Why Poverty Is Like a Disease

On paper alone you would never guess that I grew up poor and hungry.

My most recent annual salary was over $700,000. I am a Truman National Security Fellow and a term member at the Council on Foreign Relations. My publisher has just released my latest book series on quantitative finance in worldwide distribution.

None of it feels like enough. I feel as though I am wired for a permanent state of fight or flight, waiting for the other shoe to drop, or the metaphorical week when I don’t eat. I’ve chosen not to have children, partly because—despite any success—I still don’t feel I have a safety net. I have a huge minimum checking account balance in mind before I would ever consider having children. If you knew me personally, you might get glimpses of stress, self-doubt, anxiety, and depression. And you might hear about Tennessee.

Meet anyone from Tennessee and they will never say they are from “just” Tennessee. They’ll add a prefix: East, West, or Middle. My early life was in East Tennessee, in an Appalachian town called Rockwood. I was the eldest of four children with a household income that couldn’t support one. Every Pentecostal church in the surrounding hillbilly heroin country smelled the same: a sweaty mix of cheap cleaner and even cheaper anointing oil, with just a hint of forsaken hope. One of those forsaken churches was effectively my childhood home, and my school.

Class was a single room of 20 people running from kindergarten through twelfth grade, part of an unaccredited school practicing what’s called Accelerated Christian Education. We were given booklets to read to ourselves, by ourselves. We scored our own homework. There were no lectures, and I did not have a teacher. Once in a while the preacher’s wife would hand out a test. We weren’t allowed to do anything. There were no movies, and no music. Years would pass with no distinguishing features, no events. There was barely any socializing.

On top of it all, I spent a lot of my time pondering basic questions. Where will my next meal come from? Will I have electricity tomorrow? I became intimately acquainted with the embarrassment of my mom trying to hide our food stamps at the grocery store checkout. I remember panic setting in as early as age 8, at the prospect of a perpetual uncertainty about everything in life, from food to clothes to education. I knew that the life I was living couldn’t be normal. Something was wrong with the tiny microcosm I was born into. I just wasn’t sure what it was.

As an adult I thought I’d figured that out. I’d always thought my upbringing had made me wary and cautious, in a “lessons learned” kind of way. Over the past decades, though, that narrative has evolved. We’ve learned that the stresses associated with poverty have the potential to change our biology in ways we hadn’t imagined. It can reduce the surface area of your brain, shorten your telomeres and lifespan, increase your chances of obesity, and make you more likely to take outsized risks.

Now, new evidence is emerging suggesting the changes can go even deeper—to how our bodies assemble themselves, shifting the types of cells that they are made from, and maybe even how our genetic code is expressed, playing with it like a Rubik’s cube thrown into a running washing machine. If this science holds up, it means that poverty is more than just a socioeconomic condition. It is a collection of related symptoms that are preventable, treatable—and even inheritable. In other words, the effects of poverty begin to look very much like the symptoms of a disease.

That word—disease—carries a stigma with it. By using it here, I don’t mean that the poor are (that I am) inferior or compromised. I mean that the poor are afflicted, and told by the rest of the world that their condition is a necessary, temporary, and even positive part of modern capitalism. We tell the poor that they have the chance to escape if they just work hard enough; that we are all equally invested in a system that doles out rewards and punishments in equal measure. We point at the rare rags-to-riches stories like my own, which seem to play into the standard meritocracy template.

But merit has little to do with how I got out.

We may not remember 1834 as a banner year, but it was in the field of organic chemistry. It was then that chemists Jean-Baptiste Dumas and Eugène Péligot distilled and analyzed a clear liquid—what they called methylene, and what we’d call methanol today—from softly heated wood chips. At its heart was a methyl group, consisting of one carbon atom bound to three hydrogen atoms. As it would turn out 150 years later, methyl groups play a critical role in gene expression.

In the fall of 1991, Aharon Razin and Howard Cedar published the extraordinary paper “DNA Methylation and Gene Expression,” which showed that gene expression works much like a snake tightly coiled around the Rod of Asclepius.¹ Perched atop the indissoluble warp and weft of our genetic code are methyl groups that control how tightly our genetic code wraps around special proteins, called histone proteins. The tighter a portion of code is wrapped, the less likely it is to have any effect (or in the jargon, the less likely it “gets expressed”). This, we now know, is one pillar of the mechanism of the epigenome: Who you are as a person is not just defined by your DNA, but by which parts of it your epigenome permits to be expressed.

