Tag: The Conversation

Categories : Substance Use UrogenitalTags :

Ketamine is Giving More Young People Bladder Problems – An Expert Explains

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A growing number of people in the UK are using ketamine recreationally. Photo by Colin Davis on Unsplash

Heba Ghazal, Kingston University

Urology departments in England and Wales have reported seeing an increase in the number of 16- to 24-year-olds being admitted for bladder inflammation associated with ketamine use.

This appears to coincide with an increase in ketamine use – with the number of adults and teens entering treatment for ketamine abuse last year jumping substantially compared to even just a few years previously.

Ketamine abuse can have many affects on the bladder, causing frequent urination, night-time urination, sudden urges, leakage, inflammation, pain in the bladder or lower back and blood in the urine. These symptoms can be severe, make daily life very difficult and may even be permanent in some cases.

Ketamine was first approved in 1970 for human use as an anaesthetic. More recently, studies have suggested that ketamine used at low doses may have antidepressant effects.

But a growing number of people are now using ketamine recreationally. It acts as a dissociative drug, causing users to feel detached from themselves and their surroundings. It can produce hallucinogenic, stimulant and pain-relieving effects, which last one to two hours.

Users typically snort or smoke powdered ketamine, or inject liquid ketamine or mix it into drinks in order to experience the drug’s effects. Snorting usually produces stronger effects and more noticeable symptoms than swallowing it.

Ketamine users can develop tolerance to the drug quickly, needing higher doses to get the same effects. This is probably due to the body and brain adapting to become more efficient at breaking down the drug. Frequent users often need to take twice the amount of occasional users to get the same effect.

Bladder damage

Frequent, high-dose ketamine use can cause serious damage to the bladder, urinary tract and kidneys. In severe cases, the bladder may need to be removed.

The first recorded cases of ketamine affecting the bladder were reported in Canada in 2007, where nine people who used ketamine recreationally had severe bladder problems and blood in their urine. Later, a bigger study in Hong Kong found the same issues in 59 people who had used ketamine for more than three months.

Ketamine, as with any other drug, is metabolised in the body where it’s broken down and excreted in urine.

When ketamine is broken down, it turns into chemicals that can seriously harm the bladder. When these by-products stay in contact with the urinary tract for a long time, they irritate and damage the tissue.

The bladder is damaged first, because it holds urine the longest. Later, the ureters (tubes connecting the kidney to the bladder) and the kidneys can also be affected.

Over time, the bladder can shrink and become stiff, causing strong urinary symptoms. The ureters can become narrow and bent, sometimes described as looking like a “walking stick.” This can lead to backed-up urine in the kidneys (hydronephrosis).

Ketamine also increases oxidative stress, which damages cells and causes bladder cells to die. This breaks the protective bladder lining, making it leaky and overly sensitive.

All these changes can make the bladder overactive, extremely sensitive and painful, often causing severe urges to urinate and incontinence.

Bladder damage from ketamine use happens in stages.

In the first stage, the bladder becomes inflamed. This can often be reversed by stopping ketamine and taking certain medication – such as anti-inflammatory drugs, pain relievers or prescription drugs that reduce bladder urgency and help the bladder lining heal.

In the second stage, the bladder can shrink or become stiff. In this stage, treatment is similar to stage one, but a bladder wash may also be required. This is where a catheter is used to put liquid medication directly into the bladder. The drug coats the bladder’s inner lining, helping to restore its protective layer and reduce inflammation.

Botulinum toxin injections may also be used to relax the bladder and reduce pain and urgency. Stopping ketamine remains essential to prevent further damage.

In the final stage, permanent damage occurs to the bladder and kidneys. Over time, if the kidneys are affected, it can lead to kidney failure. Dialysis (a treatment where waste products and excess fluid are filtered from the blood) or even surgery may be required to repair kidney function and the urinary system.

Although ketamine has been a class B drug since 2014, it’s unfortunately affordable and accessible – costing as little as £3 per gram in some parts of the UK. Raising awareness about the risks of ketamine use is essential to prevent these serious health problems.

Heba Ghazal, Senior Lecturer, Pharmacy, Kingston University

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

Categories : CancerTags :

The Next Cancer Breakthrough may be Stopping it Before it Starts

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Source: Unsplash CC0

Ahmed Elbediwy, Kingston University and Nadine Wehida, Kingston University

Cancer treatment follows a familiar pattern: doctors spot symptoms, diagnose the disease and start treatment. But scientists are now exploring a radical shift in how we tackle cancer. Instead of waiting for tumours to appear, they want to catch the disease decades before it develops.

This approach is called “cancer interception”. The idea is simple: target the biological processes that cause cancer long before a tumour ever forms.

Researchers are hunting for subtle early warning signs. These include genetic mutations that quietly build up in our cells, giving them advantages against our immune defences.

They’re also looking at precancerous lesions like moles or polyps, and early visible changes in tissue. All of these appear long before cancer becomes obvious.

Large genetic studies reveal that as people age, their bodies accumulate small groups of mutated cells called clones that grow silently. Scientists have studied this particularly well in blood. These clones can help predict who might develop blood cancers like leukaemia, and the genetics, inflammation and environmental factors strongly influence them.

Crucially, doctors can measure and track these changes over time. This opens up possibilities for early intervention.

A 16-year study followed around 7,000 women and uncovered how these mutations work. Some mutations helped clones multiply faster, while others made them particularly sensitive to inflammation.

When there was inflammation, these sensitive clones expanded. Breaking down these patterns helps researchers identify people with a higher chance of developing cancer later.

Not a sudden event

The research reveals something fundamental about cancer. It’s not a sudden event that instantly produces a tumour.

Instead, cancer develops through a slow, multi-step process with detectable warning signs along the way. These early signs could become powerful targets for stopping cancer before it starts.

Scientists are developing blood tests to spot cancer long before symptoms appear. These tests, called multi-cancer early detection tests (MCEDs for short), search for tiny fragments of DNA in the blood.

MCEDs work by looking for circulating tumour DNA, or ctDNA – DNA fragments that cancerous or precancerous cells release into the bloodstream. Even very early cancers shed this DNA, so the tests might detect disease long before it shows up on a scan.

The results so far look promising. MCEDs can boost survival rates through early detection, especially for colorectal cancer. When doctors diagnose colorectal cancer at stage one, 92% of patients survive five years. But when they catch it at stage four, only 18% survive that long.

If colon cancer is caught at stage one, most patients are still alive after five years. Credit: National Cancer Institute

The tests aren’t perfect, though. They miss some cancers entirely, and positive results still need follow-up tests to confirm.

Even so, research suggests MCEDs could become crucial for catching cancers that usually go unnoticed until much later. The potential to save lives is significant.

Heart doctors already use a similar approach. They calculate a person’s risk using age, blood pressure, cholesterol and family history, then prescribe drugs like statins years before a heart attack happens.

Cancer researchers want to copy this model. They envision combining genetic mutations, environmental factors and MCED results to guide early cancer prevention.

But cancer differs from heart disease in important ways. Cancer doesn’t follow a predictable path, and some early lesions shrink or never progress.

There’s also the risk of over-diagnosis. Being told you’re at higher risk when you feel perfectly healthy creates anxiety.

Cancer prevention tools also vary widely in their effectiveness, unlike statins that work broadly across different cardiovascular risk groups. The risk-based model shows promise, but needs careful handling.

Treating cancer risk instead of cancer itself raises difficult ethical questions. When someone feels completely healthy, judging whether intervention will truly help them becomes harder.

There’s a danger of causing unnecessary worry or harm. Scientists warn that doctors sometimes overestimate benefits and underestimate risks, particularly for older adults.

MCED tests bring their own ethical concerns. Accuracy isn’t the only issue that matters.

The tests sometimes flag cancer when none exists, leading to follow-up scans and biopsies that patients don’t actually need. The anxiety from all of this carries a high cost, both for patients and the healthcare system.

If these tests are expensive or only available privately, they could make health inequalities worse. This concern hits hardest in low-income countries.

In the US, the medicines regulator is investigating how MCED blood tests should work. They’re examining how reliable the tests need to be and what follow-ups doctors should require to keep patients safe.

The UK is following suit. The National Cancer Plan for England, published on February 4, 2026, commits to providing 9.5 million extra diagnostic tests through the NHS each year by March 2029.

The plan also states that ctDNA biomarker testing will continue in lung and breast cancer. It will extend to other cancers if proven to be cost effective.

What all this shows is clear. Cancer doesn’t suddenly appear; it’s a steady process that begins decades earlier. Catching it before it grows could save countless lives. The question now is how to do that safely, fairly and effectively.

Ahmed Elbediwy, Senior Lecturer in Cancer Biology & Clinical Biochemistry, Kingston University and Nadine Wehida, Senior Lecturer in Genetics and Molecular Biology, Kingston University

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

Categories : Metabolic DisordersTags :

High Cholesterol and Insulin Resistance are Rising Among Young South Africans – What that Means for Public Health

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Photo by Elizeu Dias on Unsplash

Themba Titus Sigudu, University of the Witwatersrand

In a small mining town in South Africa’s Limpopo province, young people are showing worrying signs of diseases that were once thought to affect only older adults.

These include type 2 diabetes, high blood pressure, high cholesterol, obesity and insulin resistance. This is not unique to Limpopo or South Africa. It reflects a global trend, where young adults in many low- and middle-income countries are increasingly experiencing early-onset metabolic diseases due to rapid urbanisation, lifestyle changes, unhealthy diets and reduced physical activity.

The World Health Organization says non-communicable diseases now account for 75% of all non-pandemic-related deaths globally. Also, 82% of premature deaths before age 70 occur in low- and middle-income countries.

I’m a public health researcher specialising in epidemiology, metabolic health, infectious diseases and environmental health. My colleagues and I conducted a study in the town of Lephalale and found that many young adults there have abnormal cholesterol levels. They also have reduced sensitivity to insulin, a condition known as insulin resistance.

Both are key risk factors for type 2 diabetes and heart disease.

Our findings suggest that these health problems are appearing much earlier in life than expected. This is particularly concerning in communities undergoing rapid social and economic change, where access to health services and screening programmes remains limited.

New jobs, new lifestyles

Lephalale, formerly known as Ellisras, offers a window into these transitions. Once a quiet rural area in the north of South Africa, it has changed rapidly over the past two decades. It is now the site of expanding mining and industrial activities, driven by the expansion of coal mining operations and the development of power stations.

This industrial growth has attracted thousands of workers from surrounding provinces and neighbouring countries, bringing new economic opportunities. It is also reshaping daily life. Increasingly, residents are doing sedentary work and eating energy-dense diets, including fast food. These lifestyle transitions make Lephalale an important setting for studying emerging health risks in young adults.

Long hours sitting at work and reduced physical activity create fertile ground for metabolic disorders. When people eat more processed, high-fat, high-sugar foods and move less, the body begins storing excess energy as fat.

Over time, this can lead to weight gain, elevated blood glucose and abnormal cholesterol levels. These changes make it harder for the body to regulate insulin, causing insulin resistance, the first step towards type 2 diabetes. Also, inactivity and poor diet increase unhealthy cholesterol and triglycerides (types of fat in the blood), raising the risk of heart disease. In rapidly transitioning communities, these health shifts can happen quickly.

Non-communicable diseases such as diabetes, hypertension and heart disease are now among the leading causes of death in South Africa. In 2020, diabetes was reported to be the second biggest underlying cause of death in South Africa, accounting for 6.6% of all deaths.

Our research

We examined 781 young adults aged 18 to 29 years living in Lephalale as part of a long-running study. We have been tracking health patterns in this community since 1992.

Participants provided fasting blood samples that were analysed for glucose, insulin and cholesterol levels. We grouped them into diabetic and non-diabetic categories based on clinical definitions used by the American Diabetes Association.

The results were striking:

  • Diabetic participants had significantly higher total cholesterol, low-density lipoprotein (the “bad” cholesterol) and triglycerides, and lower levels of high-density lipoprotein (the “good” cholesterol) than their non-diabetic peers.
  • Over half (52.7%) of the diabetic group had high total cholesterol, compared with 23% of non-diabetic participants.
  • Insulin resistance, when the body needs more insulin to manage blood sugar, was also much higher among diabetics.
  • Even some non-diabetic participants showed early signs of these metabolic changes.

Unhealthy cholesterol patterns and poor insulin sensitivity tend to occur together, each making the other worse. This combination sets the stage for early heart disease, stroke and diabetes.

Why young adults?

Most public-health strategies focus on older adults because that’s when chronic diseases usually become visible.

But our research adds to growing evidence that the seeds of non-communicable diseases are planted early, often in young adulthood or even adolescence.

Young adults in rural or semi-urban areas may seem healthy, yet many are already developing risks due to diet changes, stress and limited exercise opportunities. The modernisation of small towns, while positive economically, brings hidden health costs.

Without early detection, these individuals may enter middle age already carrying high risk of health problems. This will put pressure on health systems that are already stretched.

What makes this community unique?

Lephalale may be changing, but it still lacks many of the urban services, infrastructure and health resources found in South Africa’s big cities.

Health resources are scarce, and screening for cholesterol or insulin resistance is rare. Public clinics focus on infectious diseases such as HIV or tuberculosis. Silent metabolic disorders go unnoticed until symptoms appear.

Our study shows that rapid industrialisation without parallel investment in public-health education and preventive services risks creating a generation of young adults who are chronically unwell by their thirties.

What can be done?

Three priorities stand out:

Early screening and prevention

Regular cholesterol and glucose testing should be part of routine primary-care visits, especially for adults under 30. Mobile health campaigns, school outreach and workplace screenings could help identify those at risk.

Community-based education

Local awareness campaigns must make the link between diet, physical activity and metabolic health easy to understand. They should show, for example, how frequent consumption of fried or sugary foods contributes to cholesterol build-up and insulin resistance.

Healthy-environment policies

Urban planners and municipalities can support healthy lifestyles by ensuring there are safe spaces for exercise. They must also limit marketing of unhealthy foods, and encourage availability of affordable, nutritious options. Similar “health-in-all-policies” approaches have shown success in other countries. such as Finland’s long-running HiAP strategy, which reduced cardiovascular disease rates and improved population health outcomes.

Young people should be in peak health. Without intervention, today’s young adults risk becoming tomorrow’s chronic-disease patients, burdening families, workplaces and health systems.

Themba Titus Sigudu, Lecturer, University of the Witwatersrand

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

Categories : Obstetrics & GynaecologyTags :

Africa’s Hidden Stillbirth Crisis: New Report Exposes Major Policy and Data Gaps

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Mary Kinney, University of Cape Town

Photo by ManuelTheLensman on Unsplash

Nearly one million babies are stillborn in Africa every year. Behind every stillbirth is a mother, a family and a story left untold. Most of these are preventable, many unrecorded, and too often invisible. Each number hides a moment of heartbreak, and every uncounted loss represents a missed opportunity to learn and to act.

As a public health researcher specialising in maternal and newborn health, I have spent the past two decades working on strengthening health systems and quality of care across Africa. My research has focused on understanding how health systems can prevent stillbirths and provide respectful, people-centred care for women and newborns. Most recently, I was part of the team that led a new report called Improving Stillbirth Data Recording, Collection and Reporting in Africa. It is the first continent-wide assessment of how African countries record and use stillbirth data.

The study, conducted jointly by the Africa Centres for Disease Control and Prevention, the University of Cape Town, the London School of Hygiene & Tropical Medicine and the United Nations Children’s Fund, surveyed all 55 African Union member states between 2022 and 2024, with 33 countries responding.

The burden of stillbirths in Africa is staggering. Africa accounts for half of all stillbirths globally, with nearly eight times higher rates than in Europe. Even stillbirths that happen in health facilities may never make it into official statistics despite every maternity registry documenting this birth outcome.

Part of the challenge is that there are multiple data systems for capturing births and deaths, including stillbirths, like routine health information systems, civil registration and other surveillance systems. But these systems often don’t speak to each other either within countries or between countries. This data gap hides both the true burden and the preventable causes.

Despite advances in several countries to prevent stillbirths, large gaps remain, especially on data systems. Only a handful of African countries routinely report stillbirth data to the UN, and many rely on outdated or incomplete records. Without reliable, comparable data, countries cannot fully understand where and why stillbirths occur or which interventions save lives.

Strengthening stillbirth data is not just about numbers; it is about visibility, accountability and change. When countries count every stillbirth and use the data for health system improvement, they can strengthen care at birth for mothers and newborns and give every child a fair start in life.

Findings

The report was based on a regional survey of ministries of health. This was followed by document reviews and expert consultations to assess national systems, policies and practices for stillbirth reporting and review.

The report reveals that 60% of African countries have national and sub-national committees responsible for collecting and using stillbirth data, which produce national reports to respective health ministries. But data use remains limited. Capacity gaps, fragmented systems and insufficient funding prevents many countries from translating information into action.

To guide investment and accountability, the report categorises countries into three readiness levels:

  1. Mature systems needing strengthening, such as Kenya, Rwanda and Uganda. These countries have consistent data flows but need more analysis and use.
  2. Partial systems requiring support, where reporting mechanisms exist but are not systematically implemented, like Ghana, Malawi and Tanzania.
  3. Foundational systems still being built, including fragile or conflict-affected countries like South Sudan and Somalia. Here, policies and structures for data collection and use remain absent.

The findings show both progress and persistent gaps. Two-thirds of African countries now include stillbirths in their national health strategies, and more than half have set reduction targets. Nearly all countries report that they routinely record stillbirths through their health sectors using standard forms and definitions, yet these definitions vary widely. Most systems depend on data reported from health facilities. But the lack of integration between health, civil registration and other data systems means that countless losses never enter national statistics.

For example, if a woman delivers at home alone in Mozambique and the baby is stillborn, the loss is only known to the family and community. Without a facility register entry or civil registration notification, the death never reaches district or national statistics. Even when a stillbirth occurs in a health centre, the health worker may log it in a facility register but not report it to the civil registration system. This means the loss of the baby remains invisible in official data.

What this means

Stillbirths are a sensitive measure of how health systems are performing. They reflect whether women can access timely, quality care during pregnancy and at birth. But unlike maternal deaths, which are often a benchmark for health system strength, stillbirths remain largely absent from accountability frameworks.

Their causes, like untreated infections, complications during labour, or delays in accessing emergency caesarean sections, are often preventable. The same interventions that prevent a stillbirth also reduce maternal deaths. These improve newborn survival, and lay the foundation for better health and development outcomes in early childhood.

Accurate data on stillbirths can guide clinical care and direct scarce resources to where they are needed most. When data systems are strong, leaders can identify where and why stillbirths occur, track progress and make informed decisions to prevent future tragedies.

The analysis also highlights promising signs of momentum. Over two-thirds of countries now reference stillbirths in national health plans, an important marker of growing political attention. Several countries are moving from isolated data collection to more coordinated, system-wide approaches. This progress shows that change is possible when stillbirths are integrated into national health information systems and supported by investment in workforce capacity, supervision and data quality.

What’s needed

Africa has the knowledge, evidence and experience to make change happen.

The report calls for harmonised definitions, national targets and stronger connections and data use between the different data sources within and across African countries. Above all, it calls for collective leadership and investment to turn information into impact, so that every stillbirth is counted, every death review leads to learning and no parent grieves alone.

The author acknowledges and appreciates the partners involved in developing the report and the support from the Global Surgery Division at UCT.

Mary Kinney, Senior Lecturer with the Global Surgery Division, University of Cape Town

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

Categories : Neurodegenerative Diseases New Compounds and TreatmentsTags :

A New Treatment for Huntington’s Disease Is Genuinely Promising – But Here’s Why We Still Need Caution

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Photo by Anna Shvets

Bryce Vissel, UNSW Sydney

Imagine knowing in your 20s or 30s that you carry a gene which will cause your mind and body to slowly unravel. Huntington’s disease is inherited, relentless and fatal, and there is no cure. Families live with the certainty of decline stretching across generations.

Now, a new treatment is being widely reported as a breakthrough.

Last week, gene therapy company uniQure announced that a one-time brain infusion appeared to slow the disease in a small clinical study.

If confirmed, this would not only be a landmark for Huntington’s disease but potentially the first time a gene therapy has shown promise in any adult-onset neurodegenerative disorder.

But the results, which were announced in a press release, are early, unreviewed and based on external comparisons. So, while these findings offer families hope after decades of failure, we need to remain cautious.

What is Huntington’s disease?

Huntington’s is a rare but devastating disease, affecting around five to ten people in 100,000 in Western countries. That means thousands in Australia and hundreds of thousands worldwide.

Symptoms usually start in mid-life. They include involuntary movements, depression, irritability and progressive decline in thinking and memory. People lose the ability to work, manage money, live independently and eventually care for themselves. Most die ten to 20 years after onset.

The disease is caused by an expanded stretch of certain DNA repeats (CAG) in the huntingtin gene. The number of repeats strongly influences when symptoms begin, with longer expansions usually linked to earlier onset.

Looking for a treatment

The gene that causes Huntington’s disease was identified in 1993, 32 years ago. Soon afterwards, mouse studies showed that switching off the mutant huntingtin protein even after symptoms had begun could reverse signs and improve behaviour.

This suggested lowering the toxic protein might slow or even partly reverse the disease. Yet for three decades, every attempt to develop a therapy for people has failed to show convincing clinical benefit. Trials of huntingtin-lowering drugs and other approaches did not slow progression.

What is the new treatment?

The one-time gene therapy, called AMT-130, involves brain surgery guided by MRI. Surgeons infuse an engineered virus directly into the caudate and putamen brain regions, which are heavily affected in Huntington’s.

The virus carries a short genetic “microRNA” designed to reduce production of the affected huntingtin protein.

By delivering it straight into the brain, the treatment bypasses the blood–brain barrier. This natural wall usually prevents medicines from entering the central nervous system. That barrier helps explain why so many brain-targeted drugs have failed.

What did they find?

Some 29 patients received treatment, with 12 in each group (one low-dose, and one high-dose) followed for three years. According to uniQure, those given the higher dose declined much slower than expected.

The study compared how much participants’ movement, thinking and daily function declined, compared to a matched external group from a global Huntington’s registry (meaning they weren’t part of the study). The company claimed those given the higher dose had a 75% slowing in their decline.

On a functional scale focused on independence, the company reported a 60% slowing in decline for the higher dose group.

Other tests of movement and thinking also favoured treatment. Nerve-cell damage in spinal fluid was lower for study participants than would be expected for untreated patients.

Why should we be cautious?

These findings are an early snapshot of results reported by the company, not yet peer-reviewed. The study compared treated patients to an external matched control group, not people randomised to placebo at the same time. This design can introduce bias. The numbers are also small – only 12 patients at the three-year mark – so we can’t draw solid conclusions.

The company reports the therapy was generally well tolerated, with no new serious adverse events related to the drug since late 2022. Most problems were related to the neurosurgical infusion itself, and resolved. But in a disease that already causes such severe symptoms, it is often hard to know what counts as a side effect.

The company uniQure has said it plans to seek regulatory approval in 2026 on the basis of this dataset.

Regulators will face difficult decisions: whether to allow access sooner before all the questions and uncertainties are addressed – based on the needs of a community with no effective options – and wait for further data while people are being treated, or to insist on larger trials that confirm results before approval.

What does it mean?

If upheld, these results represent the first convincing signs that a gene-targeted therapy can slow Huntington’s disease. They may also be the first evidence of benefit from a gene therapy in any adult-onset neurodegenerative disorder. That would be a milestone after decades of failure.

But these results do not prove success. Only larger, longer and fully peer-reviewed studies will show whether this treatment truly changes lives. Even if approved, a complex neurosurgical gene therapy may not be easily accessible to all patients.

The company has said the drug’s price would be similar to other gene therapies – which can cost over A$3 million per patient – and will have the added cost of brain surgery.

The takeaway

For families who carry this gene, the hope is profound. But caution is just as important.

We may be witnessing the first credible step toward slowing an inherited adult-onset neurodegenerative disease, or just an early signal that may not hold up.

Ultimately, only time and rigorous science will show whether this treatment delivers the benefits so urgently needed.

Bryce Vissel, Cojoint Professor, School of Clinical Medicine, UNSW Sydney

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

Categories : UncategorizedTags :

Prediabetes Remission Possible Without Dropping Pounds, Our New Study Finds

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Photo by Kenny Eliason on Unsplash

Andreas L. Birkenfeld, University of Tübingen and Reiner Jumpertz-von Schwartzenberg, University of Tübingen

There’s a long-held belief in diabetes prevention that weight loss is the main way to lower disease risk. Our new study challenges this.

For decades, people diagnosed with prediabetes – a condition affecting up to one in three adults depending on age – have been told the same thing by their doctors: eat healthily and lose weight to avoid developing diabetes.

This approach hasn’t been working for all. Despite unchanged medical recommendations for more than 20 years, diabetes prevalence continues rising globally. Most people with prediabetes find weight-loss goals hard to reach, leaving them discouraged and still at high risk of diabetes.

Our latest research, published in Nature Medicine, reveals a different approach entirely. We found that prediabetes can go into remission – with blood sugar returning to normal – even without weight loss.

About one in four people in lifestyle intervention programmes bring their blood sugar back to normal without losing any weight. Remarkably, this weight-stable remission protects against future diabetes just as effectively as remission achieved through weight loss.

This represents a significant shift in how doctors might treat overweight or obese patients at high risk for diabetes. But how is it possible to reduce blood glucose levels without losing weight, or even while gaining weight?

The answer lies in how fat is distributed throughout the body. Not all body fat behaves the same way.

The visceral fat deep in our abdomen, surrounding our internal organs, acts as a metabolic troublemaker. This belly fat drives chronic inflammation that interferes with insulin – the hormone responsible for controlling blood sugar levels. When insulin can’t function properly, blood glucose rises.

In contrast, subcutaneous fat – the fat directly under our skin – can be beneficial. This type of fat tissue produces hormones that help insulin work more effectively. Our study shows that people who reverse prediabetes without weight loss shift fat from deep within their abdomen to beneath their skin, even if their total weight stays the same.

Subcutaneous fat can be beneficial. Photo by Andres Ayrton on Pexels

We’ve also uncovered another piece of the puzzle. Natural hormones that are mimicked by new weight-loss medications like Wegovy and Mounjaro appear to play a crucial role in this process. These hormones, particularly GLP-1, help pancreatic beta cells secrete insulin when blood sugar levels rise.

People who reverse their prediabetes without losing weight seem to naturally enhance this hormone system, while simultaneously suppressing other hormones that typically drive glucose levels higher.

Targeting fat redistribution, not just weight loss

The practical implications are encouraging. Instead of focusing only on the scales, people with prediabetes can aim to shift body fat with diet and exercise.

Research shows that polyunsaturated fatty acids, abundant in Mediterranean diets rich in fish oil, olives and nuts, may help reduce visceral belly fat. Similarly, endurance training can decrease abdominal fat even without overall weight loss.

This doesn’t mean weight loss should be abandoned as a goal – it remains beneficial for overall health and diabetes prevention. However, our findings suggest that achieving normal blood glucose levels, regardless of weight changes, should become a primary target for prediabetes treatment.

This approach could help millions of people who have struggled with traditional weight-loss programmes but might still achieve meaningful health improvements through metabolic changes.

For healthcare providers, this research suggests a need to broaden treatment approaches beyond weight-focused interventions. Monitoring blood glucose improvements and encouraging fat redistribution through targeted nutrition and exercise could provide alternative pathways to diabetes prevention for patients who find weight loss particularly difficult.

The implications extend globally, where diabetes represents one of the fastest-growing health problems. By recognising that prediabetes can improve without weight loss, we open new possibilities for preventing a disease that affects hundreds of millions worldwide and continues rapidly expanding.

This research fundamentally reframes diabetes prevention, suggesting that metabolic health improvements – not just weight reduction – should be central to clinical practice. For the many people living with prediabetes who have felt discouraged by unsuccessful weight-loss attempts, this offers renewed hope and practical alternative strategies for reducing their diabetes risk.

Andreas L. Birkenfeld, Professor, Diabetology, Endocrinology and Nephrology, University of Tübingen and Reiner Jumpertz-von Schwartzenberg, Professorship for Clinical Metabolism and Obesity Research, University Hospital and Medical Faculty, University of Tübingen

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

Categories : Diet and NutritionTags :

What Students Eat: I Conducted a Survey at a South African University’s Cafes – the Results Are Scary

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Photo by Jonathan Borba

Tinashe P. Kanosvamhira, University of Cape Town

University students have limited spending money and their schedules are packed. Many are adapting to new lifestyles on campus. Eating a healthy diet is crucial: a poor diet leads to reduced concentration, lower grades and increased stress.

Campus cafés, especially at universities that are some distance from supermarkets, often sell mainly fast food such as white bread sandwiches, hot chips and doughnuts. It’s easy to eat on the go, but places nutritious choices out of reach.

I’m an urban geographer who researches the relationship between food, health and place. My work examines how urban agriculture, informal food systems and everyday urban infrastructures shape well-being, sustainability and spatial justice in African cities.

Research has already found that through pricing, menu design and information provision, campus cafés play a decisive role in shaping dietary behaviours among young adults. I wanted to find out how students at the University of the Western Cape in South Africa choose what to eat when they’re on campus, what they see as healthy food and what stands in the way of them buying nutritious meals.

The university is one that was underfunded during apartheid. Until 1994 it primarily taught students who were Black and people of Colour. Today, it serves about 23 000 students, many of whom are drawn from low-income backgrounds, and has few supermarkets within walking distance. The campus cafés are a key food supply area for students.

My research found that at the University of the Western Cape, only 32% of the food offered at the student café was healthy. It also cost more than the fast food. The students I surveyed knew healthy food was important. But only a small minority consistently chose nutritious meals. Nearly 40% of the group reported that the healthy options were too expensive.

When students face the twin challenges of financial hardship and inadequate access to affordable, nutritious food, this deepens inequality. It also undermines their efforts to succeed. Even worse, it can cause students to develop long term, unhealthy eating habits that damage their health.

Unless affordability, availability and awareness of healthy food choices are addressed together, students will struggle to eat well and to perform at their best.

Universities must implement targeted food subsidies, introduce clearer nutritional labelling, and expand healthy menu options to make nutritious eating more accessible and appealing to students.

Students speak out about their food choices

I conducted a survey that sampled 112 students in five campus cafés at the university. These cafés are mainly used by students in the 18-24 age group.

My survey revealed that 75.9% of students considered healthy offerings at least “somewhat important” when choosing where to eat. Yet only 6.3% always selected nutritious options; 28.6% rarely or never did so. Meanwhile, 38.4% of students described nutritious meals as “expensive” and another 8% found the healthy options “very expensive”.

My research also found that University of the Western Cape students ate very little fruit and vegetables. Just 41% of the students I surveyed ate two or more servings a day and 9.8% admitted they ate none.

I also did a detailed menu audit at one café to see what was on the menu. I found that only 32.6% of 46 distinct items met basic “healthy” criteria (they were low in saturated fats and made up of whole-grains or vegetables).

The majority of students (55.4%) had not noticed any campus healthy-eating campaigns, but agreed (57.1%) that balanced meals boosted academic performance and overall well-being:

I feel much more focused and energetic when I eat well, which helps me do better in my studies and feel healthier overall.

Only a small handful of the students said they could afford healthy campus café meals:

I choose cafés based on food quality. If the food is fresh and tasty, I’ll pay more, but it needs to be worth it.

What needs to happen next

High prices for nutritious items, narrow menu selections and barely visible information about nutrition are preventing students from eating healthy foods on campus.

Campus café offerings tend to mirror the broader inequities of national and global food systems. Food environments of big institutions like universities can prop up food inequality, even if these universities are committed to social justice.

Universities should adopt these steps to make healthy food available to students:

  1. Subsidised meal plans and discounts: Introducing a tiered subsidy for students from low-income backgrounds would directly reduce costs. For example, meal vouchers could make salads, whole-grain sandwiches and fruit bowls as affordable as a pastry or soft drink.
  2. A wider range of food on the menu and smaller portions: Partnerships between university caterers and local cooperatives or farmers could expand the range of fresh produce. Smaller portions or “light” meal options could be sold at lower prices to suit tighter budgets. Regularly rotating healthy specials and clearly labelling ingredients and calories would help students become accustomed to choosing healthy meals.
  3. Visible nutrition campaigns: Digital and printed standout posters about healthy foods could be placed around campus. Universities could hold social-media challenges and pop-up tasting events. Integrating simple tips into lecture slides or student newsletters would also help by repeatedly exposing students to healthy food tips.
  4. Peer-led workshops and cooking classes: These should be arranged to empower students to take ownership of their diets and learn about budgeting, meal planning and quick, nutritious cooking skills. Peer facilitators can demystify healthy eating and create a supportive healthy eating community.
  5. Seeking feedback: To see if their healthy food campaigns are working, universities should survey students, and analyse sales data from the cafés to see what’s being eaten. They should get feedback from students through focus groups that identify emerging needs and ensure that campaigns and projects reflect the realities of students’ lives.

My research suggests that by tackling cost, choice and communication together, universities can transform their cafés from sites of compromise into engines of student well-being. Such interventions would unlock academic potential and set young people on healthier life paths. This is an outcome as enriching as any degree.

Tinashe P. Kanosvamhira, Postdoctoral fellow, University of Cape Town

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

Categories : Medical Research & TechnologyTags :

South African Hunters Chewed the Kanna Plant for Endurance: New Study Tests its Effects on Mouse Brain Chemistry

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Sceletium tortuosum – Kougoed. Source: Wikimedia Commons.

Catherine H Kaschula, Stellenbosch University

Sceletium tortuosum is a little succulent plant that grows in the semi-arid Karoo and Namaqualand regions of South Africa. It has a long history of traditional use among the hunter-gatherers of the region.

The plant, known as kanna or kougoed by the San and Khoikhoi people, was mainly chewed or smoked to stay alert and suppress appetite during long hunts. The San were traditionally hunter-gatherers, while the Khoikhoi were pastoralists who herded livestock.

The name kanna (meaning “eland” in the click language of the San), has a symbolic reference to this large antelope, as the “trance animal”, which was called upon during religious and spiritual gatherings. Kougoed is Afrikaans for “something to chew”. The plant can be chewed after being dried and fermented, which is believed to intensify its effects.

The first colonial governor of the Cape colony, Simon van der Stel, in 1685 wrote about kanna in his journal:

They chew mostly a certain plant which they call Canna and which they bruise, roots as well as the stem, between the stones and store and preserve in sewn-up sheepskins.

I’m part of a group of scientists from different disciplines with an interest in this plant and we pooled our expertise to understand its effects on neurochemical concentrations in different parts of the brain.

Our studies were done in mice, so there is caution about establishing effectiveness on humans. Still, the results are striking.

As a chemist with an interest in natural products, I wanted to know which alkaloids in the plant were important in bringing about these effects.

Our latest study explored the effects of Sceletium tortuosum extracts on mouse brain chemistry.

We found that Sceletium increased the levels of certain brain chemicals which may balance mood and reduce stress. These findings lend support to the calming and mood-enhancing use of this plant in traditional medicine.

Plant chemistry

Our study examined how extracts from different chemotypes of Sceletium tortuosum can have different effects on brain chemistry. Chemotypes are groups of the same plant species that differ in the alkaloids they produce. This is because plants often produce alkaloids in response to external cues such as the weather or the presence of a plant-eating animal or pathogen.

Alkaloids are carbon-based compounds produced by plants. They are often toxic or taste bitter, making the plants less appealing or even harmful to the predators or invaders that want to eat or inhabit them. Alkaloids generally have physiological effects of use to humans. Some commonly used ones include caffeine, morphine and quinine.

We harvested two chemotypes of kanna from the Touwsrivier and De Rust regions of South Africa. These areas were chosen because of their interesting and unusual alkaloid profiles. The chemotypes were given to healthy mice as a supplement once a day for one month. The mice were monitored every day for behavioural or unexpected adverse reactions but none were noted.

At the end of the month, the levels of chemicals in the mouse brain were measured. Both the chemotypes were found to cause a marked increase in noradrenaline and a decrease in GABA in all brain regions studied. Both molecules are neurotransmitters that transmit nerve signals in the brain affecting memory, mood, attention and sleep.

This effect on noradrenaline supports kanna’s traditional use as an appetite suppressing drug. Increased noradrenergic stimulation is also the basis of many anti-depressants as well as drugs that improve attention and alertness.

We also found an impact on the brain chemicals serotonin and dopamine which may act together to balance mood and reduce stress. Serotonin affects emotional well-being and mood; dopamine motivates feelings of pleasure and satisfaction. These findings lend support to the calming and mood-enhancing use of this plant in traditional medicine.

Importantly, the control kanna extracts that did not have the interesting alkaloid profiles did not cause any of these chemical changes in the mouse brain.

Most studies on kanna have focused on the alkaloid mesembrine. The two specific chemotypes of kanna harvested from the Touwsrivier and De Rust regions of South Africa do have the mesembrine, but they are also packed with some other lesser-known or “minor” alkaloids. These differences in alkaloids may arise from a combination of geographic, environmental and inherent genetic factors found in a particular subset of plants.

Both the Touwsrivier and De Rust plants contained higher levels of alkaloids called mesembrine alcohols, which are different from mesembrine, and were barely present in the control extract. Another minor alkaloid, known as sceletium A4, was also identified as possibly being important. Mesembrine alcohols and sceletium A4 may be the ones responsible for the activity.

This suggests that the source of the plant, and the area in which it is grown, can influence its potential as a natural treatment for mood disorders and sleep.

What the results tell us

Stress, anxiety and depression pose a risk to the ability to lead a meaningful life. The World Health Organization has reported a 25% increase in anxiety and depression worldwide since the emergence of COVID-19.

Our study showed that the plant extracts had a broad noradrenergic effect in mice. But we have to be careful about making connections between results in mice and in humans. We need to explore the behavioural impact of these extracts in both mice and humans, especially in relation to sleep, alertness and mood.

The results also highlighted that without understanding the complex chemical composition of these plants, we risk overgeneralising their benefits, or worse, using them inappropriately.

Our findings have two implications.

First, they point towards a future of precision phytotherapy (use of plants for medicinal purposes), where natural remedies are tailored not just to individuals but to selecting certain plant chemotypes that produce certain combinations of alkaloids. Manipulating the growing conditions and genetic make-up of plants to optimise for alkaloid content is an age-old art.

Second, they remind us of the enormous, still largely untapped potential of African medicinal plants in global health innovation if we invest in research that honours both indigenous knowledge and scientific rigour.

As the world searches for safer, more sustainable ways to treat mental health conditions, South Africa’s kanna plant may hold secrets worth rediscovering.

Catherine H Kaschula, Senior Lecturer, Stellenbosch University

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

Categories : NeurologyTags :

How ‘Brain Cleaning’ While We Sleep May Lower Our Risk of Dementia

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Photo by Cottonbro on Pexels

Julia Chapman, Macquarie University; Camilla Hoyos, Macquarie University, and Craig Phillips, Macquarie University

The brain has its own waste disposal system – known as the glymphatic system – that’s thought to be more active when we sleep.

But disrupted sleep might hinder this waste disposal system and slow the clearance of waste products or toxins from the brain. And researchers are proposing a build-up of these toxins due to lost sleep could increase someone’s risk of dementia.

There is still some debate about how this glymphatic system works in humans, with most research so far in mice.

But it raises the possibility that better sleep might boost clearance of these toxins from the human brain and so reduce the risk of dementia.

Here’s what we know so far about this emerging area of research.

Why waste matters

All cells in the body create waste. Outside the brain, the lymphatic system carries this waste from the spaces between cells to the blood via a network of lymphatic vessels.

But the brain has no lymphatic vessels. And until about 12 years ago, how the brain clears its waste was a mystery. That’s when scientists discovered the “glymphatic system” and described how it “flushes out” brain toxins.

Let’s start with cerebrospinal fluid, the fluid that surrounds the brain and spinal cord. This fluid flows in the areas surrounding the brain’s blood vessels. It then enters the spaces between the brain cells, collecting waste, then carries it out of the brain via large draining veins.

Scientists then showed in mice that this glymphatic system was most active – with increased flushing of waste products – during sleep.

One such waste product is amyloid beta (Aβ) protein. Aβ that accumulates in the brain can form clumps called plaques. These, along with tangles of tau protein found in neurons (brain cells), are a hallmark of Alzheimer’s disease, the most common type of dementia.

In humans and mice, studies have shown that levels of Aβ detected in the cerebrospinal fluid increase when awake and then rapidly fall during sleep.

But more recently, another study (in mice) showed pretty much the opposite – suggesting the glymphatic system is more active in the daytime. Researchers are debating what might explain the findings.

So we still have some way to go before we can say exactly how the glymphatic system works – in mice or humans – to clear the brain of toxins that might otherwise increase the risk of dementia.

Does this happen in humans too?

We know sleeping well is good for us, particularly our brain health. We are all aware of the short-term effects of sleep deprivation on our brain’s ability to function, and we know sleep helps improve memory.

In one experiment, a single night of complete sleep deprivation in healthy adults increased the amount of Aβ in the hippocampus, an area of the brain implicated in Alzheimer’s disease. This suggests sleep can influence the clearance of Aβ from the human brain, supporting the idea that the human glymphatic system is more active while we sleep.

This also raises the question of whether good sleep might lead to better clearance of toxins such as Aβ from the brain, and so be a potential target to prevent dementia.

How about sleep apnoea or insomnia?

What is less clear is what long-term disrupted sleep, for instance if someone has a sleep disorder, means for the body’s ability to clear Aβ from the brain.

Sleep apnoea is a common sleep disorder when someone’s breathing stops multiple times as they sleep. This can lead to chronic (long-term) sleep deprivation, and reduced oxygen in the blood. Both may be implicated in the accumulation of toxins in the brain.

Sleep apnoea has also been linked with an increased risk of dementia. And we now know that after people are treated for sleep apnoea more Aβ is cleared from the brain.

Insomnia is when someone has difficulty falling asleep and/or staying asleep. When this happens in the long term, there’s also an increased risk of dementia. However, we don’t know the effect of treating insomnia on toxins associated with dementia.

So again, it’s still too early to say for sure that treating a sleep disorder reduces your risk of dementia because of reduced levels of toxins in the brain.

So where does this leave us?

Collectively, these studies suggest enough good quality sleep is important for a healthy brain, and in particular for clearing toxins associated with dementia from the brain.

But we still don’t know if treating a sleep disorder or improving sleep more broadly affects the brain’s ability to remove toxins, and whether this reduces the risk of dementia. It’s an area researchers, including us, are actively working on.

For instance, we’re investigating the concentration of Aβ and tau measured in blood across the 24-hour sleep-wake cycle in people with sleep apnoea, on and off treatment, to better understand how sleep apnoea affects brain cleaning.

Researchers are also looking into the potential for treating insomnia with a class of drugs known as orexin receptor antagonists to see if this affects the clearance of Aβ from the brain.

If you’re concerned

This is an emerging field and we don’t yet have all the answers about the link between disrupted sleep and dementia, or whether better sleep can boost the glymphatic system and so prevent cognitive decline.

