truly impactful drugs that save human lives are depressingly rare.

About 25% of these drugs approved in 2018 were for cancer treatment. We are nowhere near curing cancer but we have an army of drugs to treat it. The majority of these drugs improve patient survival by maybe two or three months, only benefit a small minority of patients at an exorbitant cost, and do little to improve quality of life. Our obsession with progress in drug development is fuelled by a culture of medical excess. What makes us so eager to sacrifice years of labour, billions of dollars and thousands of animal lives to achieve even the faintest glimmer of clinical promise?

Much of what is called scientific or medical “progress” may not in reality improve life but rather delay death. To me, delaying death in one species by sentencing death on another, does not seem to add up. Are such drugs truly worthy of the thousands of animals sentenced to death for their development?

What about the thousands of drugs which fail during the transition from bench to bedside? Are they worth the millions of lives sacrificed for them?

In cancer research, the average rate of successful translation from animal models to cancer trials in humans is less than 8%. Of the drugs that make it into clinical trials, an even smaller fraction will make it through to achieve marketing approval  (2).

The idea that animal experimentation is “taking one like to save another” is extremely flawed. In animal research we are rarely, if ever, presented with the stark situation in which we can save the life of a human by taking the life of an animal (3).

Why do so many drugs fail in Clinical trials?

The main reasons for failure in clinical trials are lack or efficacy and lack of safety – either the drug doesn’t work well enough, or it causes some harmful side-effect that detracts from any clinical benefit it may possess.

90% of drugs entering clinical trials in humans fail to make it through, and many so-called “silent failures” happen before human testing even begins. This is the pre-clinical stage, where animals come into the picture. Before we can give a drug to a human – which will begin with a small group of healthy volunteers – scientists are required to first prove its safety in both rodent and non-rodent animal models.

All major reasons for failure in clinical trials can be attributed to the use of animal models, which due to inherent genetic differences, do not accurately reflect safety or efficacy endpoints in humans.

Do they suffer?

We know that animals feel pain. In fact it is quite likely that their experience of it is stronger than ours. Like us, animals have evolved the capacity to feel pain as a warning when an action is putting us in danger. “Don’t do that again” it says. Richard Dawkins – the great evolutionary biologist – suggests that those animals which have lower capacity for memory might actually require a more intense warning signal to deter the action.

“We have erected a moral wall around our human species”, Dawkins says. How is it that a human embryo, even in its very earliest stage, even before it has developed a nervous system, is somehow more worthy of our moral consideration than an adult chimpanzee?

Intelligent Humans

We humans like to think of ourselves as the most intelligent beings, often using this point as justification for the desperate measures we take towards human betterment. But consider this: the only reason humans are the most intelligent creature is because the concept of “intelligence” was created by humans. We picked out a few things our brains happen to do better than other animals, bundled them all together and called it “intelligence” and told ourselves that was what made our race great. Intelligence does not equal superiority. Our special blend of cognitive function does not make us any more worthy of life. It is difficult to argue that the human race, which in recent decades has inflicted irreversible harm on our planet, is still somehow more worthy to live here than any more peaceful branch of the evolutionary tree.

Maybe other animals are “less intelligent”; maybe they are “not quite like us”. The notion that animals are not like us is true – and this should be used as an argument against animal research – not supporting it. The quest to understand and treat human diseases by experimenting on animals which are not like us and which don’t even naturally contract most human diseases creates misleading and erroneous results which do more harm than help to human healthcare.

Some of the same arguments we make in justification of animal experiments could similarly be used to justify the practice in the severely disabled, the mentally ill, children, prisoners and people of colour.

Today we look back at our slave-owning ancestors with horror. It is absurd to us to consider such an immoral system, where treatment of other humans is based solely on the colour of their skin. But what will future generations think of us?

Ethics committees, which decide whether an animal experiment is justified, may consist of “intelligent humans” but they do not consist solely of vegans.  I can’t imaging that anyone who thinks it is somehow morally justifiable to end an animals life simply for the pleasure of taste, can possibly evaluate whether the outcome of an experiment truly justifies the means.

The Three R’s: Replace, Reduce, Refine

The use of animals in scientific research is guided by three basic principles:

  • Replacement of animals by alternative tools where available
  • Reducing the number of animals used to a minimum
  • Refining the conditions of use to improve animal welfare and reduce suffering as much as possible

The Three R’s have been embedded in international legislation and regulations for more than 50 years, but they are loosely defined and loosely enforced. Today, with promising new tools like organ-on-chip models burgeoning in this space, replacement needs to be at the top of the agenda.

Should we be getting to human trials sooner?

There is a concept called “microdosing” of “Phase 0 trials” which has recently been implemented in some drug discovery projects to reduce the high rate of failure and associated high costs. Phase 0 involves testing the drug in humans at a very tiny dose early on in the drug development pipeline (4) .

At the small doses used, avoiding risks of toxicity and sparing costs of large scale production, microdosing would give us an idea of how the human body processes the drug and whether it is effectively hitting its target in the right place in the body. Scientists can monitor the tiny dose as it passes through the body using highly sensitive imaging techniques, to see for example whether the chemical passes across the gut wall, how long it lasts in the body and which organs it distributes to, how it is broken down, and how it is excreted.

Collectively these processes make up what is called the drug’s pharmacokinetic properties. Normally, pharmacokinetics is first assessed in animals, but animal models are often poor predictors of pharmacokinetics in humans, and can obscure interpretations of how effective a drug will actually be.

Lost in Translation

Let’s for a moment imagine a world where animals don’t suffer, where they are merely dolls with robot hearts and unfeeling brains. Separate from any moral predicament, the use of animals in research is still, I believe, unjustified. Not only is it extremely costly to breed and home these genetically manipulated beings, but they don’t actually work very well. The ability of animal models to predict human drug responses is tenuous at best.

Findings which appear highly promising in animal studies most often fail to translate to human trials and rarely make a dent in human clinical practice. On the other hand, we can assume  that many drugs which are abandoned after fruitless studies in animals, may actually have held some clinical benefit. This is true across a wide range of disease areas (5).

A systematic review published in the British Medical Journal in 2007, compared all animal data and human data collected for six different treatments across a broad spectrum of diseases (6). For 50% of treatments, the authors reported major discordance between the results form animal and human experiments. In other words, the animal data was no more likely to predict whether these treatments would be safe and effective in humans than a toss of a coin.

It is important to understand that this is not solely an ethical debate for animal welfare, but for human welfare too.

Mouse and man share only about 80% of genes. It is no wonder that they replicate complex biological endpoints with such limited accuracy.

The paradox is that the more similar an animal is to humans in its physiology, the more useful a model it is to address biomedical problems, but also the more likely it is to experience similar mental states.

“The more justified the use of a species is on scientific grounds, the less justified it is on moral grounds”, says Hal Herzog, author of the book “Some we love, Some we hate, Some we eat”. Herzog, an anthrozoologist and psychologist, has written extensively about the complex psychology of human animal interactions, including the moral disconnectedness in our attitude towards animal research.

“But remember that one time when something good came out of it?”

