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Someone asked me:
If a striped cat is the result of a white and a black cat, why the result of a white woman and a black man is not a striped child?
I know the answer. I also know that the result of a black cat and a white one is not a striped cat. But I'm looking for a simple answer. I'm looking for an explanation without a genetics background required. I'm looking for a metaphor or something similar.
The reason that there are no stripes when black and white people get babies is the fact that the number of pigment cells is the same for black and white people. What is different is the amount of pigment produced, and it will be different in the kids as well (lighter than the dark parent, darker than the light parent) See references 1 and 2 for details on the melanocyte density. Skin color is a multigenic trait, so the genetic background of both parents and their effects on pigmentation come into full play here.
Besides this effect, humans do have stripes, although they are mostly not visible. They are called Blaschko's lines and look like below:
These develop from the migration pattern of the melanocytes (and their precursor cells) in the developing embryo. They can get visible in some rare genetic conditions or by diseases. See reference 3 for a more popular explanation and reference 4 for a review on this field.
- The Regional Anatomy of the Human Integument with Special Reference to the Distribution of Hair Follicles, Sweat Glands and Melanocytes
- General Biology of Mammalian Pigmentation
- Blaschko's Lines
- Lines of Blaschko.
Skin colour is determined by additive effects. That is, the amount of pigment is determined additively by the genes. For the basic genetics of it I will give a simple example, which is just illustrative and a gross oversimplification, it's probably much more complex (many loci all acting at once).
Suppose skin colour is affected by a single locus (at one position) within the DNA, which determines the amount of pigment produced. At this locus there are two alleles within a population, that is two versions of the DNA (e.g. ACGTCCATT and GACTTAACT are different DNA sequences). Allele one ($A_1$) produces a small amount of pigment, and allele 2 ($A_2$) produces a large amount. Thus people with $A_1 A_1$ genotype (people are diploid, i.e. they get a version from each parent) have light skin, $A_2 A_2$ genotypes have dark skin, and $A_1 A_2$ have an intermediate skin colour.
This is analogous to mixing fruit juice with water - if you mix blackcurrant cordial with water the colour is determined by the proportions. If you put out two bottles, one with cordial and one with water, allow two people to randomly choose a bottle, and use their choices to mix a glass of drink, 50% of the time you will end up with 1/2 water mixed with 1/2 cordial, while 25% of the time just a glass full of water, and the remaining 25% of the time just a glass full of cordial.
Why stripes don't occur
Note: although stripes occur in animals including humans (see chris' answer), it's not I'm the way your question insinuates
For stripes to occur you would have to have structure in the skin with two different types of skin cell, where bands/stripes of type occur - alternating between expressing the allele inherited from the mother, and that inherited from the father. That would require structure in the skin and something called genomic imprinting so parent of origin could be a factor.
The analogy with the glass of cordial is what going on in each cell, for stripes you would have to have organised and alternating clusters of glasses (cells) which get their contents determined by one individuals choice of cordial, with the selector alternating with the cluster of glasses.
Breeding Horses For Color
Genetic researchers are discovering Nature&aposs secrets for producing horses with tobiano, overo and appaloosa horse breed patterns. Horse breeders are putting the recipes to work.
Horsemen and women have long been fascinated by the various coat patterns displayed by the equine species, from the zebra&aposs stripes, to the Appaloosa breed&aposs spots and varnishes, to the Paint breed&aposs bold splashes of color. While it may sometimes seem that such breed patterns appear randomly in nature, the more we learn about genetics, the more we&aposve been able to reproduce these patterns in the horses we breed. Although we can&apost yet precisely control how these patterns are expressed (sometimes as lots of white, and sometimes as just a little), that knowledge is adding to the popularity of Paints, Pintos and Appaloosas as it reduces the risk of producing "solid-colored" horses.
The fact of the matter is, by selective breeding for dominant traits, we can introduce colorful patterns to virtually any "type" of horse we like… creating tobiano-patterned Saddlebreds, or leopard-spotted warmbloods, if that&aposs what suits our fancy.
There are a lot of myths and old wives tales when it comes to white markings on horses. Some people like the appearance of blazes and white stockings on horses, while others are prejudiced against them. Have you ever heard the saying, "One white foot, buy him. Two white feet, try him. Three white feet, there&aposs some doubt about him. Four white feet, you can do without him." Or: "One white foot, ride him for your life. Two white feet, give him to your wife. Three white feet, give him to your man. Four white feet, sell him if you can."
It is easy to refute such prejudices. Secretariat and Northern Dancer, two of the most outstanding racehorses and sires of this century, both had three white feet, and Northern Dancer&aposs outstanding son, The Minstrel, had four. However, it is true that white lower legs are more likely than colored legs to be affected by scratches and photosensitization.
If you breed Paints, Pintos, Appaloosas and Ponies of theAmericas, an attractive pattern can make a significant difference in the economic value of your foal crop.
Color genetics are complicated enough when confined to solid-colored horses. However, the rules governing the inheritance of white markings and patterns are even more complex.
The background color on every horse, with or without white markings or a white pattern, is one of the basic colors: bay, black, chestnut/sorrel, brown, dun, buckskin, palomino, cream, roan and gray. Like a horse&aposs background color, his genes control his distribution of white hair.
A number of different genes determine white markings on the face and legs. The horse&aposs base color apparently influences these genes, since white markings on chestnuts tend to be more extensive than those on bays and white markings on bays are more extensive than those on blacks. Complex relationships between the different genes determine the presence, absence and extent of the white leg and facial markings. Because of this, it is difficult or impossible to predict the white markings to be expected on a foal from any given mating.
Since fewer genes are involved, we can more easily predict the inheritance of white areas on the bodies of horses. Just as with solid colors, a pair of genes, one from the sire and one from the dam, determines any spotting pattern. Every horse of every breed, no matter what his color, has a pair of genes for every possible spotting pattern. However, the pattern is seen only when one of the genes is dominant.
In this article, dominant genes are designated by capital letters (e.g., T = tobiano, O = overo, L = leopard/appaloosa complex). The corresponding recessive genes are designated by small letters (e.g., t, o and l). When the two genes for a given trait differ, the horse is heterozygous for the trait (e.g., Tt). When the two genes are the same, the horse is homozygous for the trait (designated TT or tt, for example).
All white patterns are dominant to nonspotting, so heterozygotes are always patterned. The white areas may be difficult to see on a cream, pale palomino, dun or buckskin, or light gray or roan, but if the horse has a dominant gene for a pattern, it is there. We can be 99% certain that any solid-colored horse with no white areas is homozygous recessive (ttooll).
Predicting White Patterns
The fact that any gene for a white pattern is dominant to the gene for no pattern both simplifies and complicates predicting the pattern to be expected from a given mating. Making a prediction is simplified by the fact that we can be 99% certain that a solid-colored horse is homozygous recessive for all patterns, but it is complicated because we can&apost tell by looking at a spotted horse whether he is homozygous or heterozygous for the pattern.
When a horse that is homozygous for a pattern is mated with a horse of any color, all offspring will have the pattern. For example, if a homozygous tobiano (TT) stallion is bred to a group of chestnut, black, bay, dun and palomino mares, all of the offspring will be Tt and will have the tobiano pattern.
When two heterozygous horses (Tt) are mated, there are three chances out of four that the resulting foal will have the pattern (1 TT and 2 Tt) and one chance out of four that he will not (tt). When a heterozygous horse (Tt) is mated with a solid-colored horse, the chances of the offspring having the pattern are equal (2 Tt and 2 tt).
If a patterned stallion (or mare) has even one foal without the pattern, you can be certain that the parent horse is heterozygous for the pattern. It doesn&apost work the other way, however. That is, even if a patterned horse consistently has foals displaying that pattern, you cannot be certain that the horse is homozygous for the pattern. The horse might, by chance, have consistently passed on his dominant gene, even though he also has a recessive gene.
For certain patterns (e.g., tobiano), genetic tests are available to determine whether a horse is homozygous or heterozygous. Undoubtedly, as knowledge of the equine genome increases, tests for genes determining other patterns will be developed.
The hallmark of the tobiano pattern is that the white color crosses the center of the horse&aposs back between the neck and the croup. In addition, all four lower legs are white and the head (although possibly having a star, stripe or blaze on the face) is indistinguishable from that of a solid-colored horse.
Inheritance of the tobiano pattern is straightforward. That is, essentially all TT and Tt horses display the pattern, and there are no adverse effects associated with the genes.
