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Ernest Drucker, Public-Health Advocate for the Scorned, Dies at 84

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Ernest Drucker, Public-Health Advocate for the Scorned, Dies at 84

Ernest Drucker, a pioneering public-health researcher who approached drug addiction with compassion, invigorated needle-exchange programs to stem the AIDS epidemic and diagnosed the destructive impact of what he called a “plague” of mass incarceration, died on Jan. 26 at his home in Manhattan. He was 84.

The cause was complications of dementia, his son, Jesse Drucker, said.

For more than three decades, Dr. Drucker, primed with epidemiological evidence, waged cutting edge campaigns to improve the lot of prison inmates; the homeless; patients with tuberculosis; workers exposed to asbestos; and HIV-infected drug users and their families, who had been ravaged by the repercussions of AIDS. He was an early and vocal proponent of rethinking the country’s approach to illicit drugs, advocating “harm reduction” — a strategy that prioritizes reducing negative consequences over criminal prosecution.

A clinical psychologist by training, he was professor emeritus of family and social medicine at Montefiore Medical Center/Albert Einstein College of Medicine in the Bronx and had been a senior research associate and scholar in residence at John Jay College of Criminal Justice of the City University of New York in Manhattan, where he biked to work from the Upper West Side.

Dr. Helene Gayle, an epidemiologist and a former president of Spelman College in Atlanta, described Dr. Drucker this way in an email to his son: “Unapologetic about taking on issues that others wouldn’t touch. Unapologetic about the humanity in all including those who had suffered the most injustice.”

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Having run a drug rehabilitation program in the Bronx, Dr. Drucker knew firsthand the destructive capabilities of addictive drugs. But the criminal prosecution of addicts, he argued, only compounded the problem, forcing addicts underground, where dangerous practices like sharing needles resulted in the spread of H.I.V., and saddling them with criminal records that could make them unemployable.

“Our demonization of heroin has transformed otherwise benign and controllable patterns of its use into a lethal gamble and has raised the threshold for seeking help when problems do arise,” he wrote in a letter to The New York Times in 1995. “Other countries are adopting ‘harm reduction’ strategies that (without legalizing drugs) acknowledge their widespread use and employ methods (such as needle exchange) to make even injectable use safer.”

He added that “our stubborn failure to acknowledge the enduring appeal of drugs, and learn how to control (rather than prohibit) their use” had tragic consequences.

Instead, he contended in his book “A Plague of Prisons: The Epidemiology of Mass Incarceration in America” (2011), that for the 90 percent of drug crimes that are nonviolent “criminalization can be replaced with a public health and therapeutic model.”

Dr. Drucker established some of the world’s first syringe exchange programs and in 1991, after he testified in favor of them, four members of the AIDS Coalition to Unleash Power, known as Act Up, were acquitted in Jersey City, N.J., of charges related to running a needle exchange program to prevent the spread of AIDS.

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He warned that the AIDS epidemic was not only afflicting gay men but was also increasingly devastating poor, nonwhite families. He said that heterosexual relations in certain Bronx neighborhoods had become a form of “sexual Russian roulette” that was orphaning children.

“No one, by a long shot, spun out more novel ideas for research, policy and advocacy, many of which resulted in influential publications, new organizations and changes in policy on all aspects of harm reduction as well as drug treatment, public health and criminal justice reform,” Ethan A. Nadelmann, the founder of the Drug Policy Alliance, which has opposed the war on drugs, said in an email.

Dr. Drucker was a founder and chairman of Doctors of the World/USA from 1993 to 1997, was the founding editor in chief of Harm Reduction Journal, and a founder of the International Harm Reduction Association.

In his eulogy, Professor David Michaels of George Washington University’s Milken Institute School of Public Health and a former administrator of the federal Occupational Safety and Health Administration, said Dr. Drucker was “a true public health Renaissance man, driven by a deep commitment to fairness, and justice. He cared deeply about people — you can see it in his work on harm reduction, insisting we should not punish people for who they are and the decisions they make, but instead we should help them become healthier and more fulfilled.”

Ernest Mor Drucker was born on March 29, 1940, in Brooklyn. His father, Joseph, was a machinist for ITT. His wife, Beatrice (Strull) Drucker, managed the household.

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Ernest was raised in the borough’s Brighton Beach section, and graduated from Brooklyn Technical High School with plans to become an engineer, but he gravitated toward psychology as a major at City College of New York, where he earned a bachelor’s degree in 1962 followed by a doctorate.

At Montefiore/Einstein, where he was a disciple of Drs. H. Jack Geiger and Victor Sidel, two proponents of health care for the poor, he was the director of Public Health and Policy Research and the founding director of a 1,000-patient drug treatment program, where he served until 1990.

He would periodically reinvent himself professionally, shifting his focus to and from heroin addiction, public health, occupational safety, AIDS and alternatives to prison.

In addition to his son, Jesse, an investigative reporter for The New York Times, he is survived by his wife, Jeri (Rosner) Drucker, an artist; his brother, Alan Drucker; and two grandchildren.

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Aging process could accelerate due to ‘forever chemicals’ exposure, study finds

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Aging process could accelerate due to ‘forever chemicals’ exposure, study finds

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A new study suggests that middle-aged men may be more vulnerable to faster biological aging, potentially linked to exposure to “forever chemicals.”

The research, published in the journal Frontiers in Aging, examined how perfluoroalkyl and polyfluoroalkyl substances, more commonly known as PFAS, could impact aging at the cellular level.

PFAS are synthetic chemicals commonly used in nonstick cookware, food packaging, water-resistant fabrics and other consumer products, the study noted. 

Their chemical structure makes them highly resistant to breaking down, allowing them to accumulate in water, soil and the human body.

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Chinese researchers analyzed blood samples from 326 adults enrolled in the U.S. National Health and Nutrition Examination Survey between 1999 and 2000.

A new study suggests that middle-aged men could face accelerated biological aging at the cellular level due to exposure to PFAS. (iStock)

The researchers measured levels of 11 PFAS compounds in participants’ blood and used DNA-based “epigenetic clocks” — tools that analyze chemical changes to DNA to estimate biological age — to determine how quickly their bodies were aging at the cellular level, the study stated.

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Two compounds, perfluorononanoic acid (PFNA) and perfluorooctanesulfonamide (PFOSA), were detected in 95% of participants.

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Higher concentrations of those chemicals were associated with faster biological aging in men of certain age groups, but not in women.

“People should not panic.”

The compounds most strongly linked to accelerated aging were not the PFAS chemicals that typically receive the most public attention, the researchers noted.

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“The associations were strongest in adults aged 50 to 64, particularly in men,” Dr. Xiangwei Li, professor at Shanghai Jiao Tong University School of Medicine and the study’s corresponding author, told Fox News Digital. 

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“While this does not establish that PFAS cause aging, it suggests that these widely present ‘forever chemicals’ may be linked to molecular changes related to long-term health and aging.”

The study found that two of the compounds were detected in 95% of participants, and higher levels were linked to faster biological aging in men ages 50–64. (iStock)

Midlife may represent a more sensitive biological period, when the body becomes more vulnerable to age-related stressors, according to the researchers.

Lifestyle factors, such as smoking, may influence biological aging markers, potentially increasing vulnerability to environmental pollutants.

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While Li said “people should not panic,” she does recommend looking for reasonable ways to reduce exposure. 

That might mean checking local drinking water reports, using certified water filters designed to reduce PFAS, and limiting the use of stain- or grease-resistant products when alternatives are available.

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Meaningful reductions in PFAS exposure will likely depend on broader regulatory action and environmental cleanup efforts, Li added.

The researchers noted that midlife could be a particularly sensitive stage, when the body is more susceptible to stressors associated with aging. (iStock)

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Study limitations

The researchers outlined several important limitations of the research, including that the findings show an association, but do not prove that PFAS directly causes accelerated aging.

“The study is cross-sectional, meaning exposure and aging markers were measured at the same time, so we cannot determine causality,” Li told Fox News Digital.

The study was also relatively small, limited to 326 adults age 50 or older, which means the findings may not apply to younger people or broader populations.

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Researchers measured PFAS levels using data collected between 1999 and 2000, and today’s exposure patterns may differ.

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Li added that while PFAS is known to persist in the environment and the body, these results should be validated through larger, more recent studies that follow participants over time.