Considering the sheer quantity of animals being used, animal research will inevitably stumble upon a few handsome successes simply by chance. Communities involved in animal research continue to back  claims for its indispensable value with the same handful of selected instances, where use of an animal model once upon a time produced some significant clinical benefit. Here is a table provided by the National Institute of Health (7). These seven feeble examples are feats we accomplished decades ago.

animal research saves lives

I would love to see some examples from the last decade, during which about a quarter of a billion rodents, and lesser millions of other animals have been created, used and killed for medical progresses that were never fulfilled. It more current examples were out there, they would be the ones being advertised.

This report attempts to justify animal experimentation with cringeworthy arguments like this one:

“Scientists study animals because they are a lot like people when it comes to basic body functions like breathing, eating, hearing, and seeing.”

Oh look! Here’s a thing that breathes! That must mean surely that it is similar to a human in every meaningful way – surely every molecular pathway and enzymatic reaction going on inside its body is carried out exactly like ours. What’s more, it even eats, sees and hears! Indeed, we are essentially twins.

These instances of successful translation are few and far between. Meaningful genetic and epigenetic differences between man and rodent, and even non-human primates, gives rise to interspecies variation in molecular pathways and metabolic processes which control a body’s response to a drug.

How we process drugs largely comes down to enzymes – the biological catalysts which break drugs down, inactivate them, and in some cases activate them. Often, mouse enzymes differ from ours in small but important ways. Rodents express more of particular enzymes and less of others. They differ in their rates of activity and how strongly they bind to drugs and mediate their effects.

This is not “animal testing in the name of scientific progress”. It may even be “animal testing in the name of scientific detriment”.

Humane Killing

In some cases, animals die as direct result of the experiment. For example in drug lethality testing, substances are forcibly fed to animals at increasing doses, for the purpose of calculating the amount which will kill 50% of animals, called the LD50.

However, most experiments do not require the animals to be killed. Many experiments do not in themselves involve pain, and lab animals are usually housed and treated with much higher standards of care than animals raised for food. But even if no suffering occurs during the experiment itself, what happens afterwards?

Once all of the desired data has been collected, most animals will  meet the inevitable fate of euthanasia, usually using Carbon Dioxide (CO2).

The familiar oxymoron “humane killing” is a pervasive term in these circles. Even  if a “kind murder” did exist, CO2 would not fit the definition. Studies have found that animals exposed to even low concentrations of CO2 release high levels of the stress response hormones adrenaline and noradrenaline.

Moreover, CO2 causes what is known as “conditioned place aversion” in rodents – they learn to avoid places where they have been previously exposed to CO2. They will avoid CO2 even if it means missing out on a highly desired pleasurable food reward or exposing themselves to other painful stimuli in non-CO2 environments (8). This indicates a strong negative emotional response, and coupled with elevated stress hormones, is clear evidence that this method of euthanasia is for animals a distressing death.

Giving Animals Human Diseases

Many of the diseases which are studied using animal models do not even naturally occur in animals. Naturally, rodents rarely develop most common human diseases like cancer, heart disease and diabetes. To study such diseases in them, and to investigate the effects of drugs, the disease first needs to be created in the model.

In cancer research this is done by genetic manipulation; for heart diseases, diabetes and obesity, a mixture of genetic manipulation and dietary intervention is used.  These methods do not adequately reflect the complexity of these diseases in humans, in whom the process develops naturally and over a much longer timeframe.

Forcing the most dreaded of human diseases like cancer on innocent animals from birth to death, and pumping their bodies with massive doses of experimental drugs, is not something any sentient being would consent to if he had a voice.


What do the World’s Leading Academics have to say?

In 2015, Oxford University’s Centre for Animal Ethics, in partnership with Cruelty Free International, commissioned a report on the ethics of animal use in research entitled “Normalising the Unthinkable”.  An international group of academic experts, ethicists and scientists came together to discuss their views on the subject. The report highlights the need to denormalise and deinstitutionalise animal research (9).

“The deliberate and routine abuse of innocent, sentient animals involving harm, pain, suffering, stressful confinement, manipulation, trade, and death should be unthinkable. Yet animal experimentation is just that: the ‘normalisation of the unthinkable’”.

Doing harm to animals is especially difficult because animals cannot give or withdraw their consent. They cannot vocalise or express their own interests. They are vulnerable and relatively defenceless.

For a summary of thoughts from the Oxford Centre, have a look at this short film.

Emeritus Professor of Veterinary Medicine at University of California, Davis, Dr Nedim C. Buyukmihci, expresses his views at the Oxford Summer School for Animal Ethics:

“We do to other animals things that we would find abhorrent if we did them to each other. We have to ask ourselves: “Why is it that we do not do these things to each other?” Because from a scientific perspective, we could learn a lot more, a lot more quickly, and with far greater benefits for ourselves, if we used people. All the experiments we do now in other animals – we don’t do these things in people because we say they have certain values and certain traits that we want to protect. My argument is that other animals – particularly mammals, for example nonhuman primates – have exactly the same traits and we cannot do things to them that we’re not willing to do to ourselves.”

Professor Stephen F. Eisenman from North Western University highlights the personal and psychological problems which permeate these settings. He says scientists are guilty of what he calls “splitting” animals seen as pets to be loved and cherished are psychologically split into a separate category from those seen as tools to be experimented on in whatever way humans desire.

“Getting scientists to recognise that the dog you have in your home is no different from the dog you’re doing research on in the laboratory, is a very hard task”.

Why is it that we react with visceral disgust when we see a man kicking a dog in the street, but not when we see a man in a clean white coat injecting a toxic substance into a mouse, or even a beagle, in a clean white laboratory?

It seems the human race is suffering from a case of Moral Schizophrenia – a term coined by American legal Scholar, Gary Francione, to describe humanity’s ambivalent relationship with other animals. The term describes the conflict between the stated desire not to cause animals unnecessary pain and suffering, and the continued support of practices that cause pain and suffering that cannot be regarded as “necessary” in any normal sense of the word.

New ways of doing things

Mouse may not be quite like man, but he is much more like man than a layer of cells in a petri dish. Mouse has a mouth, a digestive system and blood vessels. He has a liver that breaks down drugs, and two kidneys that flush drugs out. He is almost a perfect match, but not quite.

Thankfully, many in the scientific community are increasingly recognising the need to replace animal models with alternative tools – not only for ethical reasons but in order for science and medicine to flourish. Classical cell culture will not replace animals models, but it is no longer the only alternative we have.

During the past two decades, a number of impressive technological advancements have emerged which promise to replace failing animal models. These novel systems include human organs on chips, miniature organoids created using human stem cells, and computer models of disease. As these new methods become more physiologically relevant, we might envision a future of research free from animal experimentation.

The scientific community needs to shift from “progress-oriented” to “success-oriented” research. Success-oriented research requires human-relevant models that animal experimentation can never provide.

Animals are not instruments, objects, commodities, machines or tools. They have not been placed on Earth for us to breed, use and discard. They have complex interior lives, experiences and emotions that deserve respect.

Veganism in an age of Climate Emergency


What is the Climate Emergency?

Earlier this month, Ireland became the second country to declare a climate emergency, following the UK government’s commitment to achieve net zero carbon emissions by 2050. This goal, according to the Intergovernmental Panel on Climate Change (IPCC) 2018 report, will be necessary to limit warming to the critical threshold of 1.5°C, urging governments that immediate action is needed to avert disaster. Recognising climate change as the greatest challenge humanity now faces, EU leaders are placing climate action at the top of the agenda for the next five years.