Six years later, Michael Meaney, a professor at McGill University specializing in the biology of stress, published a breakthrough result together with his colleagues: The quality of maternal care alters the epigenome in rats, affecting glucocorticoid stress receptors in the hippocampus as well as the response of the hypothalamic-pituitary-adrenal axis to stress.² Similar effects were later found in zebra finches which, like humans, are socially monogamous and involve both parents in raising offspring. Messenger-RNA levels of glucocorticoid and mineralocorticoid receptors were reduced in maternally deprived birds, which made stress hormones remain elevated in adult finches for longer periods of time. The researchers wrote that epigenetic mechanisms could be responsible for the changes, but they did not prove them to be.³

In human children, epigenetic changes in stress receptor gene expression that lead to heightened stress responses and mood disorders have been measured in response to childhood abuse.⁴ And last year, researchers at Duke University found that “lower socioeconomic status during adolescence is associated with an increase in methylation of the proximal promoter of the serotonin transporter gene,” which primes the amygdala—the brain’s center for emotion and fear—for “threat-related amygdala reactivity.”⁵ While there may be some advantages to being primed to experience high levels of stress (learning under stress, for example, may be accelerated⁶), the basic message of these studies is consistent: Chronic stress and uncertainty during childhood makes stress more difficult to deal with as an adult.

From one perspective, epigenetics offers a compelling narrative of life experiences feeding back directly onto the basic programming that makes us who we are. But the field also has some foundational controversies. In June of last year, a team of researchers from the Albert Einstein College of Medicine, Bristol University, and the European Bioinformatics Institute published a paper arguing that the field is plagued with misinterpreted results. The sources of misinterpretation included confusing cause and effect (diseases can produce epigenetic markers as well as the other way around); spurious and misinterpreted statistics; confounding variables which cause apparent correlations; and a large variability among the epigenomes of individual cells, which is usually not controlled for in experiments.

John Greally, one of the study’s co-authors, argues that some of the landmark results in the field, including Meaney’s, have suffered from these problems. “At the time [of Meaney’s study],” he explains, “the idea was that if I see something like a DNA methylation change, in cells of either the rats that didn’t get licked by their mothers, or the kids from the lower socio-economic group, or whatever it might be, then I’m learning how we’re reprogrammed as a response to that environmental condition.” But the measurement of DNA methylation explains more than whether a cell has been reprogrammed or not. It is also related to the proportions of cell subtypes, each with different epigenomes, that are present in the subjects being compared. Greally and his co-authors call this the meta-epigenome.

But Greally also points out that, even if the molecular mechanism is a shift in cell subtypes rather than cellular reprogramming through methylation, there is still an interesting conversation to be had. “Even if you find that there’s a change in the proportion of say, cell subtype proportions in the peripheral blood, and it’s associated with a condition like low socio-economic status or something like that, that’s actually a pretty interesting finding,” he says. “It kind of gets back to the issue of how you define epigenetics.” It may be possible that shifts in cell subtypes are inheritable, even though they do not involve a reprogramming of a cell through methylation. Tim Spector of King’s College in London, for example, has found DNA sequence variants associated with cell subtype variation.

The science of the biological effects of the stresses of poverty is in its early stages. Still, it has presented us with multiple mechanisms through which such effects could happen, and many of these admit an inheritable component. If a pregnant woman, for example, is exposed to the stresses of poverty, her fetus and that fetus’ gametes can both be affected, extending the effects of poverty to at least her grandchildren. And it could go further.

