Food, Body + Health Naturopathic Nutrition Expert

02/03/2026

A great informative post by Kerry Bone.

A new analysis led by researchers at University College London (UCL) suggests that Alzheimer disease (AD) may depend far more heavily on one gene than scientists once believed. The study estimates that more than 90% of Alzheimer cases might not develop without the influence of a single gene called APOE. Moreover, the impact appears to extend beyond AD alone. Researchers found that nearly half of all dementia cases may also rely on this gene’s contribution.

The APOE gene has been linked to Alzheimer’s disease for many years. It exists in three common forms, or alleles, known as ε2, ε3, and ε4. Each person inherits two copies of APOE, which results in six possible combinations of these variants. The six combinations of the APOE gene are: ε2+ε2; ε2+ε3; ε2+ε4; ε3+ε3; ε3+ε4; ε4+ε4. The variants are more commonly referred to as APOE2, APOE3, APOE4, which more correctly describes the APOE protein type produced from the gene (apolipoprotein E). APOE4 is thought to be the ancestral form; APOE3 and APOE2 evolved later.

Research in the 1990s established that people who carry one or more ε4 variants (producing mainly APOE4) face a much higher risk of AD compared with those who have two copies of the more common ε3 variant. People with ε2 generally had a lower risk than ε3 carriers. However, the new study goes much further than this.

Lead author Dr. Dylan Williams (UCL Division of Psychiatry and Unit for Lifelong Health and Ageing at UCL) said: “We have long underestimated how much the APOE gene contributes to the burden of Alzheimer’s disease. The ε4 variant of APOE is well recognised as harmful by dementia researchers, but much disease would not occur without the additional impact of the common ε3 allele, which has been typically misperceived as neutral in terms of Alzheimer’s risk.

“When we consider the contributions of ε3 and ε4, we can see that APOE potentially has a role in almost all Alzheimer’s disease. Consequently, if we knew how to reduce the risk that the ε3 and ε4 variants confer to people, we may be able prevent most disease from occurring.”

The study represents the most detailed modelling so far of how common APOE variants contribute to Alzheimer’s and dementia across the population. Researchers combined evidence linking the ε3 and ε4 alleles to Alzheimer’s disease, all-cause dementia, and the brain changes that precede Alzheimer’s.

A critical element of the analysis was access to data from four very large studies involving more than 450,000 participants. This allowed researchers to identify a sizable group of people with two ε2 copies, an uncommon but low risk group, and use them as a reference point in their calculations for the first time in this type of research. Specifically, the researchers analysed electronic health record data from 171,105 older adults in the UK Biobank cohort and 289,150 older adults in the FinnGen study to determine Alzheimer and all-cause dementia diagnoses. They also examined baseline amyloid PET scans of 4,415 participants in the A4 trial and analysed data from 5,007 participants in the Alzheimer's Disease Genetics Consortium (ADGC) of autopsy-confirmed Alzheimer cases and controls to provide a comprehensive view.

Based on their analysis, the researchers estimated that 72 to 93% of Alzheimer cases would not have occurred without the ε3 and ε4 variants of APOE. They also found that roughly 45% of all dementia cases might not arise without the gene’s influence.

These estimates exceed earlier assessments of APOE’s impact, largely because the new study evaluated the combined effects of both ε3 and ε4 rather than focusing only on ε4.

Results differed somewhat across the four studies included in the analysis. These differences reflected how AD and dementia were defined and measured, including whether cases were identified through medical diagnoses, other dementia classifications, or signs of amyloid buildup seen on brain scans. Variation in follow-up length and possible recruitment biases also contributed. When considered together, the evidence suggests that APOE is likely responsible for at least three quarters of Alzheimer cases, and potentially more.

The findings indicate that APOE should receive greater attention in research aimed at understanding disease mechanisms and developing new treatments and prevention options.

APOE is a lipoprotein-binding protein that helps transport cholesterol, triglycerides and phospholipids. It acts as a ligand for LDL (low density lipoprotein) receptors and related receptors, helping shuttle lipids between tissues, particularly the brain, the vascular system and the liver. In the brain, APOE is produced mainly by astrocytes and helps redistribute cholesterol to neurons for membrane repair and synapse maintenance.

