In preparation for Stoic Camp New York 2015 I have been reading one of Plato’s dialogues, the Euthydemus. My co-organizer, Greg Lopez, and I picked it because it is crucial to understand the Stoic concept of wisdom.
The version I have is published by Focus, with an introduction by Denise Schaeffer, translation by Gregory McBrayer and Mary Nichols, and a nice and very informative accompanying essay by Nichols and Schaeffer.
It’s a bit of a weird dialogue, and it was neglected by scholars until recently. It features Socrates (of course), engaging two Sophists — Euthydemus, and his brother Dionysodorus — who sound for all the world like the caricatures of a pair of modern academic postmodernists. The strange thing, though, is that it isn’t clear the extent to which Socrates himself takes these two characters seriously, even at some point professing admiration for them and their ways, as opposed to displaying his sarcasm at…
Despite the near-universal acceptance of the benefits of vaccination, some people still worry about risks associated with their use. Luckily, scientists are vigilant about identifying possible risks, so they can be addressed before problems emerge.
Still, people sometimes forget that science is the process by which we arrive at solutions. And they worry about incremental scientific steps that often expose weakness in these solutions.
A recent study published in the journal PLOS Biology, for instance, was presented by some media as claiming that certain vaccines make viruses more dangerous. The research showed chickens treated with its vaccine are more likely to spread a highly virulent strain of Marek’s disease virus, a condition that affects poultry.
The reason was simple: the vaccine used in the study targets Marek’s disease, not the virus that causes it. These types of vaccines are known as “leaky vaccines” because they don’t affect the ability of the virus to reproduce and spread to others; they simply prevent the virus from causing disease.
Marek’s disease vaccines use a non-disease-causing virus to infect cells. This preventive infection stops tumour formation and death when those cells are infected by the Marek’s disease virus.
But the virus can replicate and still produce more virus particle, which can infect other chickens. All Marek’s disease vaccines, since their introduction in the 1970s, have been leaky; they allow chickens to carry and spread the virus without getting the disease.
The effect of leaky vaccines on how disease spreads is explained by the “imperfect-vaccine hypothesis”. It holds that, without vaccination, a very virulent virus can get into a population and kill infected hosts (people or animals) very quickly – before they have a chance to spread it. This means that the virus will die out very quickly too, as all potential hosts will be dead or immune to it.
A leaky vaccine can prevent the very virulent virus from killing the host, but doesn’t stop that host from spreading the virus to others. This means that a very virulent virus can survive for long periods in the vaccinated hosts. And it can continue to spread in this time, making it less likely to die out.
The PLOS Biology study showed chickens vaccinated against Marek’s disease were more likely to spread the disease to other chickens, than unvaccinated chickens were. The unvaccinated chickens all died in less than ten days – before they could spread the virus.
The vaccinated chickens, on the other hand, were protected from the disease so were able to spread the virus to other (unvaccinated) chickens for weeks and weeks. And they made those chickens immune to the virus in the process.
One of the reasons the researchers looked at Marek’s disease in chickens is because it has been getting progressively deadlier. Originally, the disease occurred mainly in older chickens and caused paralysis. But an acute form of the disease emerged in the 1950s and has since become the dominant form. This rather virulent version can kill up to 100% of unvaccinated birds.
Leaky but not sinking
But what does all this mean for the future of vaccination?
Well, the first thing to note is that in this study the vaccinated chickens always had the best outcome. In one experiment, only three out of 50 unvaccinated chickens survived the disease, while vaccination protected the majority of chickens (46 out of 50 survived).
The authors also noted that vaccination has been very effective in preventing deaths in chickens due to Marek’s disease. They said their study didn’t indicate whether vaccination played any role in the development of the serious form of Marek’s disease.
Vaccines prevent disease, even if they’re leaky. But it’s important to note there are currently no vaccines against viruses that infect humans that are leaky. Current human vaccines mimic the body’s own response to viruses.
But yet-to-be-developed vaccines for diseases such as HIV, Ebola or malaria, where humans have been unable to mount an effective natural defence, are likely to be leaky. And even imperfect vaccines for these illnesses would be an enormous step forward.
The possible effect of “leaky vaccines” on how viruses spread is an interesting new observation. But there are a number of other ways by which viruses can change in response to vaccination.