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Melissa Joan Hart, 49, Opens up About Weight Loss in Perimenopause

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Melissa Joan Hart, 49, Opens up About Weight Loss in Perimenopause


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Alzheimer’s prevention breakthrough found in decades-old seizure drug

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Alzheimer’s prevention breakthrough found in decades-old seizure drug

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A drug that has long been used to treat seizures has shown promise as a potential means of Alzheimer’s prevention, a new study suggests.

The anti-seizure medication, levetiracetam, was first approved by the FDA in November 1999 under the brand name Keppra as a therapy for partial-onset seizures in adults. The approval has since expanded to include children and other types of seizures.

Northwestern University researchers recently found that levetiracetam prevented the formation of toxic amyloid beta peptides, which are small protein fragments in the brain that are commonly seen in Alzheimer’s patients.

The medication was found to prevent the formation of amyloid-beta 42 in both animal models and cultured human neurons, according to the study findings, which were published in Science Translational Medicine.

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The effect was also seen in post-mortem human brain tissue obtained from individuals with Down syndrome, who are at high risk for Alzheimer’s disease.

The medication was found to prevent the formation of amyloid-beta 42 in both animal models and cultured human neurons. (iStock)

“While many of the Alzheimer’s drugs currently on the market, such as lecanemab and donanemab, are approved to clear existing amyloid plaques, we’ve identified this mechanism that prevents the production of the amyloid‑beta 42 peptides and amyloid plaques,” said corresponding author Jeffrey Savas, associate professor of behavioral neurology at Northwestern University Feinberg School of Medicine, in a press release. 

“Our new results uncovered new biology while also opening doors for new drug targets.”

HIDDEN BRAIN CONDITION MAY QUADRUPLE DEMENTIA RISK IN OLDER ADULTS, STUDY SUGGESTS

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The brain is better able to avoid the pathway that produces toxic amyloid‑beta 42 proteins in younger years, but the aging process gradually weakens that ability, Savas noted. 

“This is not a statement of disease; this is just a part of aging. But in brains developing Alzheimer’s, too many neurons go astray, and that’s when you get amyloid-beta 42 production,” he said. 

The effect was also seen in post-mortem human brain tissue obtained from individuals with Down syndrome, who are at high risk for Alzheimer’s disease. (iStock)

That then leads to tau (“tangles”) — abnormal clumps of protein inside brain neurons — which can kill brain cells, trigger neuroinflammation and lead to dementia.

In order for levetiracetam to function as an Alzheimer’s blocker, high-risk patients would have to start taking it “very, very early,” Savas said — up to 20 years before elevated amyloid-beta 42 levels would be detected.

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“You couldn’t take this when you already have dementia, because the brain has already undergone a number of irreversible changes and a lot of cell death,” the researcher noted.

The researchers also did a deep dive into previous human clinical data to determine whether Alzheimer’s patients who were taking the anti-seizure drug had slower cognitive decline. They reported that the patients in that category had a “significant delay” in the span from cognitive decline to death compared to those not taking the drug.

“This analysis supports the positive effect of levetiracetam to slow the progression of Alzheimer’s pathology,” the researcher said. (iStock)

“Although the magnitude of change was small (on the scale of a few years), this analysis supports the positive effect of levetiracetam to slow the progression of Alzheimer’s pathology,” Savas said.

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Looking ahead, the research team aims to find people who have genetic forms of Alzheimer’s to participate in testing, Savas said.

Limitations and caveats

The study had several limitations, including that it relied on animal models and cultured cells, with no human trials conducted.

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Because the study was observational in nature, it can’t prove that the medication caused the prevention of the toxic brain proteins, the researchers acknowledged.

Savas noted that levetiracetam “is not perfect,” cautioning that it breaks down in the body very quickly.

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The team is currently working to create a “better version” that would last longer in the body and “better target the mechanism that prevents the production of the plaques.”

“You couldn’t take this when you already have dementia, because the brain has already undergone a number of irreversible changes and a lot of cell death.”

The medication’s common documented side effects include drowsiness, weakness, dizziness, irritability, headache, loss of appetite and nasal congestion.

It has also been linked to potential mood and behavior changes, including anxiety, depression, agitation and aggression, according to the prescribing information. In rare cases, it could lead to severe allergic reactions, skin reactions, blood disorders and suicidal ideation.

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Funding for the study was provided by the National Institutes of Health and the Cure Alzheimer’s Fund.

Fox News Digital reached out to the drug manufacturer and the researchers for comment.

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