Poverty Is a Disease, That’s Curable

“Below this article point to an individual who describes causes of poverty and how we as a country perpetuated this ignoma. Creating a socially economic group of people who are trapped through no fault of their own. Hopefully those who thoroughly read this person’s view of poverty as a disease can help someone understand that being poor is not always their fault and can assist them in upward mobility by changing the cycle of poverty. Because this disease shows in all our outward appearances. Taking assessment of poverty areas in our country there is a diffenant relationship with poverty and obesity.”

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 accelerated by 6), 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.

We continue with Part Two of this very insightful article on poverty and the effects of those in that cycle while they are in their developing stage. Those informative years have greatly affected in their later years. Research on this disease should awaken those who have direct control over poverty in this country.