In the overo pattern, the white color never crosses the back between the neck and the croup. In addition, at least one lower leg is colored, and the horse has generally extensive white markings on the head. The overo often has a so-called "bald" face and white markings that often extend onto the lower jaw.
The terms piebald and skewbald as regards overo and tobiano horses sometimes cause confusion. Despite the "bald" in their names, these terms have nothing to do with the amount of white on the head. A piebald horse, whether tobiano, overo or leopard/appaloosa, is black and white. Piebald comes from the same root as magpie, a black and white bird. A piebald bird or animal of any species is black and white. (Killer whales, for example, are piebald.) A skewbald horse has any color besides black in association with his white pattern.
Overos have four distinct patterns: frame, calico, sabino and splashed white.
Frame overos generally have solid-colored hooves and legs (or white leg markings that are no more extensive than those on solid-colored horses), white spots with distinct borders in the middle of their bodies and necks, and extensive white on their heads. The white body spots do not connect with any white on the legs. Some frames have solid-colored bodies with no white spots, but such horses usually have bald faces. Others have nearly all-white heads and extensively white bodies, although the midline of the back and the lower legs and feet are colored.
Calico overos have white body markings that have a scattered, irregular border and often connect with white on one or more of the legs. There can be extensive, irregular white markings on the head, but the hair around the eyes is usually colored. Calicos with more than 75% white on their bodies and irregular white markings on their legs above the knees and hocks are sometimes called "loud calicos."
Sabinos are often confused with calicos and classified with them by some authorities. Dr. Elizabeth Santschi of the University of Wisconsin School of Veterinary Medicine, who has done extensive work on the overo lethal white syndrome, considers sabino to be a distinct pattern that is characterized by extensive mixing of white hairs (roaning) with colored patches that are irregularly shaped and flecked with white that blends with small white patches.
All White Tigers Are Inbred and Are Not Purebred
The ONLY way to produce a tiger or lion with a white coat is through inbreeding brother to sister or father to daughter generation after generation after generation. The kind of severe inbreeding that is required to produce the mutation of a white coat also causes a number of other defects in these big cats.
In June 2011 the board of directors for the American Zoological Association (AZA) formalized their 2008 ban on the breeding of white tigers, white lions or king cheetahs by their member zoos. Their report said, “Breeding practices that increase the physical expression of single rare alleles (i.e., rare genetic traits) through intentional inbreeding, for example intentional breeding to achieve rare color-morphs such as white tigers, deer, and alligators, has been clearly linked with various abnormal, debilitating, and, at times, lethal, external and internal conditions and characteristics, which are outlined in this paper.” This change in policy came more than 12 years after Big Cat Rescue first released Dr. Laughlin’s expose below.
The same gene that causes the white coat causes the optic nerve to be wired to the wrong side of the brain, thus all white tigers are cross eyed, even if their eyes look normal. They also often suffer from club feet, cleft palates, spinal deformities and defective organs.
The white coat is a double recessive gene so most of the cubs born through this inbreeding have normal coloring but they too suffer the same defects and are referred to in the trade as “throw away tigers.” As such, they are often killed at birth because only the white tigers are the big money makers. And because none of these cats are purebred (they are all crosses between Bengal tigers and Siberian tigers), they serve no conservation purpose.
The American Zoological Association (AZA) recognizes that these cats should not be bred and admonishes AZA accredited zoos not to breed any more of them. The leader of the tiger Species Survival Plan states openly that the only reason people breed white tigers is because people will pay to see white tigers.
You can end the misery by just Saying NO to any place that breeds or exploits white tigers.
What’s Killing America’s Black Infants?
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After she lost her son, Tonda Thompson dreamed of a baby in a washing machine. She’d stuffed in dirty clothes and closed the door. The lock clicked shut. Water rushed in. Then she saw him, floating behind the glass. Frantic, she jabbed at a keypad on the machine, searching for a code to unlock the door.
When Thompson became pregnant she was 25, living in Los Angeles and working as a model. She and her boyfriend got engaged and moved back to Milwaukee, Wisconsin. She’d grown up on the city’s north side, a predominantly African-American neighborhood with pockets of deep poverty, in a zip code known for having the highest incarceration rate in the United States. Thompson went to all of her medical appointments, took prenatal vitamins, and stayed in shape. On her birthday, she wrote on Facebook that the only gift she wanted was “a healthy mom and baby.” But she also wrote about how hard it was to be pregnant in a city where there was “nothing to do that’s fun and safe.”
What It’s Like to Be Black and Pregnant When You Know How Dangerous That Can Be
Thompson got married in April 2013, and a month later went into labor. Forty hours later, Terrell was born. He lived less than half that time, due to “complications” with the delivery. By the time Thompson got home, all of the baby’s things had been moved to the basement. She’d gotten to hold him for five minutes.
Thompson sank into a depression. She thought about suicide. On her birthday, she received divorce papers by the next summer, she was on the verge of homelessness. She often felt angry that the hospital didn’t save her son. But mostly she asked herself, “What did I do wrong?”
Each year in the United States, more than 23,000 infants die before reaching their first birthday
E ach year in the United States, more than 23,000 infants die before reaching their first birthday. Though the mortality rate varies widely by state and county, the average in the United States is higher than in the rest of the world’s wealthy countries, worse than in Poland and Slovakia. Because infants are so vulnerable, their survival is considered a benchmark for a society’s overall health. What our infant-mortality rate tells us is that, despite spending more money on health care than any other country in the world, the United States is not very healthy. Looked at closely, it reveals that particular groups of Americans are starkly unwell.
White, educated American women lose their infants at rates similar to mothers in America’s peer countries. Most of the burden of the higher mortality rate here is borne by poorer, less-educated families, particularly those headed by unmarried or black women. Across the United States, black infants die at a rate that’s more than twice as high as that of white infants. The disparity is acute in a number of booming urban areas, from San Francisco—where black mothers are more than six times as likely to lose infants as white mothers—to Washington, DC. In the capital’s Ward 8, which is the poorest in the city and over 93 percent black, the infant-mortality rate is 10 times what it is in the affluent, predominantly white Ward 3.
The year that Terrell died, a mother in war-torn Libya had better odds of celebrating her child’s first birthday than Thompson did. Milwaukee has one of the worst infant-mortality rates of all major urban centers in the United States, and the racial gap is threefold. (Four other Rust Belt cities count among the 10 with the highest rates of infant death: Cleveland, Detroit, Indianapolis, and Columbus.) Over the past decade, more than 100 babies, at least 60 of them black, have died in Milwaukee each year, about two-thirds of them because they were born early or small.
&ldquoWe literally embody the societal and ecological conditions in which we grow up and develop and live.&rdquo
Bevan Baker, Milwaukee’s commissioner of health, is one of the people trying to reverse the trend. “If 100 people died from tuberculosis, then you would have a whole different approach,” Baker said. “People would say we have a public-health emergency.” His department, working with a coalition of groups, is trying to respond with the same urgency that it would to a deadly infectious disease. The city has declared infant mortality to be a primary health priority and, in 2011, set a goal of reducing the overall rate by 10 percent, and the black rate by 15 percent, by the end of this year.
For many years, researchers have asked the same question that Thompson asked herself: What are black mothers doing wrong? Common answers included eating poorly being overweight or diabetic smoking or drinking during pregnancy not going to the doctor not being married getting pregnant too young or smothering their newborns in their sleep. In the 1980s, health officials began focusing on access to prenatal care as a way to reduce these perceived risk factors. The result, said Dr. Michael Lu, an ob-gyn and leading infant-mortality researcher, was more women getting care, but little improvement in birth outcomes. Instead, the racial gap grew. Black women who received prenatal care starting in the first trimester were still losing children at higher rates than white women who never saw a doctor during their pregnancies.
By the late 1990s, the field was at a crossroads. Lu said, “We’d dedicated the last two decades to trying to improve on access to prenatal care, but if prenatal care is not the answer, then what?” Some researchers suggested that black women were genetically predisposed to poor birth outcomes, and began to hunt for “preterm birth genes.” At the time, pharmaceutical companies were exploring race-specific drugs, and the public-health community was embroiled in a broader debate about whether race is a genetic category. That debate hasn’t fully died out. But we now know that genetic variation among humans is tiny and doesn’t correspond neatly with racial categories. If preterm birth genes did exist, we would expect to see poor outcomes for black women everywhere, but studies have found that foreign-born black women living in the United States have birth outcomes almost identical to white American women’s.
