Colin Gordon, University of Iowa

Republicans in the U.S. Senate are sparring over their version of the multitrillion-dollar budget and immigration bill the House of Representatives passed on May 22, 2025.

Some GOP senators are insisting on shrinking the budget deficit, which the House version would increase by about US$3.8 trillion over a decade.

Others are saying they oppose the House’s cost-cutting provisions for Medicaid, the government’s health insurance program for people who are low income or have disabilities.

Despite the calls from U.S. Sen. Josh Hawley of Missouri and a few other Republican senators to protect Medicaid, as a scholar of American social policy I’m expecting to see the Senate embrace the introduction of work requirements for many adults under 65 who get health insurance through the program.

The House version calls for the states, which administer Medicaid within their borders and help pay for the program, to adopt work requirements by the end of 2026. The effect of this policy, animated by the conviction that coverage is too generous and too easy to obtain, will be to deny Medicaid eligibility to millions of those currently covered – leaving them without access to basic health services, including preventive care and the management of ongoing conditions such as asthma or diabetes.

Ending welfare

The notion that people who get government benefits should prove that they deserve them, ideally through paid labor, is now centuries old. This conviction underlay the Victorian workhouses in 19th-century England that Charles Dickens critiqued through his novels.

U.S. Rep. Brett Guthrie, R-Ky., put it bluntly earlier this month: Medicaid is “subsidizing capable adults who choose not to work,” he said.

This idea also animated the development of the American welfare state, from its origins in the 1930s organized around the goals of maintaining civil order and compelling paid labor. Enforcing work obligations ensured the ready availability of low-wage labor and supported the growing assumption that only paid labor could redeem the lives and aspirations of the poor.

“We started offering hope and opportunity along with the welfare check,” Wisconsin Gov. Tommy Thompson argued in the early 1990s, “and expecting certain responsibilities in return.”

This concept also was at the heart of the U.S. government’s bid to end “welfare as we know it.”

In 1996, the Democratic Clinton administration replaced Aid to Families with Dependent Children, or AFDC, a long-standing entitlement to cash assistance for low-income families, with Temporary Aid for Needy Families, known commonly as TANF. The TANF program, as its name indicates, was limited to short-term support, with the expectation that most people getting these benefits would soon gain long-term employment.

Since 1996, Republicans serving at the state and federal levels of government have pressed to extend this principle to other programs that help low-income people. They’ve insisted, as President Donald Trump put it halfway through his first term, that unconditional benefits have “delayed economic independence, perpetuated poverty, and weakened family bonds.”

Such claims are unsupported. There is no evidence to suggest that work requirements have ever galvanized independence or lifted low-income people out of poverty. Instead, they have punished low-income people by denying them the benefits or assistance they require.

Work requirements haven’t worked

Work requirements have consistently failed as a spur to employment. The transition from the AFDC to TANF required low-income families to meet work requirements, new administrative burdens and punitive sanctions.

The new work expectations, rolled out in 1997, were not accompanied by supporting policies, especially the child care subsidies that many low-income parents with young children require to hold a job. They were also at odds with the very low-paying and unstable jobs available to those transitioning from welfare.

Scholars found that TANF did less to lift families out of poverty than it did to shuffle its burden, helping the nearly poor at the expense of the very poor.

The program took an especially large toll on low-income Black women, as work requirements exposed recipients to long-standing patterns of racial and gender discrimination in private labor markets.

Restricting access to SNAP

Work requirements tied to other government programs have similar track records.

The Supplemental Nutrition Assistance Program, which helps millions of Americans buy groceries, adopted work requirements for able-bodied adults in 1996.

Researchers have found that SNAP’s work requirements have pared back eligibility without any measurable increase in labor force participation.

As happens with TANF, most people with SNAP benefits who have to comply with SNAP work requirements are already working to the degree their personal circumstances and local labor markets allow.

The requirements don’t encourage SNAP recipients to work more hours; they simply lead people to be overwhelmed by red tape and stop renewing their SNAP benefits.

Failing in Arkansas

The logic of work requirements collapses entirely when extended to Medicaid.

Red states have been pressing for years for waivers that would allow them to experiment with work requirements – especially for the abled-bodied, working-age adults who gained coverage under the Affordable Care Act’s Medicaid expansion.

The first Trump administration granted 13 such waivers for what it saw as “meritorious innovations,” building “on the human dignity that comes with training, employment and independence.”

Arkansas got the furthest with adding work requirements to Medicaid at that time. The results were disappointing.

“We found no evidence that the policy succeeded in its stated goal of promoting work,” as one research team concluded, “and instead found substantial evidence of harm to health care coverage and access.”