Studies of mice and fruit flies have shown that epigenetic traits similar to the ones Meaney proposed can be passed down, and last for dozens of generations. The effects of things like diet and prenatal parental stress have been observed to be inherited, not just through histone modifications, but also through DNA methylation and non-coding RNAs.⁷ In one 2014 study, the offspring of a mouse trained to fear a particular smell were observed to also fear that smell, even with no previous exposure to it. The effect lasted for two generations.⁸ In humans, inheritable effects of stress have been observed through at least three generations from parents who survived mass starvation (Dutch Hunger Winter),⁹ a fluctuating food supply (the Överkalix cohort)¹⁰ and the Holocaust. The effects of early paternal smoking and paternal betel quid chewing have been observed to be transmitted to children in a sex-specific manner, supporting biological epigenetic transmission in humans.¹¹ According to a 2014 survey of the field, “the few human observational studies to date suggest (male line) transgenerational effects exist that cannot easily be attributed to cultural and/or genetic inheritance.”¹⁰

Even at this stage, then, we can take a few things away from the science. First, that the stresses of being poor have a biological effect that can last a lifetime. Second, that there is evidence suggesting that these effects may be inheritable, whether it is through impact on the fetus, epigenetic effects, cell subtype effects, or something else.

This science challenges us to re-evaluate a cornerstone of American mythology, and of our social policies for the poor: the bootstrap. The story of the self-made, inspirational individual transcending his or her circumstances by sweat and hard work. A pillar of the framework of meritocracy, where rewards are supposedly justly distributed to those who deserve them most.

What kind of a bootstrap or merit-based game can we be left with if poverty cripples the contestants? Especially if it has intergenerational effects? The uglier converse of the bootstrap hypothesis—that those who fail to transcend their circumstances deserve them—makes even less sense in the face of the grim biology of poverty. When the firing gun goes off, the poor are well behind the start line. Despite my success, I certainly was.

So how did I get out? By chance.

It’s easy to attach a post-facto narrative of talent and hard work to my story, because that’s what we’re fed by everything from Hollywood to political stump speeches. But it’s the wrong story. My escape was made up of a series of incredibly unlikely events, none of which I had real control over.

At age 14, I’d had eight years of trying to teach myself using photocopied handouts, without textbooks, lesson plans, aids, or even a teacher. I was desperate to get out and terrified of winding up like the people I saw around me at the Christian compound. So, I picked up the phonebook and started dialing trade schools, colleges, anything and anyone that might give me a new option. Randomly, unexpectedly, I reached the president of the local community college, Sherry Hoppe. I was probably 12 years old the first time I met Hoppe and even at that age I could tell my story was not unique in her experience.

At that same college, I met Bruce Cantrell, a professor who wound up being like a father figure to me while I was navigating being 15 and poor. He grew up poor too but ultimately did well. We never actually talked about it but we just clicked. A few years later he ran for office and made me his campaign manager. We won and I got a priceless education in the reality of Roane County bare-knuckle politics. I’ll forever be grateful to Bruce and Sherry. With their help, I ultimately got my accredited college degree.

Did I show initiative? Sure. And there have been many people who have interpreted my escape from poverty as a confirmation of some foundational meritocracy that justifies the whole system. But the fact is hillbilly country is full of people just as desperate to get out as me, and taking just as inventive a set of measures. Yes, I am the exception that proves the rule—but that rule is that escape from poverty is a matter of chance, and not a matter of merit.

I have relatives and friends who are as bright and hard-working as I am, with roughly the same kind of educational path or better. But none of them made it out of poverty. One of them also got into community college, but not before he saw his drugged-up best friend kill himself. That proved to be a one-way ticket to a lifetime of emotional problems. Another was lucky enough to attend an accredited public school, learning far more there than I ever did in my Accelerated Christian Education. He ended up a heroin addict. They would not, as I did, find the path to graduation curiously free of obstacles. They would not become, as I did, head of a derivatives trading desk on Wall Street. They are not, as I am, writing about poverty. They are still living it. As of now, I can count around 20 friends and family who have checked out by handgun or heroin. I have no doubt I will add to that count this year.

Why do so few make it out of poverty? I can tell you from experience it is not because some have more merit than others. It is because being poor is a high-risk gamble. The asymmetry of outcomes for the poor is so enormous because it is so expensive to be poor. Imagine losing a job because your phone was cut off, or blowing off an exam because you spent the day in the ER dealing with something that preventative care would have avoided completely. Something as simple as that can spark a spiral of adversity almost impossible to recover from. The reality is that when you’re poor, if you make one mistake, you’re done. Everything becomes a sudden-death gamble.