Other researchers suggested that poverty and lack of education were to blame, as black women consistently experience higher poverty levels. Those factors matter, but they don’t account for the full racial gap. After evaluating 46 different factors, alone and in combination—including smoking, employment status, and education—the authors of one 1997 study could account for less than 10 percent of the variation in birth weight between black and white babies. Another study found that even black women with advanced degrees—doctors, lawyers, MBAs—were more likely to lose infants than white women who hadn’t graduated from high school.
Now, a growing body of evidence points to racial discrimination, rather than race itself, as the dominant factor in explaining why so many black babies are dying. The research suggests that what happens outside a woman’s body—not just during the nine months of pregnancy—can profoundly affect the biology within. One study found that black women living in poorer neighborhoods were more likely to have low-birth-weight infants regardless of their own socioeconomic status. More segregated cities have greater black/white infant-mortality disparities women whose babies are born severely underweight are more likely to report experiences of discrimination. This may help to explain how someone like Tonda Thompson, who says she did everything right during her pregnancy, could come to bury her infant son.
E arly one morning last September, a Milwaukee Health Department nurse named JoAnn went to the city’s north side to check on 9-month-old TJ and his mother, Ebony. Ebony participates in one of the department’s four home-visiting programs, which are a key component of the city’s strategy to reduce infant deaths. Similar intensive home-visiting programs in other cities have been shown to be effective. In a study conducted in Cincinnati, babies who received home visits were more than twice as likely to survive as those who didn’t.
Ebony lives in a corner apartment above her church, in the same neighborhood where Tonda Thompson was raised. Ebony grew up in Chicago, but when she was a teenager, her mother sent her to live with her father in Milwaukee, to get her away from violence. Back then, she remembers, Milwaukee was safe enough for her to sleep on the porch when it got too hot inside. Now, she’s reluctant even to take TJ out, because she thinks the city has gotten too dangerous. “Milwaukee has [gone] from beautiful to garbage,” Ebony said. Even the inside of her apartment isn’t totally safe. Around the time Ebony got pregnant, an electrical fire forced her to move temporarily into a Red Cross shelter. Now she worries about lead paint on the windowsills and puts blankets down on the floor before she lets TJ crawl around on the old carpet. “I just want a house, where my baby can play in a yard, but, you know—where?” she said.
Ebony’s impression of decline is real, although Milwaukee has always been hostile to its black population. During the 1940s and ’50s, the manufacturing boom created high-paying jobs, and the city flourished. But African Americans came more slowly to Milwaukee than other Midwestern cities, in part because the labor force was already filled by European immigrants. In the 1920s, the Milwaukee Real Estate Board had begun to steer black renters and home buyers to a small area northwest of downtown. By 1940, according to the sociologist Juliet Saltman, all of the city’s 8,821 black residents lived in a three-by-four-block area. The City Council repeatedly rejected a fair-housing ordinance, passing it only after Congress passed the Fair Housing Act in 1968.
&ldquoIf 100 people died from tuberculosis, people would say we have a public-health emergency.&rdquo
The city’s black population began to grow in the 1960s. But as Alec MacGillis recounted in a 2014 article in The New Republic, there was little time for the city’s black community to build wealth before the local economy collapsed. Between 1961 and 2001, the city of Milwaukee lost 69 percent of its manufacturing jobs. In 2007, the city got walloped again by the housing crisis, which wiped out much of the black wealth the city had. Milwaukee was one of the cities hardest hit by the real-estate crash, with 40 percent of its homes—nearly half of those in Ebony’s neighborhood—underwater as of 2014.
More than a decade ago, Ebony had a daughter. She lived for eight months. Just before she died, Ebony bathed her and put her in a swing. She went to check on the chicken she was cooking and came back to find her daughter unconscious. The official cause of death was sudden-infant-death syndrome. SIDS, one of the leading causes of infant death in the United States, still mystifies researchers. But what happened to Ebony’s daughter is part of a broader trend that defines America’s high infant-mortality rate: Where the United States really lags is in keeping babies alive after they’ve left the hospital, when they’re between 1 month and 1 year old.
After her daughter died, Ebony was in an abusive relationship and had several miscarriages. She assumed she’d never have another child. “I didn’t want to bring any kids into this world or this time,” she said as she laid TJ across her lap to change his diaper. “But God said otherwise, and of course I’m going to accept my blessing.”
Ebony has had high blood pressure since she was 11, and when she was pregnant with TJ, she developed preeclampsia. He was born on Christmas Eve, several weeks early. For the next couple of months, JoAnn visited every week to check on his health and set parenting goals with Ebony. TJ grew quickly, and JoAnn’s encouragement showed Ebony that she was on the right track. “Every time she’d weigh or measure him, she’d say, ‘Oh, he gained a pound or two!’” Ebony said. “The fact that he was progressing made me real happy.”
Parenting is difficult under the best of circumstances, but Ebony and women living in other poor, segregated neighborhoods face a particularly brutal slate of risk factors and stressors—having to move during pregnancy, for instance. Harvard sociologist Matthew Desmond found that 30 percent of the people evicted in Milwaukee each year are women living in black neighborhoods, though they make up less than 10 percent of the city’s population. Then there’s the fact that Wisconsin locks up more of its black men than any other state in the country, leaving more women to parent alone, or with partners whose criminal record makes it difficult for them to get a job.
Chronic stress raises amounts of cortisol, a hormone that at elevated levels triggers labor. It can also cause an inflammatory response that restricts blood flow to the placenta, stunting infant growth. But it’s not just stress during pregnancy that matters: Health experts now think that stress throughout the span of a woman’s life can prompt biological changes that affect the health of her future children. Stress can disrupt immune, vascular, metabolic, and endocrine systems, and cause cells to age more quickly.
All of these effects together create what scientists call “allostatic load,” or “the cumulative wear and tear on the body’s systems owing to repeated adaptation to stressors,” according to a 2006 study published by Arline Geronimus and others in the American Journal of Public Health. Geronimus, a University of Michigan professor, developed what she calls the “weathering” hypothesis, which posits that black Americans’ health deteriorates more rapidly than other groups’ because they bear a heavier allostatic load. “These effects may be felt particularly by Black women because of ‘double jeopardy’ (gender and racial discrimination),” Geronimus and her co-authors noted. (Infant mortality is just one of many forms of disease that fall disproportionately on black Americans. The list includes cervical cancer, asthma, diabetes, and cardiovascular disease.)
&ldquoIt&rsquos easier to say &lsquoWe need to make sure women take folic acid&rsquo than it is to fix racism and poverty.&rdquo
Researchers now link much of that higher stress burden to racial discrimination. Dr. Camara Phyllis Jones, president of the American Public Health Association, proposed a now widely cited framework for understanding how discrimination affects health outcomes, breaking it down into three categories: internalized, personally mediated, and institutionalized. Personally mediated experiences include things like being treated differently at a doctor’s office than white patients black women who report these kinds of experiences have been found more likely to have low-birth-weight babies. But institutional discrimination—which refers to the ways in which unequal treatment has been baked into our social, economic, and political systems—impacts individual health too. It’s apparent in the disparities in the criminal-justice system, in education, in predatory lending practices that target African Americans, and in the siting of polluting industrial facilities near communities of color. These problems are particularly acute in most of the cities with large racial gaps in their infant mortality rates. In none of America’s peer countries is racism so embedded—and that may explain why racial gaps in infant mortality and other health outcomes are worse here. These various forms of discrimination, stacked up over a lifetime, can cause chronic stress, which in turn can damage the biological systems necessary for a healthy pregnancy and birth.
Institutional racism is like a thicket of thorny plants: After a woman spends a few decades walking through it, it can be hard to tell which particular prick led to her child’s death, or if it was all of them together. But there’s growing recognition that a woman’s entire life experience matters, maybe even her parents’. “We literally embody, biologically, the societal and ecological conditions in which we grow up and develop and live,” said Dr. Nancy Krieger, a professor of social epidemiology at Harvard University. “Infant mortality is affected by not only the immediate conditions in which the infant is conceived and born, but also the health status of the mother and, some evidence indicates, the father as well.” In 2013, Krieger and her colleagues compared infant deaths in states with and without Jim Crow laws they found that black infant deaths were significantly higher in Jim Crow states, but that after the passage of the 1964 Civil Rights Act, the gap shrank and, by 1970, had disappeared (although the overall black/white gap persisted). The study suggests that discriminatory policy does indeed shape health outcomes. If this is true, then the infant-mortality gap can’t be closed without addressing broader inequities in employment, education, health care, criminal justice, and the built environment—in other words, without ending racial discrimination altogether.