The Biden administration slowed down the implementation of these waivers by directing the Centers for Medicare and Medicaid Services to suspend or stem any state programs that eroded coverage. Meanwhile, state courts consistently ruled against the use of Medicaid work requirements.

In Trump’s second term, Iowa, Arizona and at least a dozen other states have proposed “work requirement” waivers for federal approval.

Trying it again

The waiver process is meant to allow state experiments to further the statutory objectives of the Medicaid program, which is to furnish “medical assistance on behalf of families with dependent children and of aged, blind, or disabled individuals, whose income and resources are insufficient to meet the costs of necessary medical services.”

On these grounds, the courts have consistently held that state waivers imposing work requirements not only fail to promote Medicaid’s objectives but amount to an arbitrary and capricious effort to undermine those objectives.

“The text of the statute includes one primary purpose,” the D.C. Circuit ruled in 2020, “which is providing health care coverage without any restriction geared to healthy outcomes, financial independence or transition to commercial coverage.”

Changing Medicaid in all states

The House spending bill includes a work requirement that would require all able-bodied, childless adults under 65 to demonstrate that they had worked, volunteered or participated in job training for 80 hours in the month before enrollment.

It would also allow states to extend such work requirements to six months and apply the new requirements not just to Medicaid recipients but to people who get subsidized health insurance through an Affordable Care Act exchange.

If passed in some form by the Senate, the House spending bill would transform the landscape of Medicaid work requirements, pushing an estimated 4.8 million Americans into the ranks of the uninsured.

Colin Gordon, Professor of History, University of Iowa

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Danielle Wilhour, University of Colorado Anschutz Medical Campus

Cerebrospinal fluid, or CSF, is a clear, colorless liquid that plays a crucial role in maintaining the health and function of your central nervous system. It cushions the brain and spinal cord, provides nutrients and removes waste products.

Despite its importance, problems related to CSF often go unnoticed until something goes wrong.

Recently, cerebrospinal fluid disorders drew public attention with the announcement that musician Billy Joel had been diagnosed with normal pressure hydrocephalus. In this condition, excess CSF accumulates in the brain’s cavities, enlarging them and putting pressure on surrounding brain tissue even though diagnostic readings appear normal. Because normal pressure hydrocephalus typically develops gradually and can mimic symptoms of other neurodegenerative diseases, such as Alzheimer’s or Parkinson’s disease, it is often misdiagnosed.

I am a neurologist and headache specialist. In my work treating patients with CSF pressure disorders, I have seen these conditions present in many different ways. Here’s what happens when your cerebrospinal fluid stops working.

What is cerebrospinal fluid?

CSF is made of water, proteins, sugars, ions and neurotransmitters. It is primarily produced by a network of cells called the choroid plexus, which is located in the brain’s ventricles, or cavities.

The choroid plexus produces approximately 500 milliliters (17 ounces) of CSF daily, but only about 150 milliliters (5 ounces) are present within the central nervous system at any given time due to constant absorption and replenishment in the brain. This fluid circulates through the ventricles of the brain, the central canal of the spinal cord and the subarachnoid space surrounding the brain and spinal cord.

CSF has several critical functions. It protects the brain and spinal cord from injury by absorbing shocks. Suspending the brain in this fluid reduces its effective weight and prevents it from being crushed under its own mass. Additionally, CSF helps maintain a stable chemical environment in the central nervous system, facilitating the removal of metabolic waste and the distribution of nutrients and hormones.

If the production, circulation or absorption of cerebrospinal fluid is disrupted, it can lead to significant health issues. Two notable conditions are CSF leaks and idiopathic intracranial hypertension.

Cerebrospinal fluid leak

A CSF leak occurs when the fluid escapes through a tear or hole in the dura mater – the tough, outermost layer of the meninges that surrounds the brain and spinal cord.

The dura can be damaged from head injuries or punctured during surgical procedures involving the sinuses, brain or spine, such as lumbar puncture, epidurals, spinal anesthesia or myelogram. Spontaneous CSF leaks can also occur without any identifiable cause.

CSF leaks were originally thought to be relatively rare, with an estimated annual incidence of 5 per 100,000 people. However, with increased awareness and advances in imaging, health care providers are discovering more and more leaks. They tend to occur more frequently in middle-aged adults and are more common in women than men.

Risk factors for the condition include connective tissue disorders such as Ehlers-Danlos syndrome as well as postural orthostatic tachycardia syndrome.

