By Christian H. Cooper
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.
more
The Grim Biology of Being Poor
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.
more
The Grim Biology of Being Poor
