Mind Health Matters

26/06/2026

The Interview They Sacked Karl Stefanovic Over

by George Christensen [Commentary]

The interview that has cost Karl Stefanovic his job at Nine was not some crazed rant. It was not an extremist broadcast. It was not even, despite all the noise that followed, especially shocking.

It was an interview.

That is what makes the whole thing so revealing.

Karl Stefanovic sat down with Tommy Robinson and did the thing journalists used to do without needing permission from a woke approval committee. He asked questions. He let Robinson answer.

He pushed him at times on his past tactics, the street protests, the clashes that followed some of those events, and whether all of that had hurt the message he was trying to get across.

Robinson spoke about censorship, the grooming-gang scandals in Britain, immigration, prison, free speech, national identity, Christianity, working-class voters, and why he believes so many ordinary people have been frightened into silence.

You can agree with Robinson. You can disagree with him. You can think some of his claims need challenging, and fair enough. But there was nothing untowards or extreme in the conversation itself. Nothing that should make a major media company panic like someone had smuggled contraband into the studio.

The real offence, it seems, was that Karl allowed viewers to hear the man speak at length. Not a seven-second grab. Not a hostile panel discussion with everyone talking over each other. Not the usual media treatment where the label is slapped on first and the public is told to stop listening.

Just a conversation. And that, apparently, was too much.

The interview was pulled from platforms, Nine distanced itself from the podcast, and the reports began flying that Karl was either being pushed out, sacked, or negotiating his exit after the backlash. The exact corporate wording may be massaged by lawyers and PR people, as it always is, but ordinary Australians can see what happened here. A journalist interviewed the wrong person, in the wrong way, for too long, and the machine came down on him.

That is the part people should sit with for a minute.

We have seen interviews with criminals, dictators, terrorists, fraudsters, radical activists, anti-Western academics, and every fashionable left-wing firebrand you can imagine. They are treated as complex. Misunderstood. Worth hearing. Worth analysing. Sometimes they are practically given a lounge chair and a cup of tea.

But Tommy Robinson? No. He must only be spoken about, not spoken to.

Robinson’s views should be questioned. Of course they should. He is a controversial figure, and he has said plenty over the years that people will argue about. But if the media response to an interview is to erase it and reportedly end the interviewer’s career, then we are no longer talking about whether Tommy Robinson is right or wrong.

We are talking about whether Australians are still allowed to hear uncomfortable conversations and make up their own minds.

That is what I object to. Not that people criticised the interview. They are free to do that. Not that people dislike Robinson. Plenty do. What I object to is the idea that the public must be protected from hearing him speak, as if we were children who might catch a dangerous thought if the adults left the room.

People are smarter than that. A bloke at the pub, a mum doing the school run, a truckie listening on the highway, a small business owner catching up on podcasts late at night, they can listen to an interview and decide for themselves. They do not need woke media executives deciding which voices are safe enough to enter their ears.

This was not really about Tommy Robinson. It was not even really about Karl Stefanovic. It was about the boundaries of acceptable speech in this country, and who gets to draw them.

Listen for yourself and decide: https://dailydeclaration.org.au/2026/06/26/sacked-karl-stefanovic/

26/05/2026

A pilot clinical study evaluated a traditional dried rosemary leaf (Rosmarinus officinalis) infusion in untreated grade 1 hypertensive patients (defined as systolic BP 140 to 159 mmHg and/or diastolic BP 90 to 99 mmHg) using a pragmatic but loosely controlled design. Over 45 days, participants consumed a daily tea made from 2 g powdered rosemary leaf infused in 100 mL hot water for 15 minutes, delivering approximately 38 mg polyphenols including 18 mg of rosmarinic acid. The use of powdered leaf is noteworthy, as it substantially increases extraction yield compared with intact leaf.

In the hypertensive group (n=30 completers), the herbal intervention produced statistically significant reductions in ambulatory blood pressure, including −6.3 mmHg systolic and −4.9 mmHg diastolic (24-hour averages). These translate to moderate within-subject effect sizes (0.5 to 0.65), suggesting a potentially meaningful clinical effect. There was no impact in a smaller group of normotensive participants, no change in nocturnal BP, and no effect on pulse pressure or heart rate. While these effect sizes are clinically relevant for early hypertension, interpretation is limited by the absence of a randomised placebo-controlled design, meaning regression to the mean and behavioural factors cannot be excluded.

Methodologically, the study’s main strength is the use of 24-hour ambulatory BP monitoring, which improves reliability over clinic readings, along with phytochemical characterisation of the intervention. However, it is constrained by a small sample size and lack of blinding and a proper control group. Safety signals were reassuring over the 45 days, with no adverse events and stable biochemistry. Clinically, this study should be viewed as hypothesis-generating: it suggests rosemary infusion may exert modest antihypertensive effects, but requires confirmation in well-powered, randomised, dose-ranging trials before integration into standard care.

Beyond blood pressure, rosemary tea shows a range of emerging clinical effects, particularly in the neurocognitive space. Small human studies suggest improvements in mood, anxiety, and cognitive performance, and notably, a pilot trial has reported a marked increase in circulating brain-derived neurotrophic factor (BDNF) following short-term rosemary tea consumption, pointing to a potential role in neuroplasticity and stress resilience. Mechanistically, this aligns with its polyphenols (such as rosmarinic acid and carnosol) acting via Nrf2, anti-inflammatory and CREB-related pathways (cAMP response element-binding protein). Hence the dried leaf is suitable in this context (since the polyphenols are retained on drying), even though it is lower in essential oil compared to fresh rosemary.

So at this point there is no harm and possibly great benefit in the suggestion that hypertensive patients could start taking rosemary leaf tea as part of their overall regime.

For more information see: https://www.sciencedirect.com/science/article/pii/S2667031325000569?via%3Dihub

25/05/2026

A new study from researchers at Penn State has proposed a fascinating new mechanism by which ordinary body movement may help support brain health. Using mice, advanced imaging and computer modelling, the researchers found that contraction of the abdominal muscles can mechanically transmit pressure through the vertebral venous plexus into the craniospinal system, producing subtle movement of the brain within the skull. Their modelling suggested that this movement may help drive cerebrospinal fluid (CSF) flow through and around the brain, potentially supporting the clearance of metabolic waste products, some of which have been associated with neurodegenerative disease.

Over the past decade, human imaging studies have increasingly shown that CSF dynamics are strongly influenced by physiological rhythms such as breathing, vascular pulsation and sleep. Real-time MRI studies in humans have demonstrated that inspiration is a major driver of CSF movement, while sleep studies have linked slow-wave brain activity with coordinated CSF oscillations thought to support metabolic clearance. Together, these findings are contributing to the broader ‘glymphatic’ model of brain housekeeping, in which CSF fluid circulation helps remove waste products from brain tissue.

What makes this new study especially interesting is that it extends this concept beyond sleep and respiration into the realm of ordinary movement. The authors propose that even mild abdominal contractions associated with standing, walking or postural adjustments may generate small forces that help circulate fluid through the brain. This raises the intriguing possibility that low-level physical movement throughout the day may contribute to continuous maintenance and cleaning of the CNS, rather than brain clearance occurring predominantly during sleep alone.

These findings also create interesting parallels with practices such as diaphragmatic breathing, yoga breathing exercises (pranayama), and movement systems that deliberately coordinate abdominal contraction, posture and respiration (again such as yoga).

However, it is essential to stress that this remains early-stage science for humans. The new work was performed in mice. At present, the findings should be viewed as a biologically plausible mechanistic hypothesis that aligns with emerging human imaging data, rather than proof of a therapeutic effect. Nonetheless, the study raises the intriguing possibility that part of the brain’s ‘housekeeping’ system may operate continuously during the day through movement itself — with walking, diaphragmatic breathing, postural shifts and targeted breathing or abdominal exercises all potentially contributing small rhythmic mechanical forces that help circulate our CSF and support metabolic waste clearance from the brain.

How does this sit with the understanding that deep slow-wave sleep (stage 3 NREM) is the primary state where large-scale glymphatic clearance occurs from the brain? A useful analogy is to think of sleep as the brain’s ‘deep cleaning cycle,’ whereas movements and respiration during waking life may provide a background circulation push that assists CSF fluid dynamics and ultimately waste clearance.

For more information see: https://scitechdaily.com/this-simple-movement-could-be-secretly-cleaning-your-brain/

18/05/2026

08/05/2026

Big conversations are happening right now around , , and how we assess risk—and Dr. Nick Norwitz is right in the middle of it.