Unfortunately, it’s common for health care providers to misdiagnose a CSF leak as another condition, like migraine, sinus infections or allergies. What can make diagnosing a CSF leak challenging is its broad symptoms. Most people with a CSF leak have a positional headache that improves when lying down and worsens when standing. Pain is usually felt in the back of the head and may involve the neck and between the shoulder blades. In addition to headaches, patients may experience ringing in the ears, vision disturbances, memory problems, brain fog, dizziness and nausea.

Imaging may help guide diagnosis, including an MRI of your brain or entire spine, or a myelogram of the space surrounding your spinal cord. Features of a CSF leak that are visible in a scan include your brain sagging down in the base of your skull as well as a fluid collection outside of your dura. However, an estimated 19% of people with a CSF leak can have normal scans, so not seeing signs of a leak on imaging does not entirely rule it out.

Conservative treatment for a CSF leak involves rest, lying flat and increasing your fluid intake to give your spine time to heal the puncture. Increasing your caffeine consumption to an equivalent of three to four cups of coffee per day can also help by increasing CSF production through stimulating the choroid plexus. Caffeine also relieves pain by interacting with adenosine receptors, which are key players in the body’s pain perception mechanisms.

If a conservative approach is not successful, an epidural blood patch may be necessary. In this procedure, blood is drawn from your arm and injected into your spine. The injected blood can help form a covering over the hole and promote the healing process. Headache improvement can be fast, but if the patch does not work or the results are short-lived, additional testing may be needed to better locate the site of the leak. In rare cases, surgery may be recommended. Most patients with a CSF leak respond to some form of these treatments.

Idiopathic intracranial hypertension

Idiopathic intracranial hypertension is a disorder involving an excess of CSF that elevates pressure inside the skull and compresses the brain. The term “idiopathic” indicates that the cause of the raised pressure is unknown.

Most patients with idiopathic intracranial hypertension have a history of obesity or recent weight gain. Other risk factors include taking certain medications such as tetracycline, excessive vitamin A, tretinoin, steroids and growth hormone. Middle-aged obese women are 20 times more likely to be diagnosed with idiopathic intracranial hypertension than other patient groups. As obesity becomes more prevalent, so too does the incidence of this condition.

Patients with idiopathic intracranial hypertension typically experience headaches and vision changes, tinnitus or eye pain. Papilledema, or swelling of the optic disc, is the hallmark finding on a fundoscopic examination of the back of the eye. Clinicians may also observe paralysis of the patient’s eye muscles.

Normal pressure hydrocephalus, Joel’s diagnosis, is a form of this condition that commonly results in difficulty walking, loss of bladder control and cognitive impairment, sometimes referred to as the “wet, wobbly and wacky” triad. Joel’s diagnosis has brought awareness to this underrecognized but potentially treatable disorder, which is often managed through surgically placing a shunt to divert excess fluid and relieve symptoms.

Brain imaging of patients suspected of having idiopathic intracranial hypertension is crucial to excluding other causes of elevated CSF pressure, such as brain tumors or blood clots in the brain. A lumbar puncture or spinal tap to measure the pressure and composition of CSF is also central to diagnosis.

Since high intracranial pressure can damage the optic nerve and lead to permanent vision loss, the primary goal of treatment is to decrease pressure and preserve the optic nerve. Treatment options include weight loss, dietary changes and medications to reduce CSF production. Surgical procedures can also reduce intracranial pressure.

Future directions and unknowns

Cerebrospinal fluid is indispensable for brain health. Despite advances in understanding diseases related to CSF, several aspects remain unclear.

The exact mechanisms that lead to conditions like CSF leaks and idiopathic intracranial hypertension are not fully understood, though there are many theories. Further research is vital to enhance diagnostic accuracy and effective treatments for CSF disorders.

This is an updated version of an article originally published on Aug. 14, 2024.

Danielle Wilhour, Assistant Professor of Neurology, University of Colorado Anschutz Medical Campus

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Bill Sullivan, Indiana University

Male fertility rates have been plummeting over the past half-century. An analysis from 1992 noted a steady decrease in sperm counts and quality since the 1940s. A more recent study found that male infertility rates increased nearly 80% from 1990 to 2019. The reasons driving this trend remain a mystery, but frequently cited culprits include obesity, poor diet and environmental toxins.

Infectious diseases such as gonorrhea or chlamydia are often overlooked factors that affect fertility in men. Accumulating evidence suggests that a common single-celled parasite called Toxoplasma gondii may also be a contributor: An April 2025 study showed for the first time that “human sperm lose their heads upon direct contact” with the parasite.