The APOE ε4 variant is thought to increase dementia risk by impairing amyloid-β clearance, amplifying tau pathology and neuroinflammation, disrupting brain lipid transport and synaptic repair, and compromising vascular integrity, thereby lowering the brain’s resilience to age-related neurodegenerative stress over time. Further research is needed to confirm these processes and to explain why ε3 increases dementia risk compared with ε2.

Despite its strong influence, APOE is not the sole cause of Alzheimer or other dementias. Even among people with the highest genetic risk, those who carry two ε4 variants, lifetime risk of AD is still estimated to be below 70%. See my recent posting on the 14 modifiable risk factors in AD and the key role they play.

This invites some more sober commentary on the study’s findings. For example, claiming that most Alzheimer cases would not occur without the contribution of APOE was a bit like saying most road traffic deaths wouldn't occur without the contribution of cars, according to geneticist Dr Timothy Frayling of the University of Geneva. (This is not entirely true because only ε3 and ε4 appear to account for risk.) "People should not worry if they have the risk versions of the gene, because 99.4% of us do," he added.

To my mind, the true value of this study lies in the mechanistic lens it provides. Specifically, are there any natural interventions that can mitigate the risk imposed by APOE variants? See my next posting for a few promising leads.

For more information see: https://bit.ly/40837KO
and
https://scitechdaily.com/one-overlooked-gene-may-shape-nearly-all-alzheimers-risk/

31/01/2026

Even with unprecedented investment, the dementia drug pipeline continues to deliver modest and uncertain gains at best. Despite the media fanfare, recent agents largely target late-stage amyloid pathology, offering small statistical benefits that translate into limited real-world clinical impact, while carrying substantial costs and safety concerns. There is little in the current pipeline that convincingly alters disease trajectory once neurodegeneration is established. This sobering reality underlines a critical truth: dementia is unlikely to be “cured” pharmacologically after onset. The greatest opportunity lies earlier—shifting focus toward prevention and delay through vascular health, metabolic resilience, inflammation control, and lifelong neuroprotection—where the biological leverage, population impact, and cost-effectiveness are far greater.

A recent umbrella review underlines that we already know a good deal about what to do. A total of 45 reviews covering 212 meta-analyses (including around 10,000 individual studies in total) were synthesised. From this the authors identified 14 broadly defined modifiable risk factors that were significantly associated with dementia disorders.

They were: alcohol consumption, body weight, depression, diabetes mellitus, diet, hypertension, less education, physical inactivity, sensory loss, sleep disturbance, smoking, social isolation, traumatic brain injury and vitamin D deficiency. All 14 factors were associated with the risk of major neurocognitive disorders (NCD), and five were associated with mild NCD. Of note, the scientists found considerably less research for vascular dementia and mild NCD.

The study highlighted the role of a key nutrient in prevention, namely vitamin D. Beyond vitamin D, several B vitamins and selected herbs may contribute meaningfully to dementia prevention. Folate and vitamin B12 are central to homocysteine metabolism; elevated homocysteine is strongly linked to brain atrophy, white-matter damage and faster cognitive decline, with trials suggesting benefit when deficiencies or low-normal levels are corrected. Among herbs, Ginkgo biloba has the most consistent human evidence, supporting cerebral microcirculation and endothelial function and mitochondrial activity. Turmeric (particularly bioavailable curcumin) targets neuroinflammation, oxidative stress and amyloid pathology. Low-dose lithium, even at trace nutritional levels, has emerging epidemiological and clinical support for neuroprotection, possibly reduced tau phosphorylation and enhanced neuronal resilience.

For more information see: https://pubmed.ncbi.nlm.nih.gov/38346414/

18/11/2025

An area of health that I specialise in is cognitive health where I see patients who would like to prevent cognitive decline and patients who have been diagnosed with mild cognitive impairment (MCI) or have very early Alzheimer's disease. I also see the adult children of people with dementia or Alzheimer's who want to care for their cognitive health as best as possible. Unfortunately dementