Less melanin in white people leads to less folate for blood production

Less melanin in white leads to less folate and more melanin in dark colored skin people affects Vitamin D and Calcium absorption

White people must get sunshine to help in folate absorption (folic acid – important nutrient for the blood ) while dark-colored skin people must eat whole foods rich in Vitamin D3 , calcium , omega 3 , Vitamin K2 and magnesium to protect them from diseases related to the heart and circulation/vascular system.

As a result, depression is prevalent among whites while circulatory health issues are common among dark colored skin.

See your doctor for more preventive measures.

Connie Dello Buono

The color of skin is influenced by a number of pigments, including melanin, carotene, and hemoglobin. Recall that melanin is produced by cells called melanocytes, which are found scattered throughout the stratum basale of the epidermis. The melanin is transferred into the keratinocytes via a cellular organelle called a melanosome (Figure 5.7).

This figure consists of two diagrams side by side. The right diagram shows development of light colored skin; the left shows development of dark-colored skin. In both, a brown melanocyte sits at the border between the dermis and epidermis. The melanocyte has a large nucleus and six finger-like extensions. These reach between cells of the stratum basalis. Sections of the extensions detach and travel through the skins. These are melanosomes. In the left diagram, both the melanocyte and melanosomes contain melanin particles, shown as dark dots. Melanosomes travel upwards to outer skin layers, releasing melanin. As a result, keratinocytes in the left diagram contain several melanin particles that darken skin color. In light colored skin, the melanocyte contains no melanin. It still releases melanosomes into upper layers of the skin; however, these melanosomes contain no melanin. Therefore, the skin does not darken and remains light.
Figure 5.7. Skin Pigmentation
The relative coloration of the skin depends of the amount of melanin produced by melanocytes in the stratum basale and taken up by keratinocytes.

Melanin occurs in two primary forms. Eumelanin exists as black and brown, whereas pheomelanin provides a red color. Dark-skinned individuals produce more melanin than those with pale skin. Exposure to the UV rays of the sun or a tanning salon causes melanin to be manufactured and built up in keratinocytes, as sun exposure stimulates keratinocytes to secrete chemicals that stimulate melanocytes.

The accumulation of melanin in keratinocytes results in the darkening of the skin, or a tan. This increased melanin accumulation protects the DNA of epidermal cells from UV ray damage and the breakdown of folic acid, a nutrient necessary for our health and well-being.

In contrast, too much melanin can interfere with the production of vitamin D, an important nutrient involved in calcium absorption.

Thus, the amount of melanin present in our skin is dependent on a balance between available sunlight and folic acid destruction, and protection from UV radiation and vitamin D production.

It requires about 10 days after initial sun exposure for melanin synthesis to peak, which is why pale-skinned individuals tend to suffer sunburns of the epidermis initially. Dark-skinned individuals can also get sunburns, but are more protected than are pale-skinned individuals. Melanosomes are temporary structures that are eventually destroyed by fusion with lysosomes; this fact, along with melanin-filled keratinocytes in the stratum corneum sloughing off, makes tanning impermanent.

Too much sun exposure can eventually lead to wrinkling due to the destruction of the cellular structure of the skin, and in severe cases, can cause sufficient DNA damage to result in skin cancer.

When there is an irregular accumulation of melanocytes in the skin, freckles appear. Moles are larger masses of melanocytes, and although most are benign, they should be monitored for changes that might indicate the presence of cancer (Figure 5.8).

Five photos of moles. The three upper photos show moles that are small, flat, and dark brown. The bottom left photo shows a dark black mole that is raised above the skin. The bottom right photo shows a large, raised, reddish mole with protruding hairs.
Figure 5.8. Moles
Moles range from benign accumulations of melanocytes to melanomas. These structures populate the landscape of our skin. (credit: the National Cancer Institute)


The first thing a clinician sees is the skin, and so the examination of the skin should be part of any thorough physical examination. Most skin disorders are relatively benign, but a few, including melanomas, can be fatal if untreated. A couple of the more noticeable disorders, albinism and vitiligo, affect the appearance of the skin and its accessory organs. Although neither is fatal, it would be hard to claim that they are benign, at least to the individuals so afflicted.

Albinism is a genetic disorder that affects (completely or partially) the coloring of skin, hair, and eyes. The defect is primarily due to the inability of melanocytes to produce melanin. Individuals with albinism tend to appear white or very pale due to the lack of melanin in their skin and hair. Recall that melanin helps protect the skin from the harmful effects of UV radiation. Individuals with albinism tend to need more protection from UV radiation, as they are more prone to sunburns and skin cancer. They also tend to be more sensitive to light and have vision problems due to the lack of pigmentation on the retinal wall. Treatment of this disorder usually involves addressing the symptoms, such as limiting UV light exposure to the skin and eyes.

In vitiligo, the melanocytes in certain areas lose their ability to produce melanin, possibly due to an autoimmune reaction. This leads to a loss of color in patches (Figure 5.9). Neither albinism nor vitiligo directly affects the lifespan of an individual.

This photo shows the back of a man’s neck. There is a large, discolored patch of skin at the base of his hairline. The discolored area extends over the ears onto the cheeks, toward the front of the face. The man’s head and facial hair are mostly gray, but white patches of hair are seen above the discolored skin.
Figure 5.9. Vitiligo
Individuals with vitiligo experience depigmentation that results in lighter colored patches of skin. The condition is especially noticeable on darker skin. (credit: Klaus D. Peter)

Other changes in the appearance of skin coloration can be indicative of diseases associated with other body systems. Liver disease or liver cancer can cause the accumulation of bile and the yellow pigment bilirubin, leading to the skin appearing yellow or jaundiced (jaune is the French word for “yellow”). Tumors of the pituitary gland can result in the secretion of large amounts of melanocyte-stimulating hormone (MSH), which results in a darkening of the skin. Similarly, Addison’s disease can stimulate the release of excess amounts of adrenocorticotropic hormone (ACTH), which can give the skin a deep bronze color.

A sudden drop in oxygenation can affect skin color, causing the skin to initially turn pale (white), a condition called pallor. With a prolonged reduction in oxygen levels, dark red deoxyhemoglobin becomes dominant in the blood, making the skin appear blue, a condition referred to as cyanosis (kyanos is the Greek word for “blue”).

This happens when the oxygen supply is restricted, as when someone is experiencing difficulty in breathing because of asthma or a heart attack. However, in these cases the effect on skin color has nothing do with the skin’s pigmentation.


This ABC video follows the story of a pair of fraternal African-American twins, one of whom is albino. Watch this video to learn about the challenges these children and their family face. Which ethnicities do you think are exempt from the possibility of albinism?

Calcium and magnesium balance 60:40 ratio

White opioids: Pharmaceutical race and the war on drugs that wasn’t

White opioids: Pharmaceutical race and the war on drugs that wasn’t


The US ‘War on Drugs’ has had a profound role in reinforcing racial hierarchies. Although Black Americans are no more likely than Whites to use illicit drugs, they are 6–10 times more likely to be incarcerated for drug offenses. Meanwhile, a very different system for responding to the drug use of Whites has emerged. This article uses the recent history of White opioids – the synthetic opiates such as OxyContin® that gained notoriety starting in the 1990s in connection with epidemic prescription medication abuse among White, suburban and rural Americans and Suboxone® that came on the market as an addiction treatment in the 2000s – to show how American drug policy is racialized, using the lesser known lens of decriminalized White drugs. Examining four ‘technologies of whiteness’ (neuroscience, pharmaceutical technology, legislative innovation and marketing), we trace a separate system for categorizing and disciplining drug use among Whites. This less examined ‘White drug war’ has carved out a less punitive, clinical realm for Whites where their drug use is decriminalized, treated primarily as a biomedical disease, and where their whiteness is preserved, leaving intact more punitive systems that govern the drug use of people of color.

Keywords: addiction, whiteness, prescription opioids, heroin


The US ‘War on Drugs’ has had a profound role in reinforcing racial hierarchies. Drug offenses accounted for two-thirds of the rise in the federal inmate population and more than half of the rise in state prisoners between 1985 and 2000, with more than half of young Black men in large cities in the United States currently under the control of the criminal justice system (Alexander, 2010), and middle aged Black men more likely to have been in prison than in college or the military (Rich et al, 2011). Although Black Americans are no more likely than Whites to use illicit drugs, they are 6–10 times more likely to be incarcerated for drug offenses (Bigg, 2007Goode, 2013). Alexander (2010)Wacquant (2009)Hart (2013) and others make the case that the criminal justice system is, in effect, a new state-sponsored racial caste system.

Meanwhile, a very different system for responding to the drug use of Whites has emerged. Beginning in the 1990s, rates of prescription opioid misuse – primarily OxyContin® – began to rise dramatically, particularly among Whites. The press reported a suburban and rural White prescription opioid epidemic (Tough, 2001Ung, 2001ab) as prescription drug overdose deaths rose 117 per cent between 1999 and 2012 (CDC, 2014). By 2010, the National Institute on Drug Abuse (NIDA) noted increasing numbers of prescription opioid dependent people turning to heroin as prescription opioids became harder to misuse (Volkow, 2014) because of new prescription monitoring programs and tamper resistant opioid formulations. Thousands of White addicted people found themselves the center of media and political debates about how the country should respond to the latest drug crisis.

The public response to White opioids looked markedly different from the response to illicit drug use in inner city Black and Brown neighborhoods, with policy differentials analogous to the gap between legal penalties for crack as opposed to powder cocaine. This less examined ‘White drug war’ has carved out a less punitive, clinical realm for Whites where their drug use is decriminalized, treated primarily as a biomedical disease, and where White social privilege is preserved. This ‘White drug war’ has historical precedents in which predominantly White populations have used social privilege to invoke ‘medical need’ to secure or maintain access to powerful sedatives or stimulants in the mid to late twentieth century (see Herzberg, 2013). But in the case opioids, addiction treatment itself is being selectively pharmaceuticalized in ways that preserve a protected space for White opioid users, while leaving intact a punitive, carceral system as the appropriate response for Black and Brown drug use.

Whiteness is a sociocultural achievement: it is actively maintained through the shoring up of social boundaries distinguishing White and from not White (Frankenberg, 1993Allen, 1994Fine et al, 1996Daniels, 1997Wray, 2006Roediger, 2007Twine and Gallagher, 2008Hughey, 2010). The seeming inevitability and naturalness of whiteness allows those within the category ‘White’ to be unmarked, to think of themselves as simply human and without race, while those who fall outside the bounds of whiteness are the racialized Other (Dyer, 1988). Scholars have explored the ways in which whiteness shapes housing (Low, 2009), education (Leonardo, 2009), politics (Feagin, 2012), law (Lopez, 2006), research methods (Zuberi and Bonilla-Silva, 2008) and our understanding of society (Lipsitz, 2006 [1998]Feagin, 2010). Yet, despite almost two decades of research in the field of whiteness studies, there remains relatively little literature that explores the myriad connections between whiteness and health in the US context (Katz Rothman, 2001Daniels and Schulz, 2006Jones, et al, 2008Daniels, 2012Daniels, 2013) and only a few studies exploring the issue of whiteness and psychoactive substances (Steiner and Argothy, 2001Murakawa, 2011Daniels, 2012Linnemann and Wall, 2013).