Now imagine that, on top of that, your brain is wired to multiply the subjective experience of stress by 10. The result is a profound focus on short-term thinking. To those outsiders who, by fortune of birth, have never known the calculus of poverty, the poor seem to make sub-optimal decisions time and time again. But the choices made by the poor are supremely rational choices under the circumstances. Pondering optimal, long-term decisions is a liability when you have 48 hours of food left. Stress takes on a whole new meaning—and try as you might, it’s hard to shake.

The standard American myth of meritocracy misinterprets personal narratives like mine. The accumulated social capital of American institutions—stable transfer of power, rule of law, and entrepreneurship—certainly create economic miracles every day. But these institutions are far more suited to exponentially growing capital where it already exists, rather than creating new capital where society needs it. Stories such as mine are treated as the archetype, and we falsely believe they are the path to escape velocity for an entire segment of the population. In doing so, they leave that population behind. I am the face of the self-made rags-to-riches success story, and I’m here to say that story is a myth. The term “meritocracy” was coined in 1958 as a mockery of the very idea of evaluation by merit alone. We’ve forgotten to laugh, and the joke is on us.

It’s time for us to update our response to poverty to take into account the new science that describes it.

Take education. One of the strongest voices connecting the dots from poverty to performance in the classroom and economic struggles later in life is Harvard’s Roland G. Fryer. In their seminal work, “It May Not Take a Village: Increasing Achievement Among the Poor,” Fryer and his colleagues focused on closing the achievement gap between rich and poor through a mosaic of strategies, primarily at school.

But the standard bearer of the achievement gap—math performance—is a symptom and not a cause. When support from well-intended social programs that address things like test scores inevitably diminish or stop, their positive outcomes fail to persist and we grow skeptical about poverty alleviation as a whole. But academic achievement isn’t the real problem—it’s uncertainty and stress. When the 2011 National Assessment of Educational Progress finds no city in America where more than 25 percent of Black or Hispanic children in the eighth grade function at grade level in reading or math, do we blame our schools, or conclude that we lost the neurological arms race long before the children were tested?

We should leverage the lessons of the science of poverty rather than ignore them. Poverty alleviation programs like conditional cash transfers, for example, reward parents or caregivers with direct payment for taking actions, like ensuring school attendance or arranging for preventative care. They encourage stress alleviation and long-term planning that is far upstream of doing well on an exam—they provide exactly the kind of certainty that the poverty-stricken brain needs. In a paper released in June of 2009, Lia Fernald and Megan Gunnar showed that such programs lowered salivary cortisol levels and reduced lifetime risk for a range of mental and physical disorders.¹² There should be more programs like these: For example so-called whole-child policies, which focus on the long-term development of children starting from birth while reducing uncertainty during the first three years of childhood development.

Our new scientific understanding of the experience of poverty can also inform medical treatments later in life. In 2009, Michael Meaney, Gustavo Turecki, Moshe Szyf and colleagues took hippocampus samples from suicide victims with a history of childhood abuse and tested for DNA methylation controlling the expression of the gene NR3C1.⁴ They discovered an increased methylation around the NR3C1 promoter, which, in other studies, has been directly linked to a reduced expression of a protein called brain-derived neurotropic factor (BDNF). BDNF is among the most active neurotrophic factors, which drive the growth and development of new neurons even in adulthood. And the degree to which it is expressed may be inheritable. A 2015 study linked NR3C1 and reduced expression of BDNF in infants born to mothers who reported prenatal depressive symptoms.¹³

It may be that BDNF is your best friend if you are an adult and want to change your neurological wiring. It could open a pathway to change brain wiring in exactly those areas that are most damaged by early stress and poverty: the prefrontal cortex, hippocampus, and the entire chain of the hypothalamic-pituitary-adrenal system. Those areas of the brain govern long-term memory, emotional control, and delayed gratification; all markers of individuals that outperform in academic settings in youth and are higher earners in adulthood.^{14, 15} Low doses of ketamine have been shown to act as a rapid anti-depressant, and that impact is directly linked to increased levels of BDNF.¹⁶

I would consider trying this treatment myself. But that is not my primary interest in the science of poverty. My interest stems from something else: worrying about the future.