C ommunity leaders working to reduce infant mortality in Milwaukee understand the complexity of their task. Operating alongside the Milwaukee Health Department’s home-visiting program is a community partnership, the Milwaukee Lifecourse Initiative, led by the United Way of Greater Milwaukee and Waukesha County. “If you look tangibly at where you can intervene, it seems easier, quite frankly, to say, ‘OK, we just need to make sure more people have primary-care providers we need to make sure women take folic acid,’ than it is to fix racism and poverty,” said Nicole Angresano, a vice president at the United Way. “It’s critical that we think more broadly. It’s also really daunting.”
The Lifecourse Initiative targets three zip codes on the city’s north side, including the neighborhood where Tonda Thompson grew up and where Ebony lives. Part of the plan focuses on fatherhood. Unlike earlier “responsible fatherhood” initiatives, which emphasized child-support enforcement, the program focuses on systemic problems, which means connecting men to jobs—a higher percentage of African Americans are unemployed in Milwaukee than in any other US city—or keeping an expectant father who’s been caught up in the criminal-justice system in contact with his family. Other programs involve faith leaders. Community gardens at several churches prioritize mothers in an attempt to compensate for the lack of fresh produce available in the inner city. Several dozen churches have been designated “safe-baby sanctuaries,” places where families can come for education and resources like diapers.
At one of those places, Ebeneezer Church of God in Christ, I met Julia Means, a nurse with a striking track record with Milwaukee’s infants. By her own count, Means has worked with 360 families in the last 12 years, through a program called Blanket of Love. Every single baby whose parents came to her group meetings lived to its first birthday, she told me. Her method is to “wrap the pregnant woman up in love.” Sometimes that’s meant finding a home for them, and furniture to fill it or role-playing, to help them feel confident speaking to doctors or educating them on safe sleeping conditions or, in a few cases, helping women escape abusive partners in the middle of the night. Another way to put it is that she does what she can to reduce the stress in these women’s lives.
In its efforts to reduce infant deaths, Milwaukee has made mistakes: A few years ago, the city launched an ad campaign focused on safe sleep featuring graphic images—one showed a baby in bed with a butcher knife, with the message “Your baby sleeping with you can be just as dangerous.” An alderwoman pushed to criminalize parents whose babies died after sleeping with them if the parents had been intoxicated. Means said the campaign “set the community on fire” it struck her as harsh and racially motivated. She warns against unsafe sleep arrangements in her own program, but because they account for only a small percentage of infant deaths, she said it made little sense for the city to direct its resources to the issue. Milwaukee Mayor Tom Barrett told me that initially he’d seen safe sleep as “low-hanging fruit,” only to realize later that it came across as scolding black women.
Barrett, who is notably engaged in the effort to lower infant mortality, pointed out that the general trend in the city is positive: Fewer babies of all races are dying in Milwaukee each year. But because the outcomes are improving more quickly for white infants, the racial disparity is growing. It’s all but certain that the city will miss its goal of a 15 percent reduction in the black infant-mortality rate this year. The state’s Republican leadership has only made things more difficult by cutting social support programs like food stamps. Last year, the state stripped hundreds of thousands of dollars in funding from Milwaukee’s home-visiting program. Wisconsin Republicans have also fought efforts to increase the minimum wage, which could have a positive effect on the infant-mortality rate. A study released last year found that a $1 increase in the minimum wage in various states between 1980 and 2011 corresponded with a 1 to 2 percent decrease in low birth weight and a 4 percent decline in deaths of infants between 1 month and 1 year.
The new buildings rising in Milwaukee’s prosperous lakeside neighborhoods stand in stark contrast with the grinding poverty on the city’s north and west sides. When I spoke with Barrett, he argued that city leaders were doing what they could to spread the benefits of that growth—for instance, by requiring construction projects that receive public funding to hire local workers. But the sheer scale of the segregation and inequality makes that kind of effort look like tinkering at the margins. The same is true on a national level. For several decades now, neither political party has applied much urgency to the task of dismantling the major drivers of racial disparity—housing and school segregation, for instance—head-on. Several social-support programs have been effective in bringing down infant-mortality rates and the black/white gap in other cities their major flaw is one of scale. Barrett acknowledged that home visits won’t be able to reach every family who needs them. As Means told me, not everyone wants city officials coming to their homes. But when I pressed the mayor on whether the city government could do more to address segregation and poverty, he threw his hands up in exasperation and shook his head. “Welcome to America,” he said.
A fter Terrell died, Tonda Thompson remembers, people assured her that she’d have another child, as if he were replaceable. “People tend to blow it off like it’s nothing,” she said. “But when a black family loses a baby, it can destroy every bit of that family.”
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Thompson did piece herself back together again. She took the dream about the baby in the washing machine as a sign—she had to help Milwaukee crack the code. In 2015, Thompson accepted an AmeriCorps position to work with the United Way on infant mortality. Later, she got a job working for a city alderwoman. She is also expecting a child, and plans to name him Jehlani, a Swahili name meaning strong and mighty.
Thompson told me that although the city has good intentions, people in her community still aren’t getting what they need: The segregation isn’t changing, the incarceration rates aren’t coming down, and people she knows don’t trust the medical community. A few weeks before we met, a police officer shot and killed a 23-year-old black man named Sylville Smith, triggering several nights of protests. There are “too many black babies dying, too many black men dying,” Thompson said. The horizon seems particularly bleak for young women who get pregnant. “We do have a stigma of ‘She’s not married she messed up she’s young—she ain’t going to be nothing.’ And that attitude gets into her mind and goes to the baby.”
Infant mortality is a wicked problem. It requires us to think about health less as a matter of biology and more as the result of political choices and socioeconomic realities. It has no single solution. But “the point is not to frame complexity as daunting,” said Nancy Krieger, the Harvard epidemiologist, “but actually as opening many avenues for effective action, and asking how different groups that are already engaged can understand how their issues relate to infant mortality.”
Bevan Baker, the health commissioner, described Milwaukee’s infant-mortality work as an opportunity to reckon with what is perhaps America’s most profoundly destructive legacy. “When you look at the racial disparity, it forces us as citizens and residents of this great nation to deal with the incomprehensible notion that race matters,” he said. “That’s something that Milwaukee, Wisconsin, and every other state will have to come to grips with.”
Editor’s note: An earlier version of this piece referred to cortisone as the hormone that can trigger labor. In fact, that hormone is cortisol. The text has been updated to correct the error.
Zoë Carpenter Twitter Zoë Carpenter is a contributing writer for The Nation.
White Baby Shocks Black Parents: Medically Possible?
Ben and Angela Ihegboro and their beautiful new baby girl Nmachi. (The Sun) The Sun
(CBS) How did Ben and Angela Ihegboro, a black Nigerian couple living in London, give birth to a white daughter?
The answer may not be so black and white, experts say.
According to the BBC, there are three potential reasons for the baby Nmachi's unexpected appearance: "dormant white genes which entered both of her parents' families long ago, a genetic mutation unique to her, or albinism."
The first reports on the family's strange case had ruled out albinism, but the BBC says Nmachi's doctors have not ruled it out.
Albinism, a condition whereby a person has little or no color in their skin, hair and eyes, can remain dormant in genes for many generations. Just because the couple's living relatives aren't afflicted by the disease, that doesn't mean they aren't carriers. It is not uncommon in Nigeria, according to the BBC.
But it's not the only possible explanation.
Doctors also say Nmachi's parents may harbor long dormant Caucasian DNA from a long forgotten interracial coupling, according to the BBC. A third possibility is perhaps the most tantalizing but also the scariest. Nmachi may have a unique genetic mutation that doctors have not seen before.
Understanding the Conversation Behind the Behavior
When reviewing records of many of the children with whom I work, I am perplexed at one particular notation I regularly see written by therapists and counselors. Under the list of negative traits of the child, it is often written, “Child exhibits attention-seeking behaviors.”
I strongly believe that children seek attention because they need attention. Nature has designed children to be completely dependent on their parents at the moment they are born. A baby crying is signaling to the parent the baby has a need—a need that the baby cannot satisfy on his own. The baby is indeed exhibiting attention-seeking behaviors.
The natural flow of the developmental journey of a child is to gradually release this need for attention, moving from a state of dependence to a state of balanced independence. The time period for this is about 18 years. We are the only animals in the animal kingdom that have our children under our care for this length of time. Expecting our children to not need our attention or to view it as a negative behavioral issue during these 18 years goes against our biology.
When children do not know how to verbally express their needs (which is predominantly the case during early childhood), they “speak” through their behaviors. In other words, behavior is a form of communication. When a parent can stop, pause, and “listen” to the behavior of a child, it can become quite obvious what the child is saying. Looking at the behavior from an objective perspective also unveils the logic behind the child’s behavior. Here is a list of 10 behaviors along with an interpretation of each behavior to demonstrate this:
1. Slamming Doors. When a child begins slamming doors, it is an indication that he does not feel like he is being heard. By slamming a door, he is making loud noises, hence forcing the parent to “hear” him. He is essentially saying, “I need to have a voice and I need you to listen to me now!”
2. Cursing. Most children know that they should not curse. They use profanity to jar the parent’s nervous system into listening. It is a way to get a parent to respond to the child, even if the response is negative. The child’s fear of not being good enough for the parent to pay attention to him is also playing out in such a scenario.
3. Shutting Down. A child who shuts down, refuses eye contact, walks away, or gives the parent the silent treatment is a child who is overwhelmed. We have traditionally labeled a child like this as defiant. This is a child who is saying, “Life is too big to handle. I’m shutting down my world in order to survive.”
4. Hitting a Sibling. Sibling rivalry is more about the relationship between the child and parent than it is between two siblings. If a child is not feeling secure in his relationship with his parent(s), he will perceive the sibling as a threat to this relationship with the parent(s). Reacting against the sibling is the basic “King of the Hill” game in order to win the attention of the parents. The child may receive negative attention from the parent (“Billy, stop picking on your brother!”) but to a child, especially a child with a trauma history, any form of attention, whether positive or negative, is love.
5. Challenging Authority. A child who challenges authority is a child who has lost his trust in authority figures. Look back into the child’s history and you will likely see a child who was abused, neglected, or abandoned by someone who was supposed to care for and nurture the child. A child who fights having someone else in charge, is a child saying, “I can’t trust anyone. It is too much of a risk.”
6. Saying, “I hate you!” Such hurtful words directed toward a parent from a child are simply a window into the child’s heart. The child is projecting his self-hatred and self-rejection back onto the parent. What he is communicating is, “I hate myself!” It is easier to hurt someone else than it is to feel the internal hurt within one’s own heart.
7. Arguing About Everything. A child who argues about everything and anything is keeping the parent looped in a conversation in order to keep the parent attuned to him. He feels that if the parent were to stop talking with him, he would cease to exist. Arguing is his way of staying connected. It is a negative form of attachment.
8. Laziness. Describing a child affected by trauma as being “lazy” is a gross misinterpretation of the child. Profound laziness is typically a sign of a child who experienced helplessness early in his childhood it is a learned behavior. Neglect happens when a child tries to elicit attention from his caregiver and the result is nothing. No attention. No help. Zilch. The child learns that his energy does not produce results and as he grows older and gets challenged by life, he will simply shut down and do nothing. He is saying, “My efforts don’t produce results so therefore I won’t even try. It’s just not worth it.”
9. Pushing Every Boundary. Many children have such intense behaviors that the adults around them in the past demonstrated a lack of ability to handle them or an unwillingness to stick with them. When parents find their child pushing every boundary, every rule, and every limit, the child is asking, “Can you really handle me?” and “You say you’re my parent, but I need to know you’re not going to give up on me so I will test you to make sure you really are committed before I put any trust into you!”
10. Becoming Unglued During Transitions. Trauma happens by surprise and when it happens, there is typically a major change in the child’s life. It is transitional trauma. The aftermath of such traumatic experiences is that the child becomes fearful of every transition, whether large or small. A child’s belief around transitions becomes, “Something bad is going to happen. Guaranteed.” Past traumatic experiences create the black and white thinking that “All change equals pain.” When a parent sees a child’s negative behaviors intensifying during a transitional time, the parent needs to remember that the child is saying, “I’m so scared that my entire world is going to fall apart in a flash just like it did in the past!”
Children’s behaviors are perfectly logical. The issue is that we’ve been looking at the behavior from our logic, not the child’s logic. Before judging the behavior as either “right” or “wrong,” look at it first from a literal perspective and ask yourself, “What is he/she trying to communicate with this behavior?” When you understand the communication behind the behavior, it will give you the solution you need to find a loving, nurturing, and relationship-based solution to the behavior.
Meeting the child’s underlying need that is activating the behavior creates the opportunity for you to help your child correct his behavior through teaching moments. Teaching children how to communicate their needs is the key. For an adopted child who has been impacted by trauma, it takes a tremendous amount of courage to come to a parent and say something simple like, “Mom, I need a hug.” or “Dad, I don’t feel like you’re listening to me.” Their traumatic histories of rejection and abandonment have left a blueprint that says not only will their needs not be met but they might be rejected for voicing their needs. Turning this blueprint around and helping them to rewire their brains to know that asking for their needs is exactly what you want them to be able to do.
Neuroscience tells us that the brain is ever changing and neuro-plasticity tells us that the brain has the ability to continually formulate new connections. In the past, it was believed that once we were hard-wired one way, we simply had to accept what we were given. However, brain scan imaging shows us that we are actually creating new connections all the time. This is even more true for children during their developmental years. Taking the time to “listen” to your child’s behavior and then teaching your child how to ask for their needs will help them to be better equipped neurologically to have a more positive long-term future.
However, when parenting a child with challenging behaviors on a day-to day basis, taking the time in every interaction to first listen to the behaviors takes a tremendous amount of time and emotional energy. Life happens and it is easy to lose sight of the idea that behavior is the language of a child. Negative behaviors are tiring and parenting adopted children who have been impacted by trauma makes this even more intense! Thus, it is imperative for parents to take care of themselves first. Their needs are equally important: you can’t give something you haven’t received yourself. When parents can keep their cup filled, they will have enough space inside of them to keep looking beyond the behaviors and listening to the behaviors instead of reacting to the behaviors.
The parent/child relationship is a dyad—a two-part system. So parents, remember that your behavioral response also signals a communication to your child. Thus, it is imperative for you to stay mindful and attuned. Give enough attention to yourself as to stay in a place of love so you are always speaking the language of truth, love, and acceptance to your child in return.
Color Patterns in Crossbred Beef Cattle
Crossbreeding provides commercial cattlemen the opportunity to combine desirable characteristics of two or more breeds (breed complementarity – see fact sheet 2014-5) and increase performance due to hybrid vigor (heterosis). The single strongest argument for crossbreeding is the advantage in fertility and longevity of crossbred cows. With all of the advantages crossbreeding provides, designing an effective mating system should be a top priority for all commercial cattlemen. To plan an effective crossbreeding system, it is helpful to consider any potential detractors that are easy to address. One such detractor exists due to market discrimination against certain breeds and/or colors and lack of uniformity in color. As we increase the number and diversity of breeds involved in crosses, we decrease our ability to maintain complete control of coat color in the offspring unless it was taken into account during breed selection. With that in mind, knowing the basics of coat color inheritance can help producers know what to expect from various breed/composite pairings relative to color pattern.
The purpose of this fact sheet is to provide guidance on how to maintain a uniform color pattern when formulating crossbreeding systems. In some breeds and breed crosses, the color is highly predictable however, in some other breeds and breed crosses, color is less predictable. A working knowledge of the inheritance of coat color will aid in planning for the color pattern to expect among calves when crossing breeds. This can be very important for evaluating marketing options either at weaning when forming large group lots or on the rail when targeting specific branded beef programs.
Many breeds of beef cattle have a fixed color pattern for that breed because selection has been placed on the color in order to maintain these characteristics. For example, all Hereford cattle have a red body color with a white face, all Charolais are white, and all Red Poll are red. However, other breeds may have more than one basic body color such as red or black Limousin or Simmental, and white, red, or roan Shorthorn. Still other breeds have multiple colors with more unpredictable inheritance patterns, such as spotting, brindling, or stripes in Longhorn and Beefmasters. Some color modifiers under genetic control have been selected against in many breeds (unless they are a feature of color in the breed, such as in Charolais or Hereford) and these features, such as “diluters” and blaze faces, are much less common than in the past which makes the process of managing color in crossbreeding systems much easier.
Table 1 shows several common breeds of beef cattle and the predominant color pattern that is most commonly associated with each breed. Recently, some breeds with unique color attributes such as spots, blaze faces, and diluter genes have selected against these traits to increase favorable perceptions by terminal buyers. Other breeds that were traditionally red have selected heavily for black coat color and are listed in Table 1 as both black and red. Introgression of other breeds (specifically Angus) into some of the Continental breeds has altered the traditional color pattern of some of these breeds. Color patterns likely to result from specific crosses are detailed in Table 2.
Table 1. Basic body colors of common cattle breeds.
Table 2. Color pattern expected in progeny resulting from the matings of bulls and cows of various colors.
All animals are carriers of mutations somewhere in their DNA for one or many recessive traits. Because an animal must inherit two copies of a given recessive mutation to be affected, and with only a few animals typically sharing the same mutation in the whole population, there is rarely a mating cross that has the potential to create affected offspring under natural selection. It is when relatives are mated that there is the possibility that offspring will inherit the mutant allele on both sides of the family tree.
When you have crossbred cows, predicting color in the offspring can be more difficult, but it helps to understand how color is inherited. All cattle basically possess one of three basic colors: black, red, or white. Black is dominant to red, and both black and red are co-dominant with white. One black or red allele with a white allele would result in either a black or red roan animal. In order for an animal to be red or white, they must have two alleles for either red or white, respectively. There is another set of alleles that controls the dilution, or intensity, of that color. Dilution causes black to be muted to gray and red to be muted to yellow. As an example, Charolais cattle are red, but possess two alleles for dilution, which results in white coat color ( Gutiérrez-Gil et al. 2007 ). This is why Charolais x Angus cattle are gray (diluted black). A very thorough discussion of coat color in cattle, including its many variations (Table 3) can be found at http://simmental.org/site/pdf/other/olsoncolor.pdf .
Table 3. Description of known coat color patterns in cattle (adapted from Olson 1999).
In a typical sale barn market, cattle are sold with little, if any, information made available about breed or performance. Many buyers will estimate performance (growth, carcass characteristics, etc.) in relation to the reputation of the breed thus, they may look for signs that indicate a certain breed or breeds within crossbred cattle. Other buyers may be looking to source animals that qualify for black- or red-hided branded beef programs and are willing to pay a premium for these types of calves. Some breeds are prone to producing calves that have certain distinguished color markings, such as white-faces, brindling, or white stockings on their legs.
Some general rules can be utilized to give the greatest chance of obtaining uniformly-colored groups of calves. Because red is recessive to black coat color, breeding solid red cows and bulls will produce solid red calves, which makes solid red an easy color to maintain in a crossbreeding system. However, because black is dominant to red, breeding solid black bulls and cows will often produce black calves, but may also yield red calves. To ensure a solid black calf crop, breed solid colored females (without diluter genes) to a homozygous black bull. If black baldy calves are desirable, use of Hereford bulls on black cows (or black bulls on Hereford cows) will yield the desired effect. If color extremes in the cowherd are a major concern, they can be masked by breeding over several generations to Charolais bulls.
In today’s market, where marketing branded beef is advantageous, knowledge of coat color inheritance is essential. Even under traditional marketing systems, uniformity in coat color can often provide premiums/discounts in the market place. Therefore, knowing the basics of color inheritance will help in planning crossbreeding systems that create animals that are suitable for desired marketing niches or branded programs.
If a Black Chicken is mated with a white chicken,and all offspring are BLACK and WHITE,This Shows_______ ?
According to Mendel's law of dominance , when two alternative alleles of a trait are present together, one of these is able to dominate over the other and expresses itself in phenotype. This allele is termed dominant allele. The other allele, though present is not able to express itself, is termed recessive allele .
In subsequent experiments to Mendel's work, it was observed that law of dominance is not universal. In Mirabilis jalapa (morning glory) , it was observed that neither of the alleles representing red and white flower color could dominate over the other. When these two alleles were present together in heterozygous plant , the flower color was pink, intermediate between red and white. This phenomenon is termed incomplete dominance .
The color of feather of chicken in question is similar to flower color of Mirabilis jalapa . The black color is represented by allele B and white color by allele W , as neither of these allele can dominate over the other.
On mating a black chicken with white chicken, the offsprings will inherit B allele from black parent and W allele from white parent. The genotype of offsprings will be BW. The color of feathers will be black and white as both alleles express in the phenotype and neiter of tese two alleles is able to dominate over the other.
The feather color in chicken in question exhibits the phenomenon of incomplete dominance.
Children of the Opioid Epidemic
In the midst of a national opioid crisis, mothers addicted to drugs struggle to get off them — for their babies’ sake, and their own.
Elizabeth and her baby at home in Rhode Island. Credit. Alec Soth/Magnum, for The New York Times
It was not until her third month of feeling unwell, in the fall of 2016, that Alicia thought to take an at-home pregnancy test. Until then, she assumed her fatigue and nausea were withdrawal symptoms from the Percocets she’d been dependent upon since the year before. “When some days you don’t get enough, you could definitely throw up or wake up feeling sick,” she told me. “It was easily confused with morning sickness.”
Alicia, who asked that I use her nickname to protect her privacy, was 26 at the time, living with her boyfriend in a tiny apartment just outside Providence, R.I. From the start of their relationship, she had been inspired by his seriousness he had a job in I.T. that paid $20 an hour. Unlike some of her previous boyfriends, this one wore collared shirts to work and did not use drugs. He had a gangly earnestness that was endearing. “He grew up as a good boy,” Alicia told me. “He did what was right, and he was smart. I wish I could have been like that.”
She had struggled with drugs and alcohol since age 15. Family life was often painful her father, a mechanic, was an alcoholic (he quit drinking years ago) she has a mentally ill sibling and her mother, a secretary who later went back to school and became a corporate manager, held the family together in a suburb outside Providence. As a teenager, Alicia was shy and often depressed — afraid of saying the wrong thing and looking foolish. “All of this paranoia and social anxiety, it made me very worked up,” she told me last May. “I could never look normal in a social setting.” At 15, she discovered that being high made her loose and funny. “I had my first drink, I tried weed, I had my first cigarette,” she told me. “I was able to go out and hang out with people. I wasn’t isolating myself and staying home. I created a whole new personality of me.” As an older teenager, she began taking the bus into Providence and hanging out with a crowd of drug-using adults, many of whom were homeless. “After 18, 19, I felt like, Whoa, I don’t even know who I am without using stuff.”
Around that time, she got what she called a “dream job” at a Macy’s Clinique counter, but she was fired for chronic lateness. She had fallen into abusing synthetic marijuana (plant particles sprayed with chemicals), known in Providence as “monkey.” At her parents’ insistence, she underwent a seven-day inpatient rehab later, when she was 22, they sent her for a second, longer rehab for excessive drinking. Toward the end of the 18-month period of sobriety that followed, she met her boyfriend and moved with him into his parents’ house. She was 24 he was 28. He encouraged her to apply to cosmetology school, and she arranged for student loans and enrolled in a two-year program. She saw a psychiatrist and was prescribed medication for her depression and anxiety, as well as for obsessive-compulsive disorder.
But other struggles persisted. She had a habit of picking at small lesions on her skin, which, early in her new relationship, worsened a staph infection she acquired from sharing makeup. Alicia went to the emergency room twice, but even as she wept from the pain, “in the back of my head I remember thinking, I wonder what they’ll give me?” She left the hospital each time with a prescription for five-milligram Percocets: oxycodone mixed with acetaminophen.
“I started doing it as prescribed, maybe one every five hours when you feel the pain,” she said. “But then I would think, If I take another half of one, I could get high from it. This is when I really made a bad move: I sniffed the pill, and it gave me a different effect. It was a lot more intense. Everything was so slow. I could see and hear everything going on around me. I could control my reactions. Oh, it’s so powerful — I don’t know what they put in there.”
Alicia prickles with intelligent awareness and self-scrutiny. She has large brown eyes thick, wavy brown hair that reaches her shoulders and a few tattoos on her ankles and shoulders. Her voice is mellow, almost purring, as if she is perpetually trying to calm someone down. The person most in need of calming is her she is prone to obsessive fretting. “Even something as small as: I need to call the dentist. I’ll keep saying it over in my head, but I won’t be able to get it done. I’m so overwhelmed I can’t get started.” These repetitive thoughts make her own mind an uncomfortable place to be in reaction, she sometimes collapses into self-sabotage. “I’ll be like, Whatever, let’s go get a pill, let’s party. Every paperwork you have, you’re like, I can’t finish this. I don’t want to go to the grocery store today. I can go from zero to extreme quickly, and that’s my weakness.”
By the time the 50 pills from her hospital visits ran out, Alicia had formed a conclusion. “I thought: This is my lifestyle. I’m not the best version of myself unless I’m on it.” She had a friend who also liked pills and had connections to buy them, and she soon found herself immersed in a demimonde of chronically ill and disabled people who supported their own addictions by selling a portion of the pills their doctors prescribed. “It happened so quickly that I became physically dependent,” she told me. “No one knew. I had a little pill counter. Everything was divided perfectly by the day, by the milligram. I felt like, I’m a safe user with a pill that a doctor has created, and also supplied.”
When cutting clients’ hair at school, she found that the pills helped her to be relaxed and personable — resulting in larger tips. “I would get a 10-milligram pill, and I would split it into three. I would take any sort of wrapper that I could fold in half, and I would put a little bit in, I would rub a lighter over it, and then I would use a credit card and get it all into one perfect little line. I would get a little straw and take it right up my nose, and then I would lick the paper and get every last bit of it, and I’d put it back in my little pouch. I’d have two milligrams before this client, another five after. I was just bouncing around like I didn’t have a problem in the world. This made people want to be around me, and I liked that. When I’m sober, I don’t want to be around people too much. I loved the idea of being a superwoman.”
As Alicia’s tolerance to the drug increased, the pressure of feeding a mounting 30-to-40-milligram-a-day habit on pills costing a dollar per milligram on the street began to take its toll. “That’s when I realized: I’m very irritable, I’m becoming like a monster because I can’t find these things.”
She began fighting with her boyfriend and acting disrespectfully to his mother, who kicked them out of the house. In a new apartment, with rent to pay, the couple’s troubles escalated. Alicia’s boyfriend suspected her of using drugs and would lurk outside the bathroom while she was sniffing pills inside. Their violent fights prompted calls to the police from neighbors, and Alicia and her boyfriend filed domestic charges against each other. In order to keep buying Percocets, she sold the Adderalls she had been prescribed by her psychiatrist for O.C.D. “I became very selfish,” she told me. “Even if I got a little euphoria, it wasn’t fun. I had to take these things just to not physically be sick. I was thinking, This is a lost cause: I’m spending $30, $40, $50 a day. How am I ever going to keep up with this?”
It was at this point that her sickness and fatigue prompted her to take an at-home pregnancy test. Doubting the positive result, she went to a women’s clinic to be retested and learned that she was in her fourth month. Her joy at the prospect of motherhood was laced with terror. “I’m thinking, Oh, my God, I’ve been using, and I’ve had this baby inside me for three and a half months. So I’m freaking out. I’m thinking, What do I do? How am I going to have an addiction and have a baby?”
Of the ESTIMATED 2.1 million Americans currently in the grip of opioid addiction, many are women of childbearing age. The young-adult population has been hardest hit, proportionately, with nearly 400,000 adults ages 18 to 25 suffering from addiction to prescription painkillers (the vast majority) or heroin. Strict adherence to a birth-control regimen — or any regimen at all — is difficult for someone whose body and mind have been hijacked by drug dependence, which may help to explain why, according to the largest recent study, nearly 90 percent of pregnancies among women who abuse opioid medications are, like Alicia’s, unintended. The number of pregnant women using opioids grew significantly between 2004 and 2013, according to recent research published in JAMA Pediatrics, with the increase disproportionately high — more than 600 percent — in rural areas. Another decade-long study found a fivefold increase in the number of newborns who experienced the opioid-withdrawal condition known as neonatal abstinence syndrome, or NAS: to eight per 1,000 hospital births from one and a half. Experts estimate that a baby with NAS is born in America every 15 minutes.
But the tally of babies born into withdrawal also includes the offspring of a great many mothers who go into treatment in the course of their pregnancies. The standard of care for a pregnant women addicted to opioids is medication-assisted treatment: a long-acting opioid substitute — traditionally methadone — that binds to the body’s opioid receptors to prevent withdrawal symptoms, usually without causing the euphoric sensations that commandeer the brain’s dopamine system into a relentless quest for more. Pregnant women on methadone or buprenorphine (a newer opioid-replacement drug) are more likely to bring their pregnancies to term, ensuring higher birth weights and better health for their babies. Federal standards mandate that methadone clinics require pregnant clients to receive prenatal care in order to get their medication. Women stabilized on medication-assisted treatment are in far less danger of relapsing, overdosing or contracting H.I.V., hepatitis C or other infections common among those who inject drugs. They experience less maternal stress, which has been shown to negatively impact the fetus’s epigenetics, or gene expression.
But because methadone and buprenorphine are still opioids, a fetus adapted to them is still at risk for withdrawal after birth. Most experts feel that this risk is justified. “As a society, if we’re thinking about the trade-off, it is much better to get Mom into treatment, for her health and her infant’s health, and then have some risk of neonatal abstinence syndrome,” Dr. Stephen Patrick, a neonatologist at Vanderbilt University Medical Center, told me. Compared with other babies in the neonatal intensive-care unit, “for the most part, infants with neonatal abstinence syndrome are just not that sick.”
Symptoms of withdrawal in newborns range from relatively benign indicators like yawning, sneezing, mottled skin and a high-pitched cry to more serious problems like diarrhea, difficulty feeding and, very rarely, seizures. Doctors can’t predict which babies will develop the syndrome, although factors like maternal smoking, anti-anxiety drugs and antidepressants have been shown to increase the likelihood. Although there are common practices, there is no uniform protocol on how to diagnose or treat NAS morphine, methadone and buprenorphine are all currently given to newborns, while some doctors believe that, except in extreme cases, swaddling and skin-to-skin contact with the mother are sufficient. Nor has it been determined what, if any, long-term effects NAS might have on a child the first longitudinal study, a multisite N.I.H. study begun in 2014, in which 117 babies treated for NAS will receive developmental tests at 18 months, is still underway.
Addiction is now widely recognized as a mental disorder, and the medical establishment and communities are more likely to treat people with drug dependency as victims of an illness. But this more generous spirit rarely extends to pregnant women in the grip of addiction, who are still widely seen as perpetrators. In 24 states and the District of Columbia, the use of any illegal substance during pregnancy constitutes child abuse, and in Minnesota, South Dakota and Wisconsin, it is grounds for civil commitment: court-ordered institutionalization — say, to a drug-treatment program — regardless of the woman’s wishes or needs (using a drug once doesn’t mean she is addicted to it). In just the past few months, authorities in Oklahoma and Montana have announced new initiatives to prosecute pregnant women who use drugs or alcohol. In Alabama, according to a report by ProPublica and AL.com, at least 479 pregnant women were prosecuted — and some imprisoned — between 2006 and 2015 under the “chemical endangerment” law originally aimed at parents who risked their children’s lives by cooking methamphetamine at home.
This results in a crazy quilt of punitive approaches to pregnant women with drug problems, which vary arbitrarily by region, county and local politics. In New Jersey, a woman on methadone was charged with child abuse in 2011 because her baby had NAS — an entirely predictable outcome of following the standard of care. In Wisconsin, a pregnant woman who told her doctor she had successfully weaned herself off painkillers was forced onto methadone in 2013 by a skeptical judge who decided she still needed treatment — thus needlessly putting her baby at risk for NAS.
Widespread horror at the thought of newborns in withdrawal has led, some experts feel, to a cultural overreaction reminiscent of the “crack baby” hysteria of the late 1980s and early 1990s, which wildly overstated the negative effects cocaine would have on the children of pregnant women who smoked it. “Crack moms” were nearly always represented as African-American, adding racism to the mix of distortions at play in that perceived crisis. Race has worked the opposite way in our current epidemic — indeed, the perception of our opioid crisis as an epidemic, rather than a racial pathology, owes much to the fact that white Americans have been hard hit. But pregnant women are often treated especially harshly. As Lynn Paltrow, executive director of National Advocates for Pregnant Women, put it, “Pregnant women are perceived as their own special class of persons, entitled to fewer constitutional and human rights.” Race and class biases may be active here, too. In a 2013 study by Paltrow and a co-author, low-income and African-American women were more likely than other women to be arrested for possibly causing harm to their fetuses during their pregnancies.