In one of the only studies to explicitly look at how drug policy is used to carve out White spaces exempt from punitive more approaches, Lassiter (2015) takes a historical look at the roots of the White opioid crisis of today. Looking back to marijuana policies of the 1970s, he states: “exemptions created for white middle-class participants in the underground market-place were not merely epiphenomenal but rather constitutive of the expansion of the carceral state (p. 127)”. The drug war operates because of a reciprocal relationship between the criminalization of blackness and the decriminalization of whiteness. Lassiter notes that, when the Rockefeller Drug Laws instituted harsh mandatory minimums, White suburban youth found themselves facing significant jail time for low-level marijuana possession. Parents of White suburban youth banded together to create policy changes that exempted marijuana from the Rockefeller Drug Laws, essentially decriminalizing low-level possession in some jurisdictions. This was possible, in part, because of the racial dynamics and the portrayal of White youth as sympathetic victims of the organized narcotics trade. The relative paucity of studies, such as Lassiter’s examining the constitutive role of whiteness in the drug war, is remarkable given the wealth of sociocultural research on pharmaceuticals, addiction and race, which has illuminated myriad ways that the biochemical stratification of people of African and Latin American origin has been represented and materially shaped in sites ranging from genetics labs, medical clinics and neighborhoods, to popular media, courtrooms and policy debates (c.f. Campbell, 2000Courtwright, 2001Fullwiley, 2007Singer, 2008Bourgois and Schonberg, 2009Roberts, 2011Tiger, 2012).

While not focused on addiction, some scholars have traced the ways that medicine has always been racialized and used to justify less punitive responses for Whites than Blacks. For example, Solinger (2013)traces how a racial divide was produced and maintained by the discourses surrounding “illegitimate” childbirth and the medicalization of abortion. While abortion became available and somewhat acceptable for Whites, the welfare system was being used to publicly shame and punish women of color who had children out of wedlock. Other studies trace how race became embedded in medical technologies and rhetoric in ways that become taken for granted and that reinforce notions of racial difference. Pollock (2012), in a study of the racialization of heart disease, notes that whiteness is reinforced by its using the famous Framingham study as the norm. Braun (2014) traces the ways that the spirometer, originally developed in the antebellum South to demonstrate the physiological inferiority of Black slaves, continues to naturalize racial difference in contemporary usage through “race correction” of “normal” reference ranges. These works remind us that racial projects are inherently implicated in medicine and that race is reified in discourses of legitimacy, normativity and technological precision.

White race is encoded into biomedical technologies and practice in particularly covert, implicit rather than explicit ways and in ways that may not be intentional on the part of key actors. Our argument here focuses on racializing consequences of pharmaceutical reason that stem from pre-existing structures of exclusion, inclusion, political pragmatism and industry that over-determine the strategies of scientists, treatment advocates, policymakers and pharmaceutical executives. Opioids in the United States are subjected to a racial biopolitics that constrains available strategies, even to those who oppose social hierarchies and strive to de-racialize drug policy. Efforts to de-racialize any arena of life in the United States, which do not directly address racism, risk reproducing racial hierarchy, because White privilege is typically reproduced by eliminating racial references from seemingly universal policies and practice; in the latter part of the twentieth century the social policy reforms that did the most to intensified racial inequalities in income, employment and incarceration were undertaken under the guise of “color blind ideology” (Alexander, 2010).

This article uses the recent history of White opioids – the synthetic opiates OxyContin® and Suboxone®that gained notoriety starting in the 1990s in connection with epidemic prescription medication abuse among White, suburban and rural Americans – to show how American drug policy is racialized, using the lesser known lens of decriminalized White drugs. Examining four ‘technologies of whiteness’ (neuroscience, pharmaceutical technology, legislative innovation and marketing), we trace a separate system that categorizes and disciplines drug use among Whites, while not naming White race explicitly, given that White is the unmarked, assumed norm. Maintaining the boundaries of whiteness under racially segregated drug policy requires constant vigilance and ongoing political work. Our thesis is that these technologies of whiteness are fueled by two biopolitical currents that trade on hidden or misrecognized racial coding: on one hand, a partnership of the pharmaceutical industry with lawmakers who are conscious of the racial symbolism of addiction risk and legitimate use of opioids, and on the other, an unconscious collusion of liberal neuroscientists seeking to decriminalize opioid misuse and democratize treatment using a discourse of addiction as a brain disease, while failing to recognize the (White) racial coding in the universal brain disease framework and its disparate consequences.

Addiction Neuroscience as a Technology of Whiteness

The mass incarceration of people of color for drug offenses is, in part, legitimated by the belief that drug use results from a failure of will or morality. People are responsible for their use and, therefore, must be held accountable or punished. However, at the same time that more punitive War on Drug policies were enforced in Black and Latino city neighborhoods, President Bush I ushered in the Decade of the Brain at the National Institute on Drug Abuse. The richly funded neuroscience program at NIDA in the 1990’s provided a scientific rationale for addiction as a clinical disease, focusing on altered brain chemistry as the source of addiction and on neuroactive pharmaceuticals and clinical (rather than law enforcement) interventions as the appropriate response. Simply put, neuroscience provided a scientific rationale for treating addictions – at least some addictions – as disease needing medical intervention rather than as crime requiring punishment. While the race of the addict was excluded from this universalizing biological discourse, the very absence of a language of race indexed White subjects. The scientists involved in this project probably did not intend to exacerbate racial inequalities with their work; on the contrary, many saw their efforts to establish the neurochemical basis for addiction as a way to counteract the social injustice of addiction stigma, and, by extension, racial injustice. Yet, the implicit racial logic of universalist clinical research, which has long held the 70 kg White male as its standard subject (Epstein, 2007), channeled the efforts of even egalitarian neuroscientists toward stratified results.

In the United States, NIDA spent millions of dollars promoting one simple message: ‘addiction is a brain disease’. In 1997, Alan Leshner, then Director of NIDA, published a landmark article entitled, “Addiction is a Brain Disease, and It Matters”. In the article, Leshner argues that addiction is as much a medical as a social problem and that the field and the public has focused too much attention on the latter:

That addiction is tied to changes in brain structure and function is what makes it, fundamentally, a brain disease. … Understanding that addiction is, at its core, a consequence of fundamental changes in brain function means that a major goal of treatment must be to either reverse or compensate for those brain changes.

(1997, p. 46)

It is this perspective that has guided NIDA since. It has also permeated the field of addictions research through the 1990s, as demonstrated by a landmark article in the Journal of the American Medical Association, co-authored by four prominent addictions researchers, and entitled “Drug Dependence, A Chronic Medical Illness”. The article argued that drug dependence was comparable to asthma, diabetes and hypertension in terms of heritability, causation, pathophysiology and adherence to treatment, and that it should be treated as a chronic medical illness for purposes of treatment approaches, insurance coverage and outcome measures (McLellan et al, 2000). In 2003, Nora Volkow, a prominent neuroscientist who pioneered the use of PET scans in addiction research, became the Director of NIDA. Since her appointment, she has vociferously championed the brain disease model in both NIDAs scientific and public education arms. For example, in 2005 NIDA underwrote a widely-cited issue of Nature devoted to addiction neurobiology. NIDA has also produced a series of curricula for elementary and high school students to explain addiction. These include: “Brain Power”, “Mind Over Matters”, “Heads Up” and “The Brain”. NIDAs educational materials closely track the scientific literature. NIDAs power in the field of addiction neuroscience has led one scholar to describe them as largely responsible for making “the neuroscientists’ laboratory … an obligatory passage point for the production of truths about addiction” (Vrecko, 2010, p. 58).

Addiction neuroscience is connected to whiteness and addiction is three key ways. First, whiteness and health are implicated in the use of brain imagery. Images, such as PET scans, of the ‘addicted brain’ are increasingly popular in addiction studies and in reporting on addiction. While images of drug-related brain damage or craving-induced brain activity are compelling and are liberally used in NIDAs educational materials, several scholars have noted that imaging technologies, far from being objective or neutral, are shaped by their social and economic context and involve a series of subjective decisions by researchers (see especially, Beaulieu, 2001Dumit, 2004Joyce, 2005). What is striking about brain images of addiction is that they are unmarked by race: they convey a sense of universality and timelessness that, by omitting racial identity, help to expunge racial identity of the addict leaving a White, because racially unmarked, backdrop. Brain scans here operate as the unmarked White norm similar to the way in which the Framingham study of predominantly White participants became the norm for heart disease (Pollock, 2012). A neuroscientific model of addiction as brain disease, which extracts the brain from the racially marked addicted body, thereby helps to unmark (biological) addiction, defining it as a human universal, and therefore White. The neuroscientific reframing of addiction is, therefore, a technique for the racial recoding of (certain types of) addiction and of (some) addicted people, which extracts addiction from the association with Black and Latino people inherent in a social, moral, or criminal framing of addiction.

Neuroscience and whiteness are further connected through the silence in neuroscientific literature about the role of environmental factors contributing to addiction. Social determinants of health, such as geography, income, education and housing are largely omitted from the description of research subjects and from the lists of relevant variables in neuroscientific papers. Environmental factors in addiction neuroscience are generally reduced to cues or triggers (for example, studies demonstrating how brain ‘lights up’ when a drug user is shown a picture of heroin or cocaine). Even when environmental forces are acknowledged, they are of interest primarily for the biochemical processes they engender. Volkow and Li explain the “neural consequences of environmental risk”:

Low socioeconomic class and poor parental support are two other factors [along with drug availability] that are consistently associated with a propensity to self-administer drugs, and stress might be a common feature of these environmental factors […T]here is evidence that corticotropin-releasing factor (CRF) might play a linking role through its effects on the mesocorticolimbic dopamine system and the hypothalamic pituitary-adrenal axis. […] If we understand the neurobiological consequences underlying the adverse environmental factors that increase the risk for drug use and addiction, we will be able to develop interventions to counteract these changes.

(2005, p. 1436)

Here, environmental influences are acknowledged but understood only in the context of how the stress they induce affects the dopamine system. Volkow and Li (2005) go on to suggest that the future addiction interventions may include medications that act synergistically with behavioral therapies to mitigate the impact of stress. Absent from their view of addiction are features of neighborhood environment or social roles that might hint at the context of drug use, and therefore the race of drug users and their stressors. They offer an individually focused clinical and physiological, rather than a public health, model of addiction.

The third connection between addiction neuroscience and whiteness is what neuroscience frames as the appropriate response to addiction. When addiction is conceptualized as a ‘brain disease’ involving genetically and physiologically determined neuroreceptors, what is called for is a medication that specifically targets faulty neuroreceptors. This stands in stark contrast to the prevalent response to addiction in the United States as part of the War on Drugs in which incarceration is the ready response. When addiction is framed as a brain disorder, rather than a crime, its cultural work to racially recode prescription opioid addiction as White is unrecognized. This ultimately leads to a bifurcated discourse of White addicts as having a ‘brain disease’ and needing ‘treatment’, and of non-White addicts as ‘criminals’ that require incarceration to protect the public.

It seems, however, that some neuroscientists are unaware of the role their work is playing in reinscribing racialized notions about drug users. Indeed, some addiction neuroscience researchers have said that their political project was to delink addiction from crime. They see themselves as reframing addiction as a brain disease for the precise purpose of destigmatizing and decriminalizing drug use and bringing it under the purview of medicine, rather than the criminal justice system. Dackis and O’Brien, for instance, claim that neuroimaging will:

substantiate the biological basis of addiction and […] ultimately erode entrenched societal attitudes that prevent addiction from being evaluated, treated, and insured as a medical disorder.

(2005, p. 1431)

Such researchers believe that promoting a neurological basis for addiction will erode the persistent idea that addiction is “a character flaw rather than a bona fide brain disease” (Chou and Narasimhan, 2005, p. 1427), leading to the end of stigma and criminalization. Importantly, both models – the moral/criminal and the medical – root the etiology of addiction at the level of the individual, absenting from consideration structural and environmental factors.

These discussions do not explicitly reference race, but it is notable that the neurobiological, universal, by extension ‘White’ and therefore less stigmatizing and criminalizing concept of addiction, was aggressively developed during a decade (the 1990s) when middle class, White heroin use was growing. This change in the demographics of heroin consumption was because of an influx of heroin from newly planted poppy fields in Colombia, whose cartels were competing with established Middle Eastern and Asian heroin distributors by dramatically lowering the price and increasing the purity of the heroin they sold in the United States cities. This attracted middle class users who found they could snort instead of injecting the purer heroin (Hamid et al, 1997). In addition, with the 1996 approval of OxyContin® as a “minimally addictive pain reliever” marketed to generalist physicians in rural and suburban areas for their use in moderate pain (Van Zee, 2009), by the late 1990s the specter of the coming White prescription opioid addiction epidemic had been raised.

By focusing on brain neurochemistry, the neuroscientific model of addiction, referred to by many neurophysiology researchers as ‘chronic relapsing brain disease’, erases and obscures the role of race and other social differences in ways that privilege whiteness. The brain disease model of addiction reduces any discussion about poverty, exposure to drugs, racism and other environmental factors to problems of the brain and its response to ‘stress’. Social issues, such as the mass incarceration of African Americans under harsh drug laws or the lack of viable economic opportunities beyond the drug trade in Black and Latino neighborhoods, have no place in neuroscientific discourse. As Nancy Campbell notes, “as an ideological code, CRBD [chronic relapsing brain disease] does not focus attention on social differences, including the differential histories and cultural geographies within which their subjects encounter drugs” (2010, p. 101).

As we discuss further below, this neuroscientific racial recoding of prescription opioid addiction was one basis for legislative innovations that created a new, separate track for treating the addiction of White opioid users.

Pharmaceutical Technologies of Whiteness

Opioids have long blurred the line between legitimate medications and drugs of abuse. Morphine went into widespread use during the Civil War in the treatment of injured soldiers, and among middle class White Victorian housewives for a range of problems including menstrual pain. Morphine ‘habits’ only began to be seen as problematic at the end of the nineteenth century; in 1898 Bayer Corporation introduced heroin as a non-addictive cure for morphine addiction as well as a cough syrup for children. However, changes in medical practice and international drug policy led the media and policymakers to associate opiates with poverty and ethnic minorities, and prohibitionists succeeded in banning opiate maintenance from clinical practice with passage of the 1914 Harrison Act (Musto, 1999Courtwright, 2001). Methadone was introduced as a synthetic opioid pain reliever in Germany during World War II when morphine supplies from Asia ran short, was re-introduced in the 1960s as a maintenance medication for heroin addiction following successful clinical trials among African Americans in Harlem (Dole and Nyswander, 1966), and was named a primary weapon in President Nixon’s War on Drugs in 1971 (White, 1998). Methadone quickly become the focus of tight surveillance and regulation by the DEA, however, based on reports of methadone abuse and diversion, and on methadone’s symbolic association with Black and Brown inner city drug use (Hansen and Roberts, 2012). New opioids have therefore undergone a predictable cycle of optimism touted as the holy grail of a non-addictive pain reliever, followed by challenges to their legitimacy as medications, their association with poverty and ethnic minorities, and stigmatization as addictive drugs.

Cleveland Ohio health data: infant mortality and heart disease


Why is there high rate of infant mortality among hispanics/latino in Wards 3, 11,14, 15 and 17?

Why is heart diease higher in Cleveland Ohio than the nation?

What quality programs were implemented to reduce heart health risks and infant mortality risks?


Preventable hospitalizations among racial groups, 2003

In 2003, racial and ethnic dis-parities existed in the rates of preventable hospitalizations, with blacks generally having the highest rates and Hispanics the second highest rates.

  • The disparities were greatest for hospitalizations for chronic conditions such as diabetes, hypertension, and asthma. Compared with non-Hispanic whites, rates of admission for these conditions were about 3 to 5 times greater among blacks, and approximately 2 to 3 times greater among Hispanics.
  • Compared with non-Hispanic whites, blacks had higher rates of preventable hospitalizations for 15 of 17 indicators, and Hispanics had higher rates of preventable hospitalizations for 14 of 17 indicators.
  • Asians were less likely than non-Hispanic whites to be ad-mitted for preventable hospitali-zations, with 9 of 17 indicators being lowest in Asians.
  • Blacks had the highest rates of preventable hospitalizations for all indicators related to diabetes and circulatory diseases. Hospi-talization rates for hypertension and for diabetes without compli-cations were 5 times higher for blacks than for non-Hispanic whites. Hospitalization rates for pediatric asthma, adult asthma, perforated appendix, dehydra-tion, and low birth weight were also highest among blacks.
  • Hispanics had the highest rates of admission for elderly asthma, pediatric gastroenteritis, and urinary tract infection.
  • Admissions for asthma among patients 65 and older were 1.8 times more likely for Asians than for non-Hispanic whites—the only indicator where hospitaliza-tion rates were higher in Asians.

This Statistical Brief is based on PQI Version 2.1, revision 3. This PQI version includes measures for hospital admission rates for the following 16 ambulatory care-sensitive conditions:

– Lower-extremity amputations among patients with diabetes (a specific, serious, long-term complication of diabetes)

– Diabetes, long-term complications (i.e., chronic conditions such as renal, visual, neurological, and circulatory disorders, including lower-extremity amputations)

– Diabetes, short-term complications (i.e., acute conditions such as diabetic ketoacidosis, hyperosmolarity, and coma)

– Uncontrolled diabetes without complications

– Angina without procedure

– Hypertension

– Congestive heart failure

– Pediatric asthma

– Adult asthma

– Chronic obstructive pulmonary disease

– Pediatric gastroenteritis

– Perforated appendix

– Urinary tract infections

– Dehydration

– Bacterial pneumonia

– Low-birth weight

This slideshow requires JavaScript.


Hormone therapy for prostate cancer may pose a risk for black men

By Lateshia Beachum

Black men treated with hormone therapy for prostate cancer may have a higher risk of death than white men undergoing the same therapy, according to a new study. But the deaths aren’t actually caused by prostate cancer.

Androgen deprivation therapy, or ADT, is a hormone treatment that shrinks prostate tumors. Researchers from the Brigham and Women’s Hospital in Boston found that black men undergoing the therapy had a 77 percent higher risk of death than non-black men.

Researchers at Brigham and Women’s Hospital looked through medical records of about 1,500 men from the Chicago Prostate Cancer Center with low- or intermediate-risk prostate cancer who were treated with ADT. About 7 percent were black.

The small study, in the journal Cancer, found that black men were usually younger, treated later and more likely to have other health issues.

Black men had a higher incidence of death after only four months of hormone therapy, the researchers found, but none of the causes of death in the study were actually prostate cancer.

Konstantin Kovtun, one of the lead researchers for the study, said the deaths seem to be related to cardiovascular health issues that existed prior to a cancer diagnosis. “African American men have an onset of cardiovascular problems that are linked to ADT use,” he said.

The study noted that earlier research has found shorter survival rates among intermediate- to high-risk prostate cancer patients using ADT because of an increased risk in fatal heart attack.

Jonathan Simons, president and chief executive officer of the Prostate Cancer Foundation, said the study was interesting but needs to be followed by more research, including a closer examination of the causes of death. “We don’t know the real reason for the number of deaths,” he said.

Black men typically fare worse with prostate cancer than white men, Simons said, and the reasons for the differences are understudied and poorly understood.

“You can have a man of European and a man of African descent,” he said. “Even if they get the same health care, insurance and doctors, black men still have it worse with prostate cancer.”

Kovtun hopes that the study helps inform decisions about treatment.

“If I was a physician and I had the data now available for the study, I would be more careful in using ADT for African American men,” he said.