Tag: The Conversation

Categories : UncategorizedTags :

Prediabetes Remission Possible Without Dropping Pounds, Our New Study Finds

On By ModernMedia
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

On By ModernMedia
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

On By ModernMedia
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

On By ModernMedia
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

On By ModernMedia
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.

Categories : Neurodegenerative DiseasesTags :

Epstein-Barr Virus: How does a Common Infection Trick the Immune System into Attacking the Brain in People with MS?

On By ModernMedia
An electron micrograph showing three Epstein-Barr virus (EBV) particles colourised red-orange. Credit: NIAID

Olivia Thomas, Karolinska Institutet; Graham Taylor, University of Birmingham, and Jill Brooks, University of Birmingham

Almost 3 million people worldwide have multiple sclerosis (MS) – an autoimmune disease caused by the immune system mistakenly attacking the brain and central nervous system.

While treatments for MS have improved over the years, there’s still no cure. This is largely because researchers still don’t fully understand what goes wrong in the immune system to cause MS. But our latest research has revealed new insights into the way certain immune cells behave in people with MS. This discovery brings us closer to understanding why some people get MS – and may also be a crucial step in developing better treatments and even cures.

Although the causes of MS aren’t fully understood, we know that genetics, lifestyle and environment factors can all influence MS risk. But the biggest risk factor for developing MS appears to be a common virus called Epstein-Barr virus (EBV).

EBV typically infects people during childhood without causing any symptoms – so most early infections go unnoticed. But if the infection occurs during adolescence, it may cause glandular fever (infectious mononucleosis) which, although debilitating in the short-term, usually has no long-term effects.

Most viral infections are rapidly cleared by the body’s immune system, but EBV is cleverer than most viruses. Although the immune system controls the infection, it is unable to completely eradicate the virus as it hides inside a type of immune cell called a B cell (which normally produce antibodies that bind to and destroy invading viruses or bacteria). Once you’re infected with EBV you carry it for life – although for most people this causes no problems.

By adulthood about 95% of people are infected with EBV, but in people with MS nearly 100% are infected. Large epidemiological studies have shown that EBV infection increases the risk of developing MS over 30-fold. For people who have had glandular fever the risk is even higher. Research has also shown that in people with MS, EBV infection occurs before the very earliest stages of disease.

Many researchers now believe being infected with EBV is more than a risk factor in MS – it’s essential.

But how does EBV cause MS – and why does a common virus only cause MS in a few people? Several theories are currently being investigated.

One theory is that in some people the immune cells activated by EBV mistakenly attack parts of the brain and central nervous system. This process, called molecular mimicry, also occurs in other autoimmune diseases, such as Guillain-Barré syndrome. This could explain why drugs which prevent immune cells from entering the brain are shown to dramatically improve MS symptoms.

Research into EBV molecular mimicry in MS has mainly focused on the viral protein EBNA1. Without EBNA1 EBV cannot live in B cells, and MS patients have higher levels of antibodies towards EBNA1.

But EBV makes over 80 different proteins during its life cycle. In our latest work we investigated immune responses to these other viral proteins in people with MS.

Altered immunity

We compared the immune responses of 31 people with MS, 33 healthy people and 11 people who had recently recovered from glandular fever. We wanted to see if each group reacted to EBV infections differently.

We found that antibodies targeting EBNA1 and another viral protein called VCA were higher in people with MS compared to the other groups. People with MS were also more likely to have antibodies targeting several other viral proteins. This suggests EBV antibodies are more altered in MS than previously thought – but it isn’t certain whether these antibodies are fighting infection or if they have a role in MS disease.

Scanning electron micrograph of a T cell lymphocyte. Credit: NIH / NIAID

Antibodies aren’t the full story. Previous research has suggested another type of immune cell, called a T cell, may also play an important role as they’re found in high numbers in MS brain lesions. As such, we wanted to understand whether T cells which fight EBV were different in people with MS.

By analysing blood samples we found that, although EBV T cell numbers were similar in MS and healthy people, these cells behaved differently in people with MS. T cells from people with MS produced slightly higher amounts of an inflammatory substance called interleukin-2. The body normally produces this substance in response to injury or infection, but too much interleukin-2 can cause chronic disease.

We also looked at molecular mimicry, wondering whether EBV T-cells mistakenly target brain proteins rather than fighting the virus.

Surprisingly, we found that in both people with MS and healthy people, their EBV T cells reacted to multiple proteins found in the brain. Notably, most people had EBV T cells that targeted a protein called myelin oligodendrocyte glycoprotein, or Mog, which surrounds the nerves.

Looking at one person with MS in more detail, we found individual T cells that directly recognised both EBNA1 and Mog. This means that, rather than just fighting infection, some EBV T cells could also target nerve cells in the brain.

This widespread misdirection between EBV T cells and the brain goes some way to suggest how infection with this common virus can lead to MS. But its presence in healthy people is slightly confusing. One possible explanation could be that EBV T cells are better able to cross the blood-brain barrier (a tight-knit lining of cells that protect the brain) in people with MS. This idea is something we’re keen to explore in future research.

While there’s still much we don’t know about these misdirected EBV T cells in the brain, our latest findings provide fresh evidence for researchers and hopefully will lead to the development of new, targeted treatments for MS.

Olivia Thomas, Assistant Professor, Department of Clinical Neuroscience, Karolinska Institutet; Graham Taylor, Associate Professor in Viral and Tumour Immunology, University of Birmingham, and Jill Brooks, Research Fellow, Institute of Cancer and Genomic Sciences, University of Birmingham

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

Categories : Mental Health NeurologyTags :

Two Reasons I’m Sceptical About Psychedelic Science

On By ModernMedia
Photo by Marek Piwnicki

Michiel van Elk, Leiden University

Since I was young, I have been intrigued by altered states of consciousness, such as out-of-body experiences, paranormal phenomena and religious visions. I studied psychology and neuroscience to gain a better understanding of how these experiences come about. And in my scientific career, I have focused on the question of why some people are more prone to having these experiences than others.

Naturally, when I came across psychedelic science a couple of years ago, this field also sparked my academic interest. Here was an opportunity to study people who had a psychedelic experience and who claimed to have had a glimpse of ultimate reality. I started to research psychedelic experiences at Leiden University and founded the PRSM lab – a group of scientists from different academic backgrounds who study psychedelic, religious, spiritual and mystical experiences.

Initially, I was enthusiastic about the mind-transforming potential of psychedelics. These substances, when administered correctly, appear to be capable of enhancing people’s mental and physical wellbeing. They also increase feelings of connectedness to and concern for the environment.

Psychedelic therapy appeared to offer great potential for treating a wide variety of disorders, including depression, anxiety, addiction and post-traumatic stress disorder. This enthusiasm about the potentially transformative effects of psychedelics was reflected in positive media attention on this topic over the past few years. Michael Pollan, an American author and journalist, has brought psychedelics to an audience of millions with his book and Netflix documentary.

However, my initial optimism about psychedelics and their potential has changed into scepticism about the science behind much of the media hype. This is due to a closer scrutiny of the empirical evidence. Yes, at face value it seems as if psychedelic therapy can cure mental disease. But on closer inspection, the story is not that straightforward.

The main reason? The empirical evidence for the efficacy of and the working mechanisms underlying psychedelic therapy is far from clear.

Two issues

I wrote a critical review paper with my colleague Eiko Fried in which we listed the problems with the current clinical trials on psychedelic therapy. The main concern is called the “breaking blind problem”. In psychedelic studies, patients easily figure out if they have been randomly assigned to the psychedelic or the placebo group, simply because of the profound mind-altering effects of psychedelic substances.

This breaking-of-the-blind can actually result in placebo effect in patients in the psychedelic group: they finally get the treatment they’d been hoping for and they start feeling better. But it can also result in frustration and disappointment in patients assigned to the control group. They were hoping to get a miracle cure but now find out they will have to spend six hours on a placebo pill with their therapist.

As a consequence, any difference in therapeutic outcomes between the psychedelic and the placebo group is largely driven by these placebo and nocebo effects. (A nocebo effect is when a harmless treatment causes side-effects or worsening of symptoms because the person believes they may occur or expects them to occur.)

Knowing who received what also affects the therapists, who may be motivated to get more out of the therapy session if their patient got the “real deal”. And this problem is impossible to control for in so-called randomised controlled trials – still the gold standard in evaluating the effectiveness of drugs and treatments.

Also, non-clinical research on psychedelics faces problems. You may recall the graphic of a brain on psilocybin compared to one on a placebo (see below). Psilocybin increases the connections between different brain areas, which is represented in a colourful array of connecting lines.

This has become known as the “entropic brain hypothesis”. Psychedelics make your brain more flexible such that it returns to a child-like state of openness, novelty and surprise. This mechanism in turn has been hypothesised to underlie psychedelic therapy’s efficacy: by “liberating your brain” psychedelics can change entrenched and maladaptive patterns and behaviour. However, it turns out the picture is much more complicated than that.

Psychedelics constrict the blood vessels in your body and brain and this causes problems in the measurement of brain signals with MRI machines.

The graphic of the entropic brain may simply reflect the fact that the blood flow in the brain is dramatically altered under psilocybin. Also, it is far from clear what entropy exactly means – let alone how it can be measured in the brain.

A recent psilocybin study, which is yet to be peer-reviewed, found that only four out of 12 entropy measures could be replicated, casting further doubt on how applicable this mechanism of action is.

Although the story about psychedelics freeing your mind is compelling, it does not yet square well with the available empirical evidence.

These are just two examples that illustrate why it is important to be really cautious when you evaluate empirical studies in psychedelic science. Don’t trust findings at face value, but ask yourself the question: is the story too good or too simple to be true?

Personally, I have developed a healthy dose of scepticism when it comes to psychedelic science. I am still intrigued by psychedelics’ potential. They offer great tools for studying changes in consciousness. However, it is too early to conclude anything definite about their working mechanisms or their therapeutic potential. For this, we need more research. And I’m excited to contribute to that endeavour.

Michiel van Elk, Associate Professor, Cognitive Psychology, Leiden University

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

Read the original article.

Categories : General Interest HospitalsTags :

South Africa’s Traditional Medicines Should be Used in Modern Health Care

On By ModernMedia
Both the Khoi and the San believed in a mythical animal, resembling a cow, whose horns were thought to have medicinal attributes. This centuries-old medicine horn contained herbal remedies used by the Khoi-san. Credit: Rodger Smith

By Zelna Booth

Traditional medicines are part of the cultural heritage of many Africans. About 80% of the African continent’s population use these medicines for healthcare.

Other reasons include affordability, accessibility, patient dissatisfaction with conventional medicine, and the common misconception that “natural” is “safe”.

The growing recognition of traditional medicine resulted in the first World Health Organization global summit on the topic, in August 2023, with the theme “Health and Wellbeing for All”.

Traditional medicines are widely used in South Africa, with up to 60% of South Africans estimated to be reliant on traditional medicine as a primary source of healthcare.

Conventional South African healthcare facilities struggle to cope with extremely high patient numbers. The failure to meet the basic standards of healthcare, with increasing morbidity and mortality rates, poses a threat to the South African economy.

In my opinion, as a qualified pharmacist and academic with a research focus on traditional medicinal plant use in South Africa, integrating traditional medicine practices into modern healthcare systems can harness centuries of indigenous knowledge, increasing treatment options and provide better healthcare.

Recognition of traditional medicine as an alternative or joint source of healthcare to that of standard, conventional medicine has proven challenging. This is due to the absence of scientific research establishing and documenting the safety and effectiveness of traditional medicines, along with the lack of regulatory controls.

What are traditional medicines?