Barry Lester, director of the Brown Center at Women and Infants Hospital in Providence and principal investigator of the Maternal Lifestyle Study, a 16-year landmark longitudinal study of babies exposed to cocaine in utero, told me, “In the ’80s and early ’90s, the initial reports were talking about cocaine causing massive brain damage: ‘These kids are going to be in wheelchairs.’ Then the real data started coming in, showing that, yes, there are cocaine effects, but you’re looking at something more like A.D.H.D. than heart effects and brain damage. You have to realize that there is a certain amount of prejudice against women who use drugs. The expectation — almost the wish — is that there’ll be something wrong with these kids so we can blame these mothers again, like we love to do.”
Health experts deplore the societal impulse to blame and punish drug-dependent women who find themselves pregnant because it discourages them from seeking treatment — even in the 19 states where a publicly funded drug-treatment program specifically for pregnant women exists. Not only does inhibiting a woman from treatment harm both fetus and mother, they say, it also squanders a rare opportunity to intervene constructively in a woman’s addiction. “Sometimes a pregnancy is when women see past their own traumas to have that clarity to move forward,” Dr. Lauren Jansson, director of pediatrics at the Center for Addiction and Pregnancy at Johns Hopkins, told me. “Treatment works, and especially for this population. They have a lot to gain.”
Alicia was alone with her quandary though her boyfriend welcomed the pregnancy, neither he nor her family knew about her addiction. The only people who did know were those who shared it, and she wanted nothing more to do with them. To her mind, taking Percocet while pregnant was out of the question. But how could she stop? After leaving the women’s clinic, where her pregnancy was confirmed, she tried calling Project Link, a treatment program in Providence for pregnant women with substance-use disorders. When she couldn’t get through on the phone, “I went right up to the building in person. I was a complete mess.” She wondered whether there was a way for her to get help without telling her boyfriend. “Because if I told him, he might not stay with me. He’ll say, ‘You’ve been lying to me this whole time, you’ve been using all of our money.’ ” Project Link advised Alicia to go to the emergency room and start opioid-replacement therapy, rather than go into withdrawal, which could cause her to miscarry. Instead, she purchased the illegal pills she needed to avoid getting sick and sniffed them through the weekend.
On Monday morning, she registered at Codac, a drug-treatment clinic in Providence, where nearly 2 percent of the clients are pregnant women. “I had no idea what methadone was,” Alicia told me. “But as long as I could be involved with something that kept the baby safe, that’s all I wanted to do.” She was prescribed an initial dose of 20 milligrams of methadone to replace the 30 to 40 milligrams of Percocet she had been taking each day, and was instructed to visit the clinic daily between 5:30 a.m. and 12:30 p.m. There, she would wait in line at a dosing window and be given a small plastic cup of clear liquid. Like all clients at Codac, she would be required to participate in drug counseling and to submit to drug tests, or “tox screens.” If she had consistently “clean urines,” as clients tend to call it, for 90 days, and followed other rules, she would be rewarded with a “take-home” dose once a week, sealed in a small plastic bottle.
After several days, Alicia screwed up her courage and told her boyfriend about her drug problem. “I was all choked up,” she recalled. “He was really shocked. He said, ‘I knew something was up, I just hoped it wasn’t that bad.’ I think it was kind of relieving to him that I wasn’t out at a club or at the casino I was just searching for these pills. But when we get into arguments, he’ll bring up things like, ‘You’re a dopehead,’ and it’s really hurtful.” She also told her mother, in a Facebook message, and her mother was loving and supportive.
After going to Codac, Alicia found an obstetrician in her town and signed a release permitting him to be in direct contact with the clinic, which was required to ensure her prenatal care. “I told him everything that I had been doing, and they did a lot more extensive ultrasounds than they would normally do on your average patient. It was causing me tons of panic attacks: I was thinking, What did I do to the baby already?”
Her tendency toward frenetic worry was worsened by the fact that her psychiatrist, on learning she was pregnant, had stopped her anxiety and depression medications. Neither Alicia nor the Codac nurse who works with pregnant clients had been able to find another doctor willing to prescribe them for a pregnant woman on methadone. Alicia smoked marijuana during her pregnancy, she said, to cope with her anxiety and nausea.
Each morning, before going to cosmetology school (and, after graduation, to her full-time hair-cutting job), Alicia stopped at Codac to be dosed. She recoiled from the clientele. “I don’t want to judge everybody, but if you can’t put some clothes on by 12:30, you’re still in a bad lifestyle. You can tell from their conversations that a lot of people are still using.” The discovery shook her she had believed that methadone blocked the potential to get high (it does for opioids, but only to a point), and this new knowledge felt dangerous. “If I wasn’t pregnant, I would be the first one to say, ‘Hey, let’s see if it still works,’ ” she told me. “But I can’t do that, and I don’t want to do it, but I’ve thought about it a million times. It’s scary, because my mind is still being controlled by the pills.” This feature of addiction — a compulsion to be high that circumvents logic, judgment and self-interest — is what can prompt relapses even years after the body has been cured of all physical dependence.
Early last May, three weeks before Alicia’s due date, I met her at Codac during a gathering of about two dozen of the clinic’s pregnant clients. The clinic sits in the shadow of an expressway, and as the 12:30 dosing deadline approaches, clients can be seen loping from underneath it to reach the doors before they’re locked. Inside, the atmosphere was gritty, with placards in the hall warning that tox screens now included a test for fentanyl.
The gathering of women was billed as a baby shower, but mostly it was a chance for pregnant clients to meet one another and talk with representatives of First Connections and Healthy Families America: groups that support high-risk women, including opioid users, and their newborns. Much of the discussion among the women centered on neonatal abstinence syndrome: dread and guilt at the idea of their babies experiencing withdrawal stories about friends whose babies had to go through it. Alicia chatted with Lyndsey, 31, who had brought along her feisty 8-month-old son. Like Alicia, Lyndsey was addicted to Percocet before switching to methadone, and her son spent three weeks being treated for NAS. “They took such good care of him,” she said of Women and Infants Hospital, where 80 percent of babies in Rhode Island are born, and where Alicia would soon deliver. “As soon as he started the medicine, he really didn’t have any symptoms. In the big picture, that was such a small glimpse. I forget that it happened.” Pregnancy had galvanized Lyndsey drug-free for 16 months, she was assembling student loans to begin nursing school.
I struck up a conversation with Elizabeth (her middle name), who was 26, petite and fair, with long straight hair, blond at the ends from grown-out highlights, and an air of apologetic sweetness. She looked impossibly young for someone with her history, which she shared with a trusting openness I’ve found to be characteristic of people in recovery. Her baby girl was due in June. Like Alicia, she had been energized and secretive in the early years of her addiction, working as a day care teacher and also assisting families of children with autism, through a state program that provides helpers in their homes. At the same time, she was addicted to Percocet and ultimately began injecting heroin. In 2015, at age 24, she started attending Alcoholics Anonymous meetings with her stepfather, a recovered alcoholic. In the two years since, she had been on and off methadone (which she hated) and buprenorphine, but she had relapsed on heroin three times, well before her pregnancy. During one relapse, she shared a needle and contracted hepatitis C, a viral infection of the liver that, according to one study, may afflict as many as 50 percent of pregnant women with opioid-use disorder.
Elizabeth returned to Codac just days before the shower, in her seventh month of pregnancy, to begin methadone yet again. Unknown to her family and her obstetrician, she had been taking Percocet since before becoming pregnant, and had hoped to taper off the pills on her own rather than go back on methadone. But weaning off the Percocet without help proved impossible — she couldn’t do it without going into withdrawal, which she feared would hurt her baby. Now that she was back on methadone, she planned to tell her obstetrician — which also meant telling him about the Percocet use that preceded it. “I’m scared,” she said.
Stool Color Guide
Visit our health section to see our collection of stool photographs to help you learn more about normal and abnormal stool color.
Stool color card
You can download a copy of a stool color guide to educate new parents about colors associated with infant liver disease like biliary atresia. The guides are available in English or Spanish. These guides are being distributed nationwide to birthing centers by Procter & Gamble Baby Care through a collaboration with the Johns Hopkins Children’s Center Division of Pediatric Gastroenterology. To order printed copies of stool guides for your hospital or pediatric practice, please call 800-543-3331.