An arms race
One response of viruses to vaccines involves the evolution of viral proteins that allow them to escape the vaccine. This is known as “epitope evolution” and it’s the reason flu vaccines change each year.
Even if a vaccine is effective in preventing a particular strain of virus, other strains may take its place. This was a concern when the human papillomavirus (HPV) vaccine was introduced nearly ten years ago. But researchers have investigated whether any HPV types not in the vaccine have become more common since the vaccine was introduced and there’s no evidence this is happening.
The interaction between viruses and their targets can change over time. In the case of Marek’s disease, the infection has become progressively deadlier. Increased use of broiler chickens, lack of genetic diversity in flocks and high-density rearing may all have played a role in the changes seen in the disease.
The benefits of vaccination far outweigh its risks. And it is research like this that helps medical researchers actively identify possible dangers so we can safely continue to avoid the diseases that terrified our parents’ generation.
Sharks have inhabited this planet for more than 400 million years, and have survived five mass extinctions. Earth is now entering its sixth – this time caused by humans – and sharks are at the pointy end, with 90% of the species already considered threatened.
It is not just an issue on NSW’s surf breaks. Humanity’s growing demand for protein has put substantial pressure on oceanic systems, and industrial fishing techniques have have reduced predatory fish populations to less than 10% of their historic numbers. Sharks are especially vulnerable because of their low reproductive rates, slow growth and delayed rates of maturity.
What’s more, sharks play a pivotal role within the ecosystems they inhabit. As apex predators, they maintain community structure and biodiversity by regulating predator and prey abundance. Even light fishing pressure such as species-target line fisheries can cause dramatic declines in populations of large coastal sharks. Meanwhile, indirect fishing via shark meshing programs can catch a range of targeted and non-targeted species of sharks.
Blanket measures don’t tend to work well as a rule. AAP Image/Dave Hunt
What would a cull do to sharks and ecosystems?
Shark culling is best thought of as an indiscriminate method of removing sharks from our coastal ecosystems. The WA and Queensland culls have led to the capture and death of many non-targeted sharks. We also know that many shark species do not cope with capture well – a recent Australian study found that 100% of hammerheads caught by line fishing will die of stress within an hour of capture.
Similarly, spinner and dusky sharks have very low survival rates within the first few hours of being hooked, and sharks that are hooked and subsequently released do not necessarily survive.
Hooking in the gut is very common. New South Wales’ flagship threatened aquatic species, the greynurse shark, will most probably die over time if hooked in the gut and then released. Stainless steel hooks do not rust out but become encapsulated in the tissue over time, causing starvation, wasting of the body (known as cachexia), and eventual death.
If we remove sharks as top predators from the ecosystem, the effects will filter down to animals lower down the food chain and cause unexpected changes to ecosystems. We are already seeing such changes in areas where sharks are overfished.
Declines in the number of blacktip sharks in North Carolina in the late 1970s and 1980s caused an increase in the relative abundance of cownose rays and a corresponding decrease in scallops over the ensuing decades. Healthy aquatic ecosystems are typified by a complexity of players in the food chain, and removing such macropredators will result in decreasing ecosystem resilience.
What can we do instead of culling?
Indiscriminately culling sharks is dangerous to marine ecosystems, not to mention expensive and futile. We would be far better off allocating resources to achieving a greater understanding of the ecology and behaviour of these large predators. We can increase knowledge of why and where sharks are likely to attack humans by tagging sharks and following their movements over time, or through genetic studies that can assess effective population sizes.
Current aerial surveys are unlikely to be a successful strategy, however. Scientific analysis has already discredited aerial programs in NSW. Aerial surveys have only a 12.5% success rate in spotting a coastal shark from a fixed-wing aircraft, and a 17.1% success rate in helicopters. As surveys are only done for a few hours per week, and pass over a particular beach in minutes, these patrols can give the public a false sense of security.
Other non-invasive methods of mitigation are currently being developed, including the use of erratic walls of bubbles to deter sharks, and the development of wetsuits and surfboards that sharks are less likely to mistake as prey.
But ultimately, we also need to take personal responsibility, and reduce the likelihood of an attack by not swimming at dawn and dusk, not entering the water at the mouth of estuaries with poor visibility, or in areas of baitfish. After all, even sharks can make mistakes.
When Charles Darwin visited the Galapagos Islands in October 1835, he and his ship-mates on board HMS Beagle collected specimens of birds, including finches and mockingbirds, from various islands of the archipelago.