Traditional medicine encompasses a number of healthcare practices aimed at either preventing or treating acute or chronic complaints through the application of indigenous knowledge, beliefs and approaches. It incorporates the use of plant, animal and mineral-based products. Plant-derived products form the majority of treatment regimens.

Traditional medicine practices also have a place in ritualistic activities and communicating with ancestors.

South Africa is rich in indigenous medicinal fauna and flora, with about 2000 species of plants traded for medicinal purposes. In South Africa the provinces of KwaZulu-Natal, Gauteng, Eastern Cape, Mpumalanga and Limpopo are trading “hotspots”. The harvested plants are most often sold at traditional medicine muthi markets.

Uses of medicinal plants

Medicinal plants most popularly traded in South Africa include buchu, bitter aloe, African wormwood, honeybush, devil’s claw, hoodia, African potato, fever tea, African geranium, African ginger, cancer bush, pepperbark tree, milk bush and the very commonly consumed South African beverage, rooibos tea.

The most commonly traded medicinal plants in South Africa are listed below along with their traditional uses:

Buchu – Urinary tract infections; skin infections; sexually transmitted infections; fever; respiratory tract infections; high blood pressure; gastrointestinal complaints.

Bitter aloe – Skin infections; skin inflammation; minor burns.

African wormwood – Respiratory tract infections; diabetes, urinary tract disorders.

Honeybush – Cough; gastrointestinal issues; menopausal symptoms.

Devil’s claw – Inflammation; arthritis; pain.

Hoodia – Appetite suppressant.

African potato – Arthritis; diabetes; urinary tract disorders; tuberculosis; prostate disorders.

Fever tea – Respiratory tract infections; fever; headaches.

African geranium – Respiratory tract infections.

African ginger – Respiratory tract infections; asthma.

Cancer bush – Respiratory tract infections; menstrual pain.

Pepperbark tree – Respiratory tract infections; sexually transmitted infections.

Milk bush – Pain; ulcers; skin conditions.

Rooibos – Inflammation; high cholesterol; high blood pressure.

There are many ways in which traditional medicine may be used. It can be a drop in the eye or the ear, a poultice applied to the skin, a boiled preparation for inhalation or a tea brewed for oral administration.

Roots, bulbs and bark are used most often, and leaves less frequently. Roots are available throughout the year. There’s also a belief that the roots have the strongest concentration of “medicine”. Harvesting of the roots, however, poses concerns about the conservation of these medicinal plants. The South African government, with the draft policy on African traditional medicine Notice 906 of 2008 outlines considerations aimed at ensuring the conservation of these plants through counteracting unsustainable harvesting practises.

Obstacles to traditional medicine use

The limited research investigating interactions posed should a patient be making use of both traditional and conventional medicine is a concern.

During the COVID-19 pandemic, many patients used traditional remedies for the prevention of infection or treatment.

Understanding which traditional medicines are being used and how, their therapeutic effects in the human body, and how they interact with conventional medicines, would help determine safety of their combined use.

Certain combinations may have advantageous interactions, increasing the efficacy or potency of the medicines and allowing for reduced dosages, thereby reducing potential toxicity. These combinations could assist in the development of new pharmaceutical formulations.

Sharing information

The WHO in its Traditional Medicine Strategy for 2014-2023 report emphasised the need for using traditional medicine to achieve increased healthcare.

Key role players from both systems of healthcare need to be able to share information freely.

The need for policy development is key. Both conventional and traditional medicine practitioners would need to be aware of and engage with patients on all the medicines they are taking.

Understanding the whole patient

Patients often seek treatment from both conventional and traditional sources, which can lead to side effects or duplication in medications.

A comprehensive understanding of a patient’s health profile makes care easier.

This could also prevent treatment failures, promote patient safety, prevent adverse interactions and minimise risks.

A harmonious healthcare landscape would combine the strengths of both systems to provide better healthcare for all.

Zelna Booth, Pharmacist and Academic Lecturer (Pharmacy Practice Division, Department of Pharmacy and Pharmacology, University of the Witwatersrand), University of the Witwatersrand

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

Source: The Conversation