So if you are concerned about your sleep or cognition, please see your doctor.

Julia Chapman, Clinical Trials Lead and Postdoctoral Research Fellow, Woolcock Institute of Medical Research and Conjoint Lecturer, Macquarie University; Camilla Hoyos, Senior Lecturer in the Centre for Sleep and Chronobiology, Macquarie University, and Craig Phillips, Associate Professor, Macquarie Medical School, Macquarie University

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

Categories : Ethics and Law GeneticsTags :

South Africa Amended its Research Guidelines to Allow for Heritable Human Genome Editing

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Source: Pixabay CC0

Françoise Baylis, Dalhousie University

A little-noticed change to South Africa’s national health research guidelines, published in May of this year, has put the country on an ethical precipice. The newly added language appears to position the country as the first to explicitly permit the use of genome editing to create genetically modified children.

Heritable human genome editing has long been hotly contested, in large part because of its societal and eugenic implications. As experts on the global policy landscape who have observed the high stakes and ongoing controversies over this technology — one from an academic standpoint (Françoise Baylis) and one from public interest advocacy (Katie Hasson) — we find it surprising that South Africa plans to facilitate this type of research.

In November 2018, the media reported on a Chinese scientist who had created the world’s first gene-edited babies using CRISPR technology. He said his goal was to provide children with resistance to HIV, the virus that causes AIDS. When his experiment became public knowledge, twin girls had already been born and a third child was born the following year.

The fate of these three children, and whether they have experienced any negative long-term consequences from the embryonic genome editing, remains a closely guarded secret.

Controversial research

Considerable criticism followed the original birth announcement. Some argued that genetically modifying embryos to alter the traits of future children and generations should never be done.

Many pointed out that the rationale in this case was medically unconvincing – and indeed that safe reproductive procedures to avoid transmitting genetic diseases are already in widespread use, belying the justification typically given for heritable human genome editing. Others condemned his secretive approach, as well as the absence of any robust public consultation, considered a prerequisite for embarking on such a socially consequential path.

In the immediate aftermath of the 2018 revelation, the organizing committee of the Second International Summit on Human Genome Editing joined the global uproar with a statement condemning this research.

At the same time, however, the committee called for a “responsible translational pathway” toward clinical research. Safety thresholds and “additional criteria” would have to be met, including: “independent oversight, a compelling medical need, an absence of reasonable alternatives, a plan for long-term follow-up, and attention to societal effects.”

Notably, the additional criteria no longer included the earlier standard of “broad societal consensus.” https://www.youtube.com/embed/XAhFoaT6Kik?wmode=transparent&start=0 Nobel laureate David Baltimore, chair of the organizing committee for the Second International Summit on Human Genome Editing, talks about the importance of public global dialogue on gene editing.

New criteria

Now, it appears that South Africa has amended its Ethics in Health Research Guidelines to explicitly envisage research that would result in the birth of gene-edited babies.

Section 4.3.2 of the guidelines on “Heritable Human Genome Editing” includes a few brief and rather vague paragraphs enumerating the following criteria: (a) scientific and medical justification; (b) transparency and informed consent; (c) stringent ethical oversight; (d) ongoing ethical evaluation and adaptation; (e) safety and efficacy; (f) long-term monitoring; and (g) legal compliance.

While these criteria seem to be in line with those laid out in the 2018 summit statement, they are far less stringent than the frameworks put forth in subsequent reports. This includes, for example, the World Health Organization’s report Human Genome Editing: Framework for Governance (co-authored by Françoise Baylis).

Alignment with the law

Further, there is a significant problem with the seemingly permissive stance on heritable human genome editing entrenched in these research guidelines. The guidelines clearly require the research to comply with all laws governing heritable human genome research. Yet, the law and the research guidelines in South Africa are not aligned, which entails a significant inhibition on any possible research.

This is because of a stipulation in section 57(1) of the South African National Health Act 2004 on the “Prohibition of reproductive cloning of human beings.” This stipulates that a “person may not manipulate any genetic material, including genetic material of human gametes, zygotes, or embryos… for the purpose of the reproductive cloning of a human being.”

When this act came into force in 2004, it was not yet possible to genetically modify human embryos and so it’s not surprising there’s no specific reference to this technology. Yet the statutory language is clearly wide enough to encompass it. The objection to the manipulation of human genetic material is therefore clear, and imports a prohibition on heritable human genome editing.

Ethical concerns

Photo by Tingey Injury Law Firm on Unsplash

The question that concerns us is: why are South Africa’s ethical guidelines on research apparently pushing the envelope with heritable human genome editing?

In 2020, we published alongside our colleagues a global review of policies on research involving heritable human genome editing. At the time, we identified policy documents — legislation, regulations, guidelines, codes and international treaties — prohibiting heritable genome editing in more than 70 countries. We found no policy documents that explicitly permitted heritable human genome editing.

It’s easy to understand why some of South Africa’s ethicists might be disposed to clear the way for somatic human genome editing research. Recently, an effective treatment for sickle cell disease has been developed using genome editing technology. Many children die of this disease before the age of five and somatic genome editing — which does not involve the genetic modification of embryos — promises a cure.

Implications on future research

But that’s not what this is about. So, what is the interest in forging a path for research on heritable human genome editing, which involves the genetic modification of embryos and has implications for subsequent generations? And why the seemingly quiet modification of the guidelines?

How many people in South Africa are aware that they’ve just become the only country in the world with research guidelines that envisage accommodating a highly contested technology? Has careful attention been given to the myriad potential harms associated with this use of CRISPR technology, including harms to women, prospective parents, children, society and the gene pool?

Is it plausible that scientists from other countries, who are interested in this area of research, are patiently waiting in the wings to see whether the law in South Africa prohibiting the manipulation of human genetic material will be an insufficient impediment to creating genetically modified children? Should the research guidelines be amended to accord with the 2004 statutory prohibition?

Or if, instead, the law is brought into line with the guidelines, would the result be a wave of scientific tourism with labs moving to South Africa to take advantage of permissive research guidelines and laws?

We hope the questions we ask are alarmist, as now is the time to ask and answer these questions.

Katie Hasson, Associate Director at the Center for Genetics and Society, co-authored this article.

Françoise Baylis, Distinguished Research Professor, Emerita, Dalhousie University

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