At the time, Darwin took little interest in the quaint finches, making only a one-word mention of them in his diary. As painstakingly shown by Frank Sulloway and more recently by John Van Whye, it wasn’t until two years later that the finches sparked Darwin’s interest.
By then he had received feedback from the leading taxonomist of the time, John Gould, that the samples comprised 14 distinct species, none of which had been previously described! Gould also noted that their “principal peculiarity consisted in the bill [i.e. beak] presenting several distinct modifications of form”.
So intrigued was Darwin by this variation in size and shape of beaks that in the second (1845) edition of Journal of Researches he included illustrations of the distinctive variation between species in the size and shape of their beaks. He added a comment that:
Seeing this gradation and diversity of structure in one small, intimately related group of birds, one might really fancy that from an original paucity of birds in this archipelago, one species had been taken and modified for different ends.
The famously varied beak shapes of the Galapagos finches, as illustrated in the second edition of Darwin’s Journal of Researches. Wikimedia
Unfortunately for Darwin, the closer he examined the available evidence on Galapagos finches, the more confusing the picture became. This was partly because the specimens available to him were not sufficiently labelled as to their island of collection.
Presumably, it was his doubt about the available evidence that resulted in Darwin making no mention of Galapagos finches in any edition of Origin of Species.
Why, then, do people now label them as “Darwin’s finches”, and why are these finches now regarded as a classical textbook example of his theory of evolution by natural selection?
Paragons of evolution
Despite not mentioning Galapagos finches, Darwin did make much use of evidence from other Galapagos species (especially mockingbirds) in Origin of Species.
As the influence of Origin of Species spread, so too did the evolutionary fame of the Galapagos Islands. Increasingly, other biologists were drawn into resolving the questions about finches that Darwin had left unanswered.
By the end of the 19th century, Galapagos finches were among the most studied of all birds. By the mid-20th century, there was abundant evidence that Galapagos finches had evolved to fill the range of ecological niches available in the archipelago – a classic example of evolution by adaptive radiation.
Beak size and shape were key attributes in determining adaptation to the different types of food available. In the second half of the 20th century, classic research by Princeton University’s Peter and Rosemary Grant provided evidence of quite strong natural selection on beak size and shape.
Under the hood
New light has also been shed on the evolution of Darwin’s finches in a paper recently published in Nature. In this latest research, the entire genomes of 120 individual birds from all Galapagos species plus two closely related species from other genera were sequenced.
The work was done by a team led by Swedish geneticist Leif Andersson, with major input from Peter and Rosemary Grant, who are still leading experts on the finches.
Comparison of sequence data enabled them to construct a comprehensive evolutionary tree based on variation across the entire finch genome. This has resulted in a revised taxonomy, increasing the number of species to 18.
The most striking feature of the genome-based tree is the evidence for matings between different populations, resulting in the occasional joining of two branches of the tree. This evidence of “horizontal” gene flow is consistent with field data on matings of finches gathered by the Grants.
A comparison of whole-genome sequence between two closely related groups of finches with contrasting beak shape (blunt versus pointed) identified at least 15 regions of chromosomes where the groups differ substantially in sequence.
Unity of life
The most striking difference between the two groups was observed in a chromosomal region containing a regulatory gene called ALX1. This gene encodes a polypeptide that switches other genes on and off by binding to their regulatory sequences.
Like other such genes, ALX1 is crucially involved in embryonic development. Indeed, mutations in ALX1 in humans and mice give rise to abnormal development of the head and face.
It is an extraordinary illustration of the underlying unity of all life on Earth that Leif Andersson and his colleagues have shown that the ALX1 gene also has a major effect on beak shape in finches, and that this gene has been subject to natural selection during the evolution of the Galapagos finches.
If Darwin were alive today, he would be astounded at the power of genomics tools such as those used in generating the results described in this paper. He would also be delighted to see such strong evidence not only in support of evolution but also in support of one of its major forces, natural selection.
As evolutionary scientists, we devote much of our working lives to exploring the behaviour of humans and other animals through an evolutionary lens. So it may come as a surprise that our show at this year’s Edinburgh Fringe is named Alas, Poor Darwin …?, borrowing from one of the most searing critiques of evolutionary psychology ever written. We’ve added a question mark, but still – it’s no simple tale of how our minds evolved.