Do we need to change our diet?

What does diet have to do with climate change? Many climate scientists, politicians and activists have admitted, sometimes grudgingly, that reducing or eliminating our consumption of meat and dairy can have a massive impact on our warming planet. Such a simple dietary shift – a decision made three times daily – may in fact do much more to reduce carbon emissions than any other lifestyle change like driving electric cars or avoiding air travel. Like any lifestyle change, going vegan alone will not save the planet, and of course changes in policy are desperately needed to augment the wave of individual action. Nevertheless, as individuals, going vegan – or at least avoiding meat and dairy – is probably the single most impactful way we can reduce environmental damage.

The Science

In May 2018, researchers from the University of Oxford released a ground-breaking study, comprehensively laying bare the true environmental cost of animal agriculture. The authors, Poole and Nemecek, insist that going vegan could reduce global farmland use  by more than 75% – an area equivalent to the US, China, European Union and Australia combined – while still growing enough food to feed the Earth’s population. “Moving from current diets to a diet that excludes animal products has transformative potential”, they conclude. As well as dramatically reducing global land use, such a transition could reduce food’s greenhouse gas emissions by 6.6 billion metric tons of CO2 equivalent (a 49% reduction); reduce acidification by ~50% and eutrophication by ~49%. These are dramatic statistics.

“If cows were a country”, says Bill Gates, founder of Microsoft, “they would be the third largest emitter of greenhouse gases”. Like slaughterhouses, greenhouse gases are invisible. This makes it easy for us to pretend that they don’t exist. We don’t perceive them with our eyes, but we are seeing their effects. Farming of animals accounts for 16.5 percent of global carbon emissions – the second contributor after the entire transportation system – yet much less talked about. The animal sector is responsible for a third of all anthropogenic methane (arising from human activity) and two-thirds of nitrous oxide emissions – both are potent greenhouse gases which trap more heat, and so cause more warming, compared to carbon dioxide. However, the myopic view that environmental issues relate solely to greenhouse gas emissions must be corrected. In this regard, the impact of animal agriculture extends far beyond greenhouse gases, contributing enormously to global acidification, eutrophication, land and water shortages and vast ocean dead zones from agricultural pollution. It uses about 70% of agricultural land, and is one of the leading causes of deforestation and biodiversity loss.

Although meat and dairy provides just 18% of calories, farming of animals for meat and dairy currently uses 83% of farmland, and accounts for 60% of agricultures greenhouse gas emissions. This is an increasingly imbalanced and inefficient system. Put simply, much more plant foods need to be grown to feed animals, therefore requiring much more land and water use to produce a calorie of meat or milk to ultimately feed a human, while much less resources are needed to directly feed the calories from vegetables and grains to the human. It takes 2500 gallons of water to produce just one pound of beef; 1000 gallons of water to produce one gallon of milk. They used to tell us, to save the planet, not to let the faucet run while you’re brushing your teeth; to take a shower instead of a bath. They never told us that agriculture was responsible for 80-90% of water consumption, as they blindly loaded its product onto our plates. Every day, humans throughout the world consume on average 5.2 billion gallons of water and 21 billion pounds of food, while livestock consume 45 billion gallons of water and 135 billion pounds of food. We act as though this makes sense.

With a growing population and an increasing demand for meat and milk, forests are being cleared at an alarming rate, leading to habitat destruction and species extinction. On May 6th 2019, a paper appeared in the journal Nature, threateningly entitled: “Humans are driving one million species to extinction.” Reporting disturbing findings from the UN’s Science-Policy Platform on Biodiversity and Ecosystem Services Intergovernmental (IPBES), the report highlights that agricultural activity has had the largest impact on ecosystems. The current rate of species extinction is already tens to hundreds of times higher than the average over the past ten million years, and is expected to increase as temperatures rise and farming continues – business as usual. I like to think that no human being would knowingly contribute to the destruction of a species, but we have, and I fear our own species may be destined to a similar dismal fate.cowspiracy_facts2-1024x1021

The Outlook

There is no longer room for ambiguity. The weight of the science is irrefutable, yet for years humans have clung to familiarity, while a few “extremists” crawled towards reform. Today, world leaders are in agreement – this is the greatest crisis the human race now faces, and without transformative economic, social and political reform, the human race may be its own Grim Reaper. We act as though eating animals is a requirement; a but it is not. We simply choose to do so. We are quick to make other small changes in our lives to save the planet, but our plates have not changed much. Emissions from animal agriculture are projected to increase by 80% by 2050 – but we want to reach net zero carbon by then. This needs to stop.

Perhaps never before has the truth been so plainly, and so stirringly put, than by 16 year old Swedish climate activist Greta Thunberg: ” If the emissions have to stop” she says, “then we must stop the emissions”, but “no one is acting as if we were in a crisis. Even most climate scientists or green politicians keep on flying around the world, eating meat and dairy.”

Collectively, human beings can be astonishingly powerful – indeed powerful enough to change the climate itself. It would be absurd to argue then that we are not capable of a simple lifestyle change – to choose bean over beef; to choose soy or oat over dairy milk. In 2019, friendlier alternatives to every animal product are available in most “normal” European supermarkets. We are all very capable of making this change, and I would argue that we have a responsibility to do so. We have a responsibility to do all in our power to repair the disaster which our species has so callously imparted on this planet. Our children and grandchildren, and the millions of other species with whom we share our lands and seas, have done nothing to deserve an uninhabitable Earth. The window of opportunity for change will never be as open as it is right now.


Transforming Cancer: When Cells Don’t Act Their Age

Inside your cells there is a peculiar molecule called Transforming growth factor beta – a fitting name for a superhero, or a super villain, and in fact TGFβ (scientists love acronyms) acts as both. As the name suggests, TGFβ’s most heralded function is to promote growth and differentiation of the cells in your body. Cell differentiation is the process whereby one specific cell type transforms into a different cell type. At times this process is critically important, such as during embryonic development, where the initial ball of undifferentiated cells gives rise to a human baby with specialised functional organs and tissues. Without TGFβ around to pull the puppet strings, none of this would be possible. Similarly, when the body is injured, TGFβ plays a role in the wound healing response. There are instances however, when this growth factor can be detrimental to your body’s condition. One of these is fibrosis, which is essentially the formation of scar tissue – this may not sound like such a dismal event, but too much fibrosis in organs such as the heart or kidney can be seriously damaging.


Another area in which TGFβ can have unfavorable effects is in cancer. The odd thing is that depending on the stage in cancer progression, TGFβ can act as either a tumour suppressor, or a tumour promoter. How can this be? Let’s consider a breast cancer cell in a newly formed tumour. At this stage, cancer cells desire nothing more than to keep on dividing. When cells accumulate cancer-causing mutations in their DNA, the cellular signalling pathways which normally tell cells to stop dividing or undergo apoptosis (programmed cell death) become deregulated, leading to the uncontrolled proliferation which is a hallmark of cancer. TGFβ can actually suppress this rogue behavior by causing growth arrest and halting cell cycle progression. But hang on… if TGFβ stops cancer growth, that’s great, right? Unfortunately the story of cancer becomes much more complex that that. Although initially a kind-hearted fellow, it is only in the later stages of cancer, when a tumour begins to leave its primary site and form distant metastasis, that TGFβ really turns rogue!