We stand at the precipice if we don’t re-evaluate our understanding of poverty and inequality. The narrative in the neo-liberal west is that if you work hard, things work out. If things don’t work out, we have the tendency to blame the victim, leaving them without any choices. Brexit, Le Pen, and the defeat of Hillary Clinton are examples of the cracks that result from inequality and poverty, symptoms of my childhood experience writ large. The Piketty pitchforks are out, and the march to global disorder can only be arrested by adopting measures that begin to price in the stacked deck that I and anyone else born into deep poverty sees, and resents.

I believe we will see the Italian Five Star Movement submit a referendum to leave the EU this year, and that Marine Le Pen has better than even odds of winning the French election. The EU is in danger of buckling under a globalist defeat and may exist in name only two years from now.

These trends are being accelerated by the blind belief that the poor have failed to seize the opportunities that the market or globalization has created. This myth deserves to be taken off life support—and the emerging, empirical, and carefully observed science of poverty can help us do so if we pay it the attention it deserves.

Christian H. Cooper is the former head of interest rate derivatives trading at an investment bank in New York City and is currently focused on raising a global macro fund. He is a Truman National Security Fellow and a Term Member at the Council on Foreign Relations.

References

1. Razin, A. & Cedar, H. DNA methylation and gene expression. Microbiological Reviews 55, 451-458 (1991).

2. Liu, D., et al. Maternal care, hippocampal glucocorticoid receptors, and hypothalamic-pituitary-adrenal responses to stress. Science 277, 1659-1662 (1997).

3. Banerjee, S.B., Arterbery, A.S., Fergus, D.J., & Adkins-Regan, E. Deprivation of maternal care has long-lasting consequences for the hypothalamic-pituitary-adrenal axis of zebra finches. Proceedings of the Royal Society B 279, 759-766 (2012).

4. McGowan, P.O., et al. Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse. Nature Neuroscience 12, 342-348 (2009).

5. Swartz, J.R., Hariri, A.R., & Williamson, D.E. An epigenetic mechanism links socioeconomic status to changes in depression-related brain function in high-risk adolescents. Molecular Psychiatry 22, 209-214 (2017).

6. Champagne, D.L., et al. Maternal care and hippocampal plasticity: Evidence for experience-dependent structural plasticity, altered synaptic functioning, and differential responsiveness to glucocorticoids and stress. Journal of Neuroscience 28, 6037-6045 (2008).

7. Lim, J.P. & Brunet, A. Bridging the transgenerational gap with epigenetic memory. Trends in Genetics 29, 176-186 (2013).

8. Dias, B.G. & Ressler, K.J. Prenatal olfactory experience influences behavior and neural structure in subsequent generations. Nature Neuroscience 17, 89-96 (2014).

9. Heijmans, B.T., et al. Persistent epigenetic differences associated with prenatal exposure to famine in humans. Proceedings of the National Academy of Sciences 105, 17046-17049 (2008).

10. Pembrey, M., Saffery, R., Bygren, L.O., & Network in Epigenetic Epidemiology. Human transgenerational responses to early-life experience: Potential impact on development, health and biomedical research. Journal of Medical Genetics 51, 563-572 (2014).

11. Pembrey, M.E., Bygren, L.O., & Golding, J. The nature of human transgenerational responses. In Jirtle, R.L. & Tyson, F.L. (Eds.) Environmental Epigenetics in Health and Disease Springer Publishing, New York, NY (2013).

12. Fernald, L.C.H. & Gunnar, M.R. Poverty-alleviation program participation and salivary cortisol in very low-income children. Social Science & Medicine 68, 2180-2189 (2009).

13. Braithwaite, E.C., Kundakovic, M., Ramchandani, P.G., Murphy, S.E., & Champagne, F.A. Maternal prenatal depressive symptoms predict infant NR3C1 1 F and BDNF IV DNA methylation. Epigenetics 10, 408-417 (2015).

14. Xu, X., et al. A significant association between BDNF promoter methylation and the risk of drug addiction. Gene 584, 54-59 (2016).

15. Kheirouri, S., Noorazar, S.G., Alizadeh, M., & Dana-Alamdari, L. Elevated brain-derived neurotrophic factor correlates negatively with severity and duration of major depressive episodes. Cognitive and Behavioral Neurology 29, 24-31 (2016).

16. Haile, C.N., et al. Plasma brain derived neurotrophic factor (BDNF) and response to ketamine in treatment-resistant depression. International Journal of Neuropsychopharmacology 17, 331-336 (2014).

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