In this new Telegraph article on Dr. Norwitz, he challenges the idea that cholesterol should be viewed in isolation and calls for more personalized, nuanced care—something that’s gaining serious traction globally.

If that sounds familiar, it should.

Dr. Norwitz is prominently featured in The Cholesterol Code, where we explore these same questions:
👉 Are we relying too heavily on single markers like LDL?
👉 What happens when real-world patient outcomes don’t match conventional expectations?
👉 And how can better tools—like imaging and metabolic context—change the conversation?

This article is a great companion to the film and a glimpse into why this discussion is only just beginning.

🔗 Read the article: https://www.telegraph.co.uk/health-fitness/conditions/heart-health/harvard-medic-cholesterol-statins/

Metabolic Mind Dave Feldman

01/05/2026

The condition once called NASH (non-alcoholic steatohepatitis) is now called MASH (metabolic dysfunction-associated steatohepatitis), and it sits within a broader category called MASLD (metabolic dysfunction-associated steatotic liver disease), formerly NAFLD (non-alcoholic fatty liver disease). These new names were introduced because fatty liver disease is now understood to be part of a wider metabolic disorder rather than just a liver problem defined by the absence of alcohol. These name changes are relevant in the context of CKD (chronic kidney disease), because the same underlying factors, such as insulin resistance, obesity, inflammation and vascular damage, can affect both the liver and the kidneys. In other words, MASH and CKD often occur together not because one directly causes the other, but because both develop from the same underlying metabolic stress.

The incidence of both MASH and CKD has been rising steadily worldwide in parallel with the epidemics of obesity and type 2 diabetes. In Australia, fatty liver disease overall affects about one in four adults, and it is estimated that around 4 to 6% of adults have MASH, the inflammatory and more progressive form. Biomedical evidence of CKD is present in roughly 11% of Australian adults (about 1.7 million people), with rates increasing sharply with age. In the United States, MASH is estimated to affect about 5 to 6% of adults, within a much larger group with fatty liver disease, and CKD affects roughly one in seven adults (around 35 million people).

Given this rather alarming epidemiological context, a recent clinical trial of bioavailable curcumin in patients with MASH and CKD is highly noteworthy. In this double blind trial, 52 patients with biopsy-confirmed MASH were studied. Most had moderate to advanced liver scarring (71% had stage F2 fibrosis or worse), and more than half also had moderate CKD (58% had stage 2 or 3). They were randomised 1:1 to receive 2 g/d of a curcumin phytosome (containing 400 mg/day curcumin) or placebo for 72 weeks.

The primary endpoint was NASH resolution with no worsening of fibrosis. The secondary endpoints included a ≥1 stage liver fibrosis improvement with no MASH worsening; regression of significant fibrosis and CKD; and improvement in renal, glucose lipid, and inflammatory parameters. The scientists also explored the treatment effect on hepatic activation of NF-kB, a key proinflammatory transcription factor and a major target of curcumin.

Fifty-one patients (26 on curcumin and 25 on placebo) completed the trial. Sixteen (62%) patients on curcumin versus 3 (12%) patients on placebo had MASH resolution (relative risk, RR = 5.33; p = 0.003). Thirteen (50%) patients on curcumin versus 2 (8%) patients on placebo had ≥1 stage fibrosis improvement (RR = 6.50; p = 0.008). Eleven (42%) patients on curcumin versus 0 (0%) on placebo had regression of significant liver fibrosis (RR = 18.01; p = 0.02). Hepatic NF-kB inhibition predicted MASH resolution and fibrosis improvement. Thirteen (50%) patients on curcumin versus 0 (0%) on placebo had CKD regression (RR = 10.71; p = 0.004). Compared with placebo, curcumin improved eGFR (difference in adjusted eGFR change: +3.59; p = 0.009), fasting glucose, HbA1c, LDL-cholesterol, triglycerides, HDL-cholesterol and inflammatory markers. Adverse events were rare, mild, and evenly distributed.

These are truly amazing results that make me wonder why findings like this receive such little attention, and why studies like this are so often overlooked by mainstream medicine and the general media, especially when we are talking about one of the central epidemics in modern healthcare.

For more information see: https://pubmed.ncbi.nlm.nih.gov/38809154/