The majority of cancer deaths are not caused by the primary tumour, but by metastasis. With that in mind, what makes a cancer cell most aggressive is not its propensity to divide, but its ability to move. Movement is generally not a feature of early cancer cells, most of which derive from epithelial cells, which are firmly anchored to a bed of connective tissue called the basement membrane. After many cell divisions, and the accumulation of further cancer-promoting mutations,  the cells within the breast tumour will begin to express a number of genes which facilitate movement and invasion. These changes allow cancer cells to migrate away from their primary site and to invade through barriers such as blood vessel linings. Once cancer cells have disseminated into the bloodstream, they can travel around your body to reach different organs and set up camp there. It is this process of metastasis that causes cells from the breast to end up in foreign lands like the lung, liver, bone or brain. When TGFβ and its fellow signalling accomplices are overexpressed, cancer cells are more likely to develop such migratory characteristics, leading them to flee from home and cause destruction elsewhere in body. This transformation which TGFβ imparts on resident tumour cells is known as Epithelial to Mesenchymal Transition (EMT). The cells which form during EMT have similar properties to stem cells – cells which are capable of giving rise to multiple different cell types.  A remarkably similar processes occurs during embryonic development. This has led many researchers to turn to developmental biology in a desperate search for clues to better understand cancer. The pioneering cancer researcher, Robert Weinberg describes metastasis as “what happens when cancer cells don’t act their age.”


Cancer is the second leading cause of death worldwide, and in 2018, it is estimated to have caused 9.6 million deaths. In 90% of cases, it is in fact not the primary tumour which causes death, but metastasis. In an attempt to reduce this dreadful burden, many cancer researchers have set their sites on TGFβ and other potent mediators of metastasis. It is their hope that targeting proteins involved in these signalling pathways may lead to more effective treatments for cancer patients, but of course any drug which targets such an essential and pleiotropic signalling molecule presents many challenges. Will it be possible to dampen the harmful effects of TGFβ during metastasis while enhancing its beneficial activity during early tumour formation? Furthermore, will it be possible to modulate this pathway without disrupting TGFβ’s many diverse roles in normal human physiology?

adult biology chemical chemist
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Neu5GC – Alien Meat Sugars in Human Cancer

About 2 million years ago in evolutionary history, just prior to the emergence of the genus Homo, a pivotal event occurred in what was soon to become the human genetic code – inactivation of a gene called CMAH (cytidine monophosphate-N-acetylneuraminic acid hydroxylase). This gene encoded an enzyme which oversees the synthesis of a small sugar molecule called N-Glycolylneuraminic acid – Neu5GC for short. As such, Neu5GC is expressed in the bodies of most non-human mammals, but is not found naturally in humans.

Our species instead evolved to express higher levels of its precursor molecule – Neu5AC – which differs only in the placement of a single hydroxyl (OH) group added onto it by CMAH. Both are negatively charged sugar molecules called sialic acids, which decorate the surfaces of cells in the body.

Although we lack the gene which codes for its production, trace amounts of Neu5GC can still be found in many humans – in those of us who consume animal products in our diet, particularly red meats.

Deactivation of the CMAH gene is believed to confer a protective effect against certain pathogens. A type of malaria which can infect other primates, but not humans, requires an interaction with Neu5GC in order to cause disease. However, lack of CMAH may also explain the negative health effects of meat consumption.

Neu5GC, Chronic Inflammation and Human Cancer

Although it is not naturally produced in the human body, Neu5GC is detectable on the surface of human epithelial cells in meat-eaters – the cells which form a lining around all of our organs and are the most common cell type to give rise to cancer. Once it is ingested, Neu5GC can be metabolised in the human body and is incorporated into human tissues. Higher levels of this alien compound are found in cells of human cancers compared to healthy tissues. Scientists have yet to elucidate the exact pathway by which dietary Neu5GC is taken up into human tissues.

The human immune system is very good at identifying what is part of the human “self” and what is not. Anything that appears foreign, like an invading bacterium, triggers the production of antibodies which label it for destruction. When incorporated into human tissues, Neu5GC is recognised as a foreign threat, and we respond to it like we would to an infection – synthesising anti-Neu5GC antibodies in an attempt to rid it from our system. Continuous ingestion of Neu5GC and production of antibodies against it fosters a state of chronic inflammation – a state which underlies the pathogenesis of many human diseases, including our most relentless and insidious enemy – cancer.

Results from a 2014 study published in PNAS suggest that this meat-derived molecule may be to blame for the well-established red meat cancer connection. When the CMAH gene is knocked out in experimental mice to mimic the human deficiency, and then fed with Neu5GC and anti-Neu5GC antibodies, the mice develop systemic inflammation, along with a five-fold increased risk or cancer occurrence with long-term exposure (1).

Neu5GC is the first identified “xeno-autoantigen” which interacts with so-called “xeno-autoantibodies”. The prefix “Xeno” means “foreign” or “different in origin”, and “auto” means “self”. In other words, the body is producing antibodies to fight against a compound which now resides in its own cells – cells belonging to “self” – but a compound which is foreign in origin.

With continued, long-term meat consumption, these antigen-antibody complexes can promote a state of chronic inflammation known as “xenosialitis”. Neu5GC thus provides a plausible mechanism for the well known epidemiological link between red meat consumption and cancer risk, and may explain the curious human-specificity of this phenomenon.

Other common diseases such as heart disease, obesity and Type 2 diabetes, which are similarly aggravated by chronic inflammation, have also been linked to red meat consumption. Neu5GC, by stimulating a chronic inflammatory state, represents a likely offender in these diseases too. Loss of the CMAH gene in human evolution may in part explain the human-specific susceptibility to heart disease and cancer, to which other meat-eating mammals scarcely fall victim.

There is little doubt that red and processed meat consumption is a threat to human health. Evidence for a cancer link – especially colorectal cancer – is stronger than ever.  The World Health Organisation – the leading international body for public health – now classifies processed meat as a Group I carcinogen (definitely causing cancer), placing it in the same category as cigarette smoking, asbestos and radon. Red meat was declared a Group IIa carcinogen (probably causing cancer).

The 2008 World Cancer Research Fund expert report lists red meat among the top 10 factors which influence cancer incidence and progression (2).


One Meat, Many Means

Numerous mechanisms have been proposed to explain the cancer-causing effects of red meat, but no single theory has been agreed upon entirely. Heterocyclic amines, N-Nitroso compounds, polycyclic aromatic hydrocarbons, heme iron and TMAO have all been under inspection. Some of these compounds are activated to cancer-causing forms through cooking processes like grilling, whereas TMAO is formed by microorganisms in the gut when we offer them a meaty meal.

All of these compounds are believed to have DNA-damaging effects, causing mutations which can lead to cancer. Epithelial cells lining the colon are understandably the most susceptible because of their proximity to the digested meal, which can hang around in the colon for several days before being excreted.

One reason why a fibre-rich diet is protective against colon cancer is because dietary fibre speeds the transit of foods through the digestive tract. Less time spent sitting around in the intestine means less contact of colonic epithelial cells to the carcinogenic substance, and less chance of it causing a harmful mutation.