I am a microbiologist, and my lab studies Toxoplasma. This new study bolsters emerging findings that underscore the importance of preventing this parasitic infection.

The many ways you can get toxoplasmosis

Infected cats defecate Toxoplasma eggs into the litter box, garden or other places in the environment where they can be picked up by humans or other animals. Water, shellfish and unwashed fruits and vegetables can also harbor infectious parasite eggs.

In addition to eggs, tissue cysts present in the meat of warm-blooded animals can spread toxoplasmosis as well if they are not destroyed by cooking to proper temperature.

While most hosts of the parasite can control the initial infection with few if any symptoms, Toxoplasma remains in the body for life as dormant cysts in brain, heart and muscle tissue. These cysts can reactivate and cause additional episodes of severe illness that damage critical organ systems.

Between 30% and 50% of the world’s population is permanently infected with Toxoplasma due to the many ways the parasite can spread.

Toxoplasma can target male reproductive organs

Upon infection, Toxoplasma spreads to virtually every organ and skeletal muscle. Evidence that Toxoplasma can also target human male reproductive organs first surfaced during the height of the AIDS pandemic in the 1980s, when some patients presented with the parasitic infection in their testes.

While immunocompromised patients are most at risk for testicular toxoplasmosis, it can also occur in otherwise healthy individuals. Imaging studies of infected mice confirm that Toxoplasma parasites quickly travel to the testes in addition to the brain and eyes within days of infection.

In 2017, my colleagues and I found that Toxoplasma can also form cysts in mouse prostates. Researchers have also observed these parasites in the ejaculate of many animals, including human semen, raising the possibility of sexual transmission.

Knowing that Toxoplasma can reside in male reproductive organs has prompted analyses of fertility in infected men. A small 2021 study in Prague of 163 men infected with Toxoplasma found that over 86% had semen anomalies.

A 2002 study in China found that infertile couples are more likely to have a Toxoplasma infection than fertile couples, 34.83% versus 12.11%. A 2005 study in China also found that sterile men are more likely to test positive for Toxoplasma than fertile men.

Not all studies, however, produce a link between toxoplasmosis and sperm quality.

Toxoplasma can directly damage human sperm

Toxoplasmosis in animals mirrors infection in humans, which allows researchers to address questions that are not easy to examine in people.

Testicular function and sperm production are sharply diminished in Toxoplasma-infected mice, rats and rams. Infected mice have significantly lower sperm counts and a higher proportion of abnormally shaped sperm.

In that April 2025 study, researchers from Germany, Uruguay and Chile observed that Toxoplasma can reach the testes and epididymis, the tube where sperm mature and are stored, two days after infection in mice. This finding prompted the team to test what happens when the parasite comes into direct contact with human sperm in a test tube.

After only five minutes of exposure to the parasite, 22.4% of sperm cells were beheaded. The number of decapitated sperm increased the longer they interacted with the parasites. Sperm cells that maintained their head were often twisted and misshapen. Some sperm cells had holes in their head, suggesting the parasites were trying to invade them as it would any other type of cell in the organs it infiltrates.

In addition to direct contact, Toxoplasma may also damage sperm because the infection promotes chronic inflammation. Inflammatory conditions in the male reproductive tract are harmful to sperm production and function.

The researchers speculate that the harmful effects Toxoplasma may have on sperm could be contributing to large global declines in male fertility over the past decades.

Preventing toxoplasmosis

The evidence that Toxoplasma can infiltrate male reproductive organs in animals is compelling, but whether this produces health issues in people remains unclear. Testicular toxoplasmosis shows that parasites can invade human testes, but symptomatic disease is very rare. Studies to date that show defects in the sperm of infected men are too small to draw firm conclusions at this time.

Additionally, some reports suggest that rates of toxoplasmosis in high-income countries have not been increasing over the past few decades while male infertility was rising, so it’s likely to only be one part of the puzzle.

Regardless of this parasite’s potential effect on fertility, it is wise to avoid Toxoplasma. An infection can cause miscarriage or birth defects if someone acquires it for the first time during pregnancy, and it can be life-threatening for immunocompromised people. Toxoplasma is also the leading cause of death from foodborne illness in the United States.

Taking proper care of your cat, promptly cleaning the litter box and thoroughly washing your hands after can help reduce your exposure to Toxoplasma. You can also protect yourself from this parasite by washing fruits and vegetables, cooking meat to proper temperatures before consuming and avoiding raw shellfish, raw water and raw milk.

Bill Sullivan, Professor of Microbiology and Immunology, Indiana University

This article is republished from The Conversation under a Creative Commons license. Read the original article.