Evolutionary theory is a bit like a chocolate ice cream in the hands of a two-year old: it’s going to get applied everywhere, but will anything useful be achieved in the process? The central tenets of Darwinian theory – variability, heredity and selection – are as beautiful as they are compelling. They completely revolutionised biology.
But applying these principles to the study of human behaviour has caused far more controversy. The evolutionary explanations for human behaviour that grab the headlines can often be neat; really neat – like tightly-plotted narratives in which everything works out perfectly in the end, usually with a guy getting a girl, where everything happens for a reason.
Real life rarely makes for such a neat story. We’ve all seen enough action movies to notice that the more satisfying the ending, the more plot holes you have to ignore as you walk out of the cinema. Neatness makes a good story, but it’s not enough for good science.
Ovulation meets evolution
One good example of this problem is the story of how women’s preferences for masculine male partners shift throughout the menstrual cycle in a strategic way. It goes like this: at the time of ovulation, when “good genes” are most important, women are attracted to more masculine men. For the rest of the menstrual cycle when faithfulness and cooperation are paramount, the opposite is true (we’re glossing over some subtleties that are explained here).
In a similar vein, there’s an elegant account of male violence. It says that men are more likely than women to behave aggressively everywhere in the world because in the Pleistocene epoch (between 10,000 and 1.7m years ago), humans had a polygynous mating system, meaning one man mating with several women. The men who succeeded in aggressive competition with other men had more partners, and therefore more children, and so more of their genes got passed on.
These stories prompt some awkward questions. For example does a change in women’s attraction have to be directly selected for? Could it be the by-product of some other evolutionary process? Can we be sure that the preferences reported in the lab by female undergraduates in 2015 are a good proxy for the real-life choices made by women 100,000 years ago? What evidence is there that our ancestors were polygynous? What selection pressures were acting on women while the men were all busy fighting? (Women’s genes also get passed on to their children, in case anyone had forgotten.)
You begin to find that very accomplished scientists who know an awful lot about evolution and human behaviour disagree. Vociferously. And there’s a good reason for this: they’re scientists. Destruction-testing of ideas is very much in the job spec.
The reality of scientific enquiry
In our own work we don’t generally find neat, satisfying stories that are easy to tell, hard to critique, and make everything fall into place. We tend to end up with tantalising hypotheses, really interesting ideas that might be true but we haven’t quite gathered the data to nail down beyond all doubt. We find theories that are dazzling in their elegance but multitudinous in their caveats.
We find that the mind steadfastly refuses to behave like a collection of perfectly adapted units, each with a single function that afforded a clear evolutionary advantage at some weirdly specific yet curiously under-specified time during human evolutionary history. Instead the human mind seems to be full of compromises and by-products, highly flexible, and intricately intertwined with this weird thing called “human culture”.
Yet having been drawn to evolutionary science for its extraordinary elegance and having found a thousand times more questions than satisfactory answers, we persist. Because if you expand your ideas about what “evolutionary” means – if you cease looking for the neat stories and embrace the fact that it’s going to get very, very messy, you can start to get somewhere really interesting.
Culture and evolution are not opposites. Evolved doesn’t have to mean adaptation. It might or might not mean “useful under some circumstances”. (It certainly doesn’t mean – and has never meant – good or right).
Refuting one evolutionary hypothesis about human behaviour doesn’t invalidate all of them. That would be like saying that evolutionary theory is felled by the old question, “But if we evolved from monkeys, why are there still monkeys?”
Arguing about the how, when and why isn’t a sign of science denialism, nor a reason to scrap the whole line of investigation – it’s healthy disagreement and we’d like to see more of it. Being an evolutionary scientist is a bit like being Dirk Gently: you might not get where you were hoping to go, but you’ll probably end up somewhere it’s worth being.
Kate and Lewis’s show, Alas Poor Darwin …?, part of the Cabaret of Dangerous Ideas, is taking place at the Edinburgh Fringe on August 16
When the University of Sydney’s Catholic Society decided to organise a debate on legalising voluntary euthanasia, it was envisaged as a modest event to be held on campus. Interest in the topic and the high profile of the speakers soon saw the debate moved to Sydney’s Town Hall, which sold out over a week in advance.
The two protagonists symbolised forces far larger than themselves. His Grace, the Most Revered Anthony Fisher, Archbishop of Sydney, represented the power and prestige of the Roman Catholic Church. He had a strong support base in the crowd, which included nuns, priests and young Catholic students.
In contrast to his stern and authoritarian predecessor, George Pell, Fisher carried himself with a relaxed charm, happy to joke about his “strange clothes” and former life of sin – he was a lawyer before studying for the priesthood.
Peter Singer is Australia’s most prominent philosopher and the current Ira W. DeCamp Professor of Bioethics at Princeton University. A key figure in the animal liberation movement and a foundational member of the Australian Greens, his advocacy, under certain circumstances, of abortion, euthanasia, infanticide – and even bestiality – has certainly courted controversy. To his religious critics, he is very much the atheist bogeyman.
Euthanasia is a sensitive topic that elicits strong emotions. The moderator, the ABC’s online editor of Religion and Ethics, Scott Stevens, urged the speakers and audience to be more civil and respectful than the Q&A norm. It was a request mostly adhered to.
Singer spoke first and his argument was relatively straightforward. The audience was asked:
Why do we consider killing an innocent person to be wrong?
The answer is twofold. First, killing someone is a violation of their autonomy. But in the case of voluntary euthanasia, a person’s autonomy is not taken away but supported.
Second, killing an innocent person deprives them of the good things in life they would have otherwise experienced. At this juncture, Singer makes an important qualification. He is not an “absolutist” about autonomy. If a healthy young person is lovesick or depressed, they may temporarily feel that life is not worth living. However, there is much reason to suspect these feelings will pass.
Singer endorses the Canadian Supreme Court’s recent ruling that allows euthanasia only for people with:
… grievous and irremediable medical conditions.
Fisher drew on the movie The Water Diviner, where a young Australian soldier agrees to kill his mortally wounded brother rather than let him slowly and painfully bleed to death. The question put to the audience was:
Is it better to kill someone than let them suffer?
Fisher asserted that comforting people through their suffering requires more from us, but it also places more value on humanity and endorses the intrinsic value of life.
Fisher’s main argument was concerned with bracket creep. If we accept some people who suffer should be able to end their lives, what about others who suffer? Rather than respect for all life, euthanasia would lead to two classes of existence. The terminally sick could soon be joined by the mentally ill, clinically depressed, severely disabled, the elderly and unwanted babies in a growing group considered better off dead.
Singer strongly rejected this claim. He argued that there was no evidence of a slippery slope towards euthanasia becoming a widespread practice to remove undesirable people for financial or other motives. He pointed to the US state of Oregon, where only 105 people took advantage of the Death with Dignity Act in 2014.
Fisher insisted that the example of the Netherlands where, he said, euthanasia has rapidly increased proves that bracket creep is real. Once you accept some people are better off dead a moral line is crossed.
The questions from the audience hinted at its makeup. Of the 12 questions asked, ten were openly hostile to Singer or supportive of Fisher. Singer was asked if he supported the killing of babies with severe disabilities or elderly people with dementia. He became increasingly impatient and regularly reminded the audience he was only advocating voluntary euthanasia – which automatically excludes babies and those unable to consent.
One questioner was even ejected by the moderator for trying to start an infanticide debate stemming from Singer’s 1979 book, Practical Ethics.
So who won the debate? No-one really. Had there been a show of hands, Fisher would have been the likely victor but that would only have reflected the Catholic Society’s strong presence.
For much of the debate, the two did not address the other’s arguments. Singer kept a small target, advocating voluntary euthanasia only for competent adults with a terminal illness.
Fisher, and the questioners, wanted a broader discussion on the sanctity of life. As one questioner demanded to much applause:
Mr Singer, who are you to decide that some lives are worth more than others?
Singer responded, also to applause, that he could not see the connection between the question and what he had advocated. It summed up the night; arguments flew in both directions but rarely met.
With the debate finished, supporters of each man formed an excited line to buy a signed book and take the obligatory selfie. As with the debates about the existence of God made so popular by Richard Dawkins and Christopher Hitchens, the goal was never to change anyone’s mind but to speak to an existing base. Both camps left the majestic building satisfied that they had won.
There seems to be a shortening gap between studies about diet, nutrition and health. And each starts another conversation about trans vs saturated vs polyunsaturated fats, or this diet vs that, or, as is today’s case, fats vs carbohydrates.
In a paper published today in the journal Cell Metabolism, researchers found that when 30% of a day’s kilojoules were restricted by cutting fats (diets with a higher intake of carbohydrates), participants in their study lost more body fat compared to when the same amount of energy was restricted by cutting carbs (diets with a higher intake of fat).
This study used a type of meticulous metabolic research, which is expensive and unsuited to lengthy periods, but valuable for exploring the physiology of reducing equal dietary contributions from fat or carbohydrate. But like much dietary analysis, it may be shining a light on the wrong issues altogether.
The good, the bad and the ugly
The most important aspect of any diet is that it should be practical and healthy enough to follow for the rest of your life. There’s no magic bullet for weight loss. While some people claim they find it easier to cut out foods high in carbohydrates, others find it easier to avoid high-fat foods.
If you need to lose weight, cutting down is what helps. But few people can stick to any extreme diet for life, so what you substitute is just as important as what you cut out – especially for long-term health.
Choices based only on macronutrients (foods required in large amounts in the diet, such as fats, carbohydrates and protein) miss important aspects of many foods and open the diet to imbalance. Carbohydrate foods, for instance, include nutritionally worthy choices – such as legumes, wholegrains, fruits, milk and yoghurt – but also a huge range of items high in sugar or refined starches with little or no nutritional attributes. “Cutting carbs” doesn’t distinguish between the good and bad foods in this category.
The same thing happens with fats. Sources of unsaturated fat – such as nuts, seeds, avocado or extra virgin olive oil – have proven health benefits. But there’s no evidence for any benefits of lard, dripping, cream, fast foods or any of the fatty snack foods that account for much of our saturated fat intake. And no long-term study shows sustained weight loss or other health benefits from a diet high in saturated fats.
Some foods are more even problematic. Most fast foods are high in saturated fat and salt, and lack dietary fibre. And they’re not only largely devoid of vegetables (apart from the odd gherkin), but often displace meals that would have contained vegetables.
Biscuits, cakes, pastries, many desserts and confectionery provide a double whammy with high levels of unhealthy fats as well as sugar and refined starches. Make that a triple whammy because most lack any nutritional virtue as well.
From bad to worse
Assumptions based on macronutrients are simply too gross to be meaningful. This is apparent in so-called meta-analyses based on a mixture of cohort and case-control studies that use different methods and time frames relating to what people eat, and fail to report all aspects of the diet.
One review, for instance, claimed that saturated fat was unrelated to cardiovascular disease. But it ignored the adverse impacts of the foods that had replaced saturated fats and provided no information about the foods that provided saturated fat in the first instance.
Worse still, such analyses are prone to many errors. A long check of every reference used in that meta-analysis showed that the conclusion would have differed if 25 studies had either not been omitted or had been reported correctly (sadly, it’s paywalled).
Another recent review also failed to show any clear association between higher saturated fat intake and all-cause mortality, heart disease, ischaemic stroke or type 2 diabetes, although the authors were unable to confidently rule out increased risk for heart disease deaths. They also noted that the certainty of associations between saturated fat and all outcomes was “very low”, which means we don’t yet understand the association between saturated fats and disease.
Hopefully, further research will distinguish between food sources of saturated fats; they are not all equal. There’s already good evidence that processed meats can have more deleterious effects than fresh meat. And that fermented dairy products, such as yoghurt and cheese, may also have health benefits and are distinctly different for heart health risk compared to butter.
Swapping saturated fat for sugar or refined starches is worse than useless for preventing cardiovascular disease. But please direct criticism of foods where fat has been replaced by sugar at the food industry. Dietary guidelines have always recommended limiting sugar as well as saturated fat.
A sorry state of affairs
Unfortunately, in most developed countries, sugar consumption remains high while intakes of vegetables, legumes, fruits, nuts and wholegrains are low. And while macronutrient intakes in countries such as Australia may look fine (31% of energy from fat and 44% from carbs), problems remain with the kinds and amounts of foods we consume.
Junk food and drinks were once consumed only as an occasional treat, but they now contribute significant portions of both adult and children’s diets – in Australia, 35% of adults’ and 41% of childrens’ energy intake. Confectionery and starchy, fatty, savoury snack food intake have also increased significantly.