Differing from other prevailing theories, Neu5GC does not directly damage colon cells – rather, it triggers systemic inflammation, suggesting that meat consumption could encourage cancer growth in organs distant from the digestive tract.

Indeed, epidemiological evidence suggests that the red meat cancer connection is not specific to the colon. Results from a large prospective cohort study published in 2018, which included more than 61,000 French men and women, reported an increased overall cancer risk, and breast cancer risk (3).

Beyond Inflammation

Sialic acids like Neu5GC are important participants in cancer progression beyond the theory of xenosialitis described above. Elevated levels of sialic acids are detected in cancer cells – a phenomenon called hypersialylation. The alien Neu5GC is particularly favoured over human Neu5AC on tumour cell surfaces.

Hypersialylation is believed to influence the interactions of tumour cells with other cells in their locality in a way which supports metastatic spread – enhancing their ability to migrate out of their primary site and ultimately form additional tumours in distant organs. Hypersialylation might also help cancer cells to evade protective anti-tumour immune defences, thus enhancing tumour growth and survival (4).


R.A. Weinberg’s prominent textbook, “The Biology of Cancer”, has designated Neu5GC as an “area to watch”! Though certainly a compelling theory, it remains unanswered whether circulating levels of anti-Neu5GC antibodies in fact correlate with cancer risk in human populations.

Scientists are continuing to explore the Neu5GC pathway and other emerging theories in an attempt to untangle the complex mechanisms underlying the meat cancer connection. There has been some talk of developing anti-Neu5GC therapies which would rid the molecule from our bodies, or block its entry into human cells. Pursuit of such a drug seems to me counterintuitive, considering that we could simply choose not to introduce Neu5GC into the body in the first place. At least in the meantime, it would be wise for all of us to eliminate, or at least largely reduce our red meat intake in favour of whole plant foods, which are free from Neu5GC and other threatening carcinogens.

Why Don’t Animals get Heart Attacks? Vitamin C, Stress & Other Stories from the Wild.

Cardiovascular diseases and related events like heart attacks and strokes are the leading causes of death in humans today, causing more than 17 million deaths every year. Remarkably though, most other animals barely ever get heart attacks! Understanding why could help us to elucidate the biological underpinnings of this deadly disease in humans, and use these insights to design new medicines and preventative strategies. Let’s begin with a short introduction.

Heart Attacks: How do they Happen?

Most heart attacks and strokes are complications of atherosclerosis – narrowing and hardening of the arteries which supply oxygen and nutrients to the heart or brain. This chronic event develops over many years, during which a cholesterol-rich plaque accumulates at sites of damage in the artery wall, causing the vessel lumen to become narrow. Over time this plaque can grow and become covered in a hard fibrous cap, which can then rupture to release a clot into the artery. Eventually this can cause a blockage, which as you might imagine, can interrupt the flow of blood to the tissues and organs that that artery supplies. So if your coronary arteries supplying the heart become blocked , there won’t be enough oxygen and nutrients flowing to the heart which it needs to function normally. This can result in a heart attack – in medical terms, it’s called a myocardial infarction. The same thing can happen in a vessel supplying the brain, which instead can lead to a stroke.

In truth, the exact sequence of events which produce an atherosclerotic plaque is not completely understood, and what I am offering you is a wildly simplified version of reality. Atherosclerosis is a chronic inflammatory process, during which gangs of hungry immune cells called macrophages infiltrate the artery walls and become engorged with an oxidised form of LDL cholesterol (commonly known as “the bad cholesterol”). These lipid-laden immune cells are now called “Foam Cells” – a hallmark of early “fatty streaks” which proceed atherosclerosis and its complications.

So now that we have an idea of how it happens, we want to know why – or more importantly, in the case of most animals, why not?

What is it about animals that has allows them to dodge this epidemic while we humans suffer? Perhaps its because they’re not sitting around working office jobs, watching Netflix, reading blogs and feasting on greasy hamburgers and fries.

I would probably tell you,  if I believed in God, that this is his way of punishing us for all the torture we’ve been putting the poor animals through, and that if we all just went vegan, perhaps he’d leave our poor hearts and arteries alone. Having had that thought now I can’t erase it, because aside from the whole God delusion, it actual would make a lot of sense… But scientists don’t think so – they’ve come up with some other intriguing explanations. It turns out that animals have got some clever tricks up their sleeves!

Is it all about Cholesterol?

We know that many of the factors which increase heart disease risk in humans are related directly or indirectly to our diets – too much fat in the blood, obesity, diabetes and high blood pressure, can all be triggered by an unbalanced diet – in particular one high in cholesterol, processed foods and saturated animal fats, and low in vitamin-rich vegetables, fruits and wholegrains (1). Cholesterol is often pinned as the primary culprit, and while high cholesterol certainly is a major risk factor for heart disease, it is not solely to blame. In fact many animals, like bears, who have much higher levels of cholesterol than even the unhealthiest of humans, still manage to evade the cardiovascular curse (2). It’s clear then that cholesterol is only part of a larger picture, and sure enough, the drugs we’ve created to lower cholesterol like statins are only somewhat effective at reducing the burden of heart disease.

The Vitamin C Factory

“So, what have animals got that we haven’t?” you ask.

L-gulono-gamma-lactone oxidase! That’s what!

Haven’t you heard?

L-gulono-gamma-lactone oxidase is an enzyme that allows animals can make their own Vitamin C. On the other hand, we humans lack this enzyme, and instead rely on our diets to provide us with this essential vitamin. Viatmin C has been linked to cardiovascular health, and is often lacking in a typical Western diet. This offer some clarity as to why heart attacks are so rare amongst the animal kingdom. Some scientists have specultated that this deficiency in our Vitamin C factories might underly our increased susceptibility.

Vitamin C isn’t a particularly difficult one to come by – you will find it in high amounts in many common fruits and vegetables, especially kiwis, citrus fruits and cruciferous vegetables, which is again great news for us broccoli enthusiasts! But many of the foods which have scourged today’s western society, like meats, dairy and processed carbohydrates, contain very low levels – the slice of pickle and lettuce in your Big Mac won’t get you very far. Relying on these foods without adequate fruit and vegetable intake can result in deficiency. Serious deficiency is rare today in developed countries but can still occur in people with limited food variety. Why does this matter?

Vitamin C is a multifunctional nutrient and offers many health benefits:

  • It is required for biosynthesis and metabolism of important proteins, such as collagen, which plays a vital role in wound healing (3)
  • It enhances immune responses to help fight off colds, flus and other infections (4)
  • It is required for the synthesis of neurotransmitters – the chemicals that send messages between cells in your brain. It has been found to improve cognitive function and protect against age-related mental decline and Alzheimer’s disease (5)
  • It can help to lower blood pressure (6) and can keep our blood vessels operating healthily by improving the function of endothelial cells lining vessel walls (7).

Vitamin C is also a powerful antioxidant. Specifically, it is known to inhibit oxidation of LDL cholesterol, which we know is a pivotal event in the formation of “Foam Cells” which leads to atherosclerotic plaques. It is no wonder then that a low Vitamin C intake, coupled with elevated cholesterol, can increase your risk of heart disease. The natural ability of many animals to synthesise this vitamin endogenously may well confer some benefit to their hearts’ health.

Linus Pauling & Lessons from Evolution

Some researchers have hypothesised that modern man’s unfortunate susceptibility to cardiovascular disease may be tracked back to a distinct evolutionary event – a genetic switch which occurred 40 million years ago. At this point in history, the emerging human genome lost its instructions for synthesising Vitamin C, and gained expression of Lipoprotein A, which negatively impacts cardiovascular health (8). So animals which make their own Vitamin C do not express Lipoprotein A, while the opposite is true of us primates and a small number of other animals like the guinea pig and European hedgehog.

Vitamin C and Lipoprotein A serve similar functions in the body during wound healing responses and in the damaged artery wall, and both also function as antioxidants to prevent oxidation of lipids. This similarity in function suggests that Lipoprotein A may serve as a surrogate for Vitamin C in certain species following this evolutionary split. So now when we find ourselves deficient in vitamin C, the body’s response is to synthesise the functionally similar Lipoprotein A in an attempt to repair damage to the artery walls.

Interestingly, the inverse correlation of these two substances in cardiovascular diseases can also be observed in cancer, diabetes and other diseases. And guess what! Not only do most animals not get heart attacks, but they are also much less prone to developing cancer and diabetes! Although aetiologically diverse, these diseases do have certain commonalities – all these diseases involve a change in the integrity or stability of the tissue – particularly the extracellular matrix. This protein-rich network of macromolecules is found between and around adjacent cells and is important in providing these cells with structural and biochemical support, and so allowing our tissues to function properly. Biosynthesis of collagen – an important protein component of this matrix – is dependent on the activity of Vitamin C.

The collagenous matrix provides strength and stability to the artery walls, which need to withstand continual stress throughout the lifetime, flattening and stretching with every heart beat. Conceivably, vitamin deficiency can cause weakening and damage to the artery wall. The body responds by producing excess cholesterol in the liver and depositing it in the injured artery. Chronic deficiency can permit the build-up of oxidised LDLs in the artery wall, which over time can produce an atherosclerotic plaque and trigger a heart attack later down the line.

If I haven’t convinced you to eat your fruits and greens, perhaps Linus Pauling will. He was a lead author of the research I have just discussed – an unwavering Vitamin C enthusiast and the only person to have won two Nobel prizes – the first in Chemistry in 1954; the second, the Nobel Peace Prize in 1962. Here is a quote of his that makes me smile:

“Facts are the air of scientists. Without them you can never fly.”

Linus Pauling would want you to believe that you can magically cure almost anything by supplementing excessive doses of this vitamin, but much of the earlier research backing his bold claims has since been criticised. Pauling sadly died of prostate cancer in 1994, though he vehemently asserted that supplementing Vitamin C had delayed the onset of the disease, and that the majority of cancers could be prevented and cured by vitamin C alone!

When it comes to reducing our own risk of heart disease, more recent studies suggest little benefit of Vitamin C supplementation (9). Epidemiological data is conflicting – some studies suggesting a meaningful benefit and others suggesting none. Most clinical intervention trials – where thousands of individuals are given the supplement once  a day for many years, and compared to a control group not consuming the supplementary dose – have failed to find any benefit of Vitamin C for primary or secondary prevention of cardiovascular disease (9).

Eat Fruit not Pills

The authors of a 2008 meta-analysis, which included more than 370,000 people and a total of 7415 incidents of coronary heart dissease, concluded that increased dietary intake of antioxidant vitamins, but not supplementary intake has encouraging prospects for disease prevention (10).

Rather than turning to supplementary megadoses, we may be better off focusing on getting enough Vitamin C in our diet to avoid deficiency. Vitamin C is a water soluble vitamin, which means that any excess we take in beyond our body’s requirements will quickly be excreted in the urine rather than being stored in our tissues. Our cells become saturated with about 100-200mg, so if we’re already taking that much in our diet, a supplement won’t make any difference. Most epidemiological studies don’t take this into account and neglect to record Vitamin C levels in participants at baseline.

Supplementation may offer cardiovascular benefits in people with inadequate dietary levels – but won’t reap all the added benefits of consuming the whole fruits and vegetables, which of course are packed with many other antioxidants, vitamins, minerals and fibre.

For healthy adults, the recommended daily allowance (RDA) for vitamin C is about 60mg (recommendations differ from country to country). A lot of us get much more than that through a healthy diet. A single kiwi or one large orange will provide just about this! Some vegetables like broccoli contains even more, although most is lost from the vegetable during cooking.

Do Humans just Live too Long?

Some have suggested that animals don’t get heart attacks because they simply don’t live as long as we do. It usually takes many years for the fats in our arteries to build up into a fully formed atherosclerotic plaque. Heart attacks usually afflict us in middle and old age, though they can occur in younger individuals. However, this theory doesn’t explain why guinea pigs, who live only 8-10 years (and who like us, can’t make their own Vitamin C), develop arterial damage within just a few weeks when Vitamin C sources are removed from their diet.

Robert Sapolsky- A Case for Stress

The Vitamin C hypothesis isn’t the only one out there. Some believe the difference all comes down to stress. A 2017 study published in The Lancet found that heightened activity in the amygdala – a region in the brain involved in stress – is associated with an increased risk of heart disease and stroke (11).

In response to a stressful event – like Climate Emergency and the Earth’s impending doom – your body starts to release higher levels of adrenaline – commonly referred to as the “stress hormone”. This causes your breathing and heart rate to temporarily speed up and your blood pressure to increase. Your body is clever – it’s not trying to give you a heart attack – this is its way of preparing for the “fight or flight” response to save you from a perceived threat or harmful event. If you were being attacked by a bear for example, your body would need to undergo certain physiological changes to provide a temporary increase in strength and reaction speed – increasing heart rate and blood flow to muscles in your legs.  But the increase in blood pressure, which adrenaline triggers, places an excess strain on the vessel walls, making them more prone to damage. Such damage then triggers a series of complex inflammatory reactions which drives the slow process of atherosclerosis. It’s hard to be human.

As well as directly impacting heart disease risk by elevating blood pressure, stress can also have indirect effects on heart health. Humans like to “manage” their stress by turning to harmful habits like smoking, excessive alcohol consumption and overeating unhealthy foods which can all increase heart disease risk. Animals experience stress too, but they don’t react to it the way we do. In recent decades, we humans, faced with increasing societal pressures and complex emotional lives, are experiencing psychosocial stress more commonly that ever before.

Robert Sapolsky, Professor of Biological Sciences and Neurology, has spent decades investigating the effects of stress on health and disease. He explains that, like other animals, our body’s have adapted well to dealing with acute physical stressors, but when the same responses are triggered in the long-term for purely psychosocial reasons, stress can wreak havoc on our physical health. Most animals don’t experience these kinds of long-term stresses – the kind brought on by social pressures, work deadlines, exams and relationship problems. Not only can chronic stress elevate blood pressure and increase our cardiovascular disease risk, but can also increase the risk of developing diabetes, gastrointestinal and neurological disorders and infections (12).


Chronic stress can also affect our gut microbes. There’s a lot of crosstalk going on between the brain and the gut. The gut even contains its own nervous system – the Enteric Nervous System or “Second Brain” which contains some 100 million neurons. Changes in the bacterial populations hanging out in our guts, which can be triggered by chronic stress, poor diet, or medications, have been linked to several human diseases including heart disease (13) .


Heart disease is an exceptionally complex and multifactorial condition. It is unlikely to be explained by any single simple theory or trigger, nor curable by any single silver bullet nutrient or wonder drug. Nevertheless it is intriguing to speculate – Why don’t animals get heart disease? Why has evolution been so cruel? Alas, this mysterious phenomenon remains a subject of debate. What’s your take?

A Vague Anxiety as the Planet Burns

Yesterday I visited the Irish Museum of Modern Art (IMMA) – one of my all time favourite spots in Dublin – and was particularly moved by one exhibition entitled “A Vague Anxiety”. A Vague Anxiety reflects on some pressing concerns of Generation Y in our rapidly evolving and increasingly fragile society – from global warming and the housing crisis, to mental health, gender identity and hookup culture. These issues hover gloomily and unmoving over the lives of todays youth. The exhibition got me thinking particularly about climate change, and how our feelings about it, and the tensions surrounding it, though ever-present, are somehow cloaked in mist. Our concerns about the changing climate vaguely occupy the shadowy background of our everyday lives. We feel a sense of urgency – overwhelming urgency – we try to act – but question the futility of our actions. We feel a disconnectedness, a fearful tension, a childish helplessness. We have been handed a dying Earth – a mysterious object of concern. We look at it despairingly, not quite sure what to be concerned about, nor to what degree concern is required. We can grasp the magnitude of the issue, yet each one of us knows he is but one person on a planet of billions. The climate is a complex and dynamic system, yet in our hurry to understand it, the media pumps us with fragmented and disordered information. We are full of information (and misinformation), yet we feel empty of knowledge, and this paralyses us. It is tempting to turn our eyes away and bury our heads as the planet burns – after all, humans have been doing it for years, as though it were a dream.


The piercing headlines scream at us:

“Humans are driving one million species to extinction”,

“250,000 deaths a year from Climate Change”,

“CO2 levels at highest for 3 million years – when seas were 20 metres higher”,

“Polar ice sheets melting faster in the last 20 years than in the last 10,000”

Yet we feel paralysed.

Is Eco-anxiety Real?

In 2017, the American Psychological Association (APA) released a report which details the impacts of climate change on mental health. It describes climate anxiety, or “Eco-anxiety” as “a chronic fear of environmental doom” – a stress caused by watching the “slow and seemingly irrevocable impacts of climate change unfold, and worrying about the future for oneself, ones children, and later generations”. It carries with it feelings of loss, helplessness and frustration as we question the ultimate avail of our well intended actions.

The 16 year old climate activist Greta Thurnberg has been a victim of climate anxiety, speaking openly about her depression for which she says the climate crisis was in part to blame. “I kept thinking about it and I just wondered if I am going to have a future,” she says, in an interview for the Guardian. “And I kept that to myself because I’m not very much of a talker, and that wasn’t healthy. I became very depressed and stopped going to school. When I was home, my parents took care of me, and we started talking because we had nothing else to do.  I told them about my worries and concerns about the climate crisis and the environment. And it felt good to just get that off my chest.”


Eco-anxiety: In Search of a Cure

If you are suffering from climate anxiety, I believe the only way out is action, and while individual action may not save the planet, collective individual action will. There are many small changes that we can make in our daily lives that really do make a difference. We can choose to reduce our own emissions by driving less, buying less and wasting less. We can choose to walk, bike or scoot, buy vintage or second-hand, use reusable cups, bottles, bags, straws and menstrual cups. We can vote for planet-conscious politicians,  join activist groups and continue to educate ourselves and others about these pressing concerns. But one of the easiest, most impactful, and often overlooked ways we can reduce our environmental burden today is through our diet. It is often underestimated just how much of an influence our food choices are having on the planet, but there are many smart changes we should be making as consumers as we strive to create a healthier Earth – and many are healthier for our bodies too!

How to Eat for the Planet

  • Going vegan is the single most impactful change you can make to help the environment – not only to reduce greenhouse gas emissions, but also land and water use, soil and water pollution and biodiversity loss. Check out my recent post on Veganism in the Age of Climate Emergency, where I look at some findings from recent research. I would also recommend taking a look at Cowspiracy facts page, and also this 2018 Study from Oxford University researchers Poole and Nemecek. Going vegan has been the most fulfilling decision I have ever made. Nothing eases the eco-anxiety more than knowing I am making conscious planet-friendly food choices three times a day, while also benefiting my own physical and mental health, and reducing the suffering and misuse of other beings who share our planet.
  • Start with small changes. Going completely plant-based in not an easy transition for everyone. Even with so many plant based options available in supermarkets today, it can be strange to stray from eating habits that have been called “normal” all of our lives. As children, we were never taught in schools how much our diet impacts the planet, so it can be difficult to come to terms with. If you’re not keen on going vegan just yet, you can still make an enormous impact simply by cutting out (or cutting down!) red meat and dairy. The livestock industry is by far the most damaging to the planet – in fact, if cows were a country, they would be the third largest emitter of greenhouse gases after China and the US! Oat and soy milk are excellent planet-friendly alternatives! The BBC have created a food impact calculator where you can check out how your own food choices are affecting our Earth. I hope we will soon see this information included in food labels alongside nutritional contents.
  • Reduce food waste. Make sure that everything you buy – especially if you’re buying animal products – is actually ending up in somebody’s belly (although it would be best if animal products did not end up in your belly!). Remember that when we waste food, we’re wasting all of the resources that go into growing it, transporting it, processing it, packaging it, as well as all the human labour going into the process, and of course our own money, and not reaping any of the benefits. 33% of all food grown globally goes to waste – 40% in the US – according to a 2012 NRDC report. As a vegan I find these statistics deeply distressing. This means that so many of the animals we kill for food are not even being eaten, and meanwhile some 795 million people in the world – about one in nine of us – do not have enough food to lead healthy active lives.
  • Choose locally made foods. Eating foods grown close to home results in a lower carbon footprint than those which need to be transported long distances. We are often told to walk or cycle, drive less and limit air travel, but it is easy to forget that everything we consume or buy needs to travel to us too! Foods can’t walk, cycle, scoot, fly or swim (well, animals can, but we’ve already established that it’s best not to eat them anyway!) – the fact is that anything produced overseas has to be transported by air or water, which automatically adds to the emissions caused by actually growing it. Food miles are the new calories! It’s time we stop thinking about food simply as something that will or will not make us fat or happy.
  • Reduce food packaging. So much of our food today is packaged in plastic and much of it is completely unnecessary – even fruits and vegetables are sold to us in plastic trays within plastic sleeves. Choosing mostly unpackaged whole foods and buying in bulk can help to minimise this. Remember too that just because something is “recyclable”, it does not mean it will be recycled. The truth is that only about 20% of plastic waste is recycled – most instead is discarded, ending up in landfills and polluting our oceans with dismal environmental consequences. You can learn more about plastic waste here.

Knowledge is Power

In the age of the internet, information is more accessible than ever, and it is certainly empowering to know that we can educate ourselves around this issue, where schools have largely failed to. I would definitely encourage reading and sharing primary research studies like that of Poole and Nemecek, but for “lighter” learning, there are many excellent and eye-opening documentaries out there too.  Check out Cowspiracy on Netflix, and Leonardo DiCaprio’s Before The Flood. I myself have been hugely inspired by a number of YouTube environmentalists who create comprehensive and accessible videos about these and other pressing issues. Some of my favourites are Kristin Leo, Sedona Christina, Madeline Olivia and of course Mic the Vegan.

Your Mental Health

Mind your head! Todays youth are growing up in a world drastically unlike that of previous generations. Of the many global issues lingering over our minds, climate change has certainly taken its toll on our mental health. The role of mental health professionals in today’s society is perhaps more important than ever. “Climate change is a human-caused problem, which is more difficult to cope with than disasters that are beyond human control.” says clinical psychologist Thomas Doherty PsyD in the APA’s 2017 report. “Mental health professionals can help give people  a sense of power over how they respond.”



So are we doomed to live in this state of vague anxiety forever? The way I see it, there are two ways to avoid it: the first is ignorance; the second is action. The urgency of climate change and its consequences demands that we choose the latter path. Whether it empowers or disables us is within our hands, but this window of opportunity will not remain open for ever. We must act now.

Food For Thought: The Choice to Eat an Animal

Why are you vegan? It’s not an easy question to answer, especially during a rushed social encounter. I find myself stumbling over my words, desperately trying to squeeze the entire bloody universe into one or two non-threatening sentences. I’ve toyed with the idea of printing out brochures, neatly bullet-pointing my “opinions” and “feelings” about animals and food.

While my lifestyle choices differ from those of most humans, I do not think I am at all unique in my actual beliefs about animals. I certainly do not love animals more than most people I know. In fact I am often blown away by the bonds I observe between humans and their dogs – the depths of their affection – the sparkle in their eyes. Many even claim to love their pets more than they love their friends, their partners, and even their children. While I too love dogs, I am not at all keen on sloppy licks, I don’t enjoy sharing my dinner, and I would never sleep in the same bed as one. The idea that eating animals and their byproducts is unethical, is not something I consider to be a personal, unique or radical opinion. It is an opinion that I believe all homo sapiens share, though all too often, it is stifled.

It takes courage to question the beliefs we have been taught since day one. Since the day you learnt to chew, your mother placed meat on your plate and sent you to school with ham and cheese sandwiches, yogurts and kisses. Daddy told you milk would make your bones grow big and strong, rewarded you with ice-cream, chocolate and cake. To your baby brain, a sausage was not a pig, a steak was not a cow, and chicken wings were never made to fly. You may have also had a cat or dog at home – a fluffy thing that likes belly rubs and walks in the park. Your mother never had to tell you not to take a knife to his throat or sink your teeth into his warm flesh. This is never something you had the desire to do. In western countries like the US and Europe, eating cats and dogs is unnatural and disgusting, while eating cows, pigs and chickens is normal and even healthy. This disconnect in our collective attitude towards other animals is taught to us from birth, and it is not backed by logic, science or reason. Pigs, like dogs, are social animals. Cows, like cats, are highly intelligent creatures. These animals, like humans, all feel pain, feel joy, and have the common ability to suffer. It is my opinion that every individual life is incredibly beautiful, valuable and important, regardless of the size of its paws, the length of its whiskers or the shape of its ears.

“You put a baby in a crib with an apple (or perhaps a bowl of apple puree, depending on the age of the baby) and a rabbit. If it eats the rabbit and plays with the apple, I’ll buy you a new car.” This famous quote by the author Harvey Diamond is meant to demonstrate that eating animals is not a natural or intuitive human behavior, but a product of our society. Let’s expand on this idea: If you place a hungry adult in a locked room with an apple and a rabbit, which will he eat? How about if you add a knife and an oven into the mix? If you were this adult, what would you eat? Unless you are allergic to apples, or have has a particularly unpleasant experience with one very violent rabbit that has made you despise the entire rabbit population, I would bet you would first eat the fruit. Then perhaps after a day or two, after the rabbit dies a natural death, you might then cook and eat it to save yourself from dying of hunger too. If you are especially kind, you might even half the apple and share it with the rabbit (but I certainly wouldn’t give up any of my final apple, unless he was incredibly fluffy rabbit). You get the idea – if you had to personally slaughter and prepare every animal you ate, I bet you would eat a lot fewer animals, if any at all.

I am not so egocentric (and I think you might think similarly) as to believe that my life is so much more valuable, that it is worth sacrificing the life of another individual, perhaps two or three times a day, for each day that I exist on Earth – certainly not when my taste buds can be equally pleasured by foods which do not require such an atrocity. Why is it that we place such value on the sense of taste, above all other human senses? If the scream of a cow was to make the most beautiful sweet song, would you slaughter it to hear that music? If the blood of a horse could produce the most exquisite works of art, would you kill it to see those paintings? Many condemn the use of fur for clothing, while eagerly sporting  leather and wool coats. Many criticise animal testing for cosmetics, while routinely purchasing meat, dairy and eggs for food. There is a murky disconnect in the way we humans think about and treat animals, and it needs to change.

Every day, I choose to be vegan because I sincerely value every individual life, and I do not want to be responsible for his/her suffering. There is a problem in the way we humans think about animal abuse and suffering – we think about “The cows” and “The chickens” as collective entities. Rarely do we consider each individual being – a being with its own family, its own unique personality, the potential to acquire passions, hopes and dreams. Every time that you pay for a chicken burger or a packet of sliced ham, you must know that you are paying for suffering, cruelty and murder of individual lives.

Now, do not think that I would ever favour the life of a cow, a pig or a chicken over the life of a human. If faced with the choice of killing a young calf or a young boy, while it would pain me to commit either murder, being a member of my own species, of course I would favour the boy. I hear this spouted sometimes as an argument against veganism – that human lives are more valuable than animal lives – but this argument is meaningless, because veganism causes not harm to human lives, it only saves animal lives.. So let’s assume that a human life is inherently more valuable than the life of a calf. How many calf lives would you say are equally valuable to the life of a single human boy? Ten calves? One hundred? One thousand? There is of course scope to argue that the human boy would likely cause the deaths of thousands of calves and other animals during his lifetime, and therefore from the perspective of limiting suffering, killing the boy would be the obvious ethical choice.

When it comes to animal exploitation, the magnitude of the suffering – the actual numbers – are rarely considered. Did you know that more animals are killed for food every day in the US than humans have been killed in all the great wars of history? Did you know that on average, a human in western society is responsible for the death of one animal per day? – given the average life expectancy in 2018 is 82 years, that’s about 29,848 individual deaths that you, as a meat eater, are paying your hard-earned money for in your lifetime. These figures only take into account land animals. Humans care more (though seemingly not much) about things with hair and legs. The amount of individual fish killed per day for food is too large to calculate, and instead is measured by mass. The estimated annual fish kill is a whopping 970-2700 billion – almost four hundred times more than the amount of humans on the planet today. I cannot provide you with the exact figures of your own daily impact, nor do I think such figures would offer you much solace. What i can do is shed a light on the magnitude of this problem, and urge you to reflect on your values and choices. Do you truly value the individual life? Are you opposed to undeserved suffering and murder? Do your everyday behaviours align with these values? If not, why? It is easy to live in denial – to continue to follow established habits and repress better judgement. It takes courage to make a change, to educate yourself and free yourself from destructive societal norms. I encourage you to be so courageous.