Consider the dozens of studies on Mediterranean diets, including randomised trials, where the fat and carbohydrate content vary but the health value depends on particular foods: extra virgin olive oil, nuts, vegetables, fruits, grains and legumes and a low intake of highly processed products. The take-home message from these is that we need to stop fussing over macronutrients and think about foods.
In some ways the False equivalence fallacy is the direct opposite of a False dilemma.
False equivalence is an informal fallacy that describes a situation where there is an apparent similarity between two things, but in fact they are not equivalent. The two things may share some common characteristics, but they have important differences that are overlooked for the purposes of the argument.
The pattern of the fallacy often looks like this: if A has characteristics c and d, and B has characteristics d and e, then since they both have characteristic d, A and B are equivalent. In practice, often only a passing similarity is required between A and B for this fallacy to be committed.
The following statements are examples of false equivalence:
‘They’re both soft, cuddly pets. There’s no difference between a cat and a dog.’
‘We all bleed red. We’re all no different from each other.’
‘Hitler, Stalin and Mao were evil atheists; therefore all atheists are evil.’
A more complex example is where somebody claims that more Australians are killed by sharks or road accidents than by terrorism, therefore we should not do anything to stop terrorism. This example ignores the fact that terrorist acts are prevented by doing something, such as surveillance and intelligence. We also choose to take the risks of swimming in the ocean and driving in cars, but we cannot avoid the risk of terrorism no matter what we do.
False equivalence is occasionally claimed in politics, where one political party will accuse their opponents of having performed equally wrong actions, usually as a red herring in an attempt to deflect criticism of their own behaviour. Two wrongs don’t make a right.
On the other hand, politicians might accuse journalists of False equivalence in their reporting of political controversies if the stories are perceived to assign equal blame to opposing parties. However, False equivalence should not be confused with False balance – the media phenomenon of presenting two sides of an argument equally in disregard of the merit or evidence on a subject (a form of argument to moderation).
Moral equivalence is a special case of False equivalence where it is falsely claimed, often for ideological motives, that both sides are equally to blame for a war or other international conflict. The historical evidence shows that this is rarely the case.
Another special case of False equivalence is Political correctness, which may be defined as language, ideas, policies, or behavior that seeks to minimise social offence in relation to occupational, gender, racial, cultural, sexual orientation, certain other religions, beliefs or ideologies, disability, and age-related contexts, to an excessive extent thus inhibiting free speech.
Moral equivalence is a form of equivocation often used in political debates. It seeks to draw comparisons between different, even unrelated things, to make a point that one is just as bad as the other or just as good as the other. Drawing a moral equivalence in this way is an informal fallacy, a special case of False equivalence.
A common manifestation of this fallacy is a claim, often made for ideological motives, that both sides are equally to blame for a war or other international conflict. Historical analyses show that this is rarely the case. Wars are usually started by one side militarily attacking the other, or mass murdering non-combatants, with or without provocation from the other side.
Some specific examples of this fallacy are as follows:
Claiming neither side in World War II was morally superior because of the British firebombing of Dresden in Germany, or the US atomic bombings of Hiroshima and Nagasaki in Japan. This is despite the fact that Germany started the war in Europe and Japan started the war in the Pacific. Whilst the morality of the British fire bombing of Dresden is questionable, the aim of the US atomic bombings was to force Japan to surrender, without the necessity of a land invasion in which millions of people were expected to die on both sides. The purpose was to end World War II as opposed to starting it.
Drawing a moral equivalence between 9/11 and U.S. policy in the Middle East, thereby attempting to justify or excuse the 9/11 atrocities against innocent non-combatants.
Drawing a moral equivalence between the Holocaust and Israeli actions toward the Palestinians.
PETA drawing a moral equivalence between the consumption of meat and the Holocaust in an ad campaign.
The excuse that slavery in the southern United States wasn’t so bad because some slaves were treated better than workers in northern factories and company towns — or the counter-use of the same examples, that conditions during the early Industrial Revolution were not that bad because the people were at least free to choose their jobs, unlike under slavery.
An early populariser of the expression was Jeane Kirkpatrick, who was United States ambassador to the United Nations in the Reagan administration. Kirkpatrick published an article called The Myth of Moral Equivalence in 1986, which sharply criticized those who she alleged were claiming that there was ‘no moral difference’ between the Soviet Union and democratic states.
 Kirkpatrick, Jeane. ‘The Myth of Moral Equivalence’, Imprimis January 1986, Vol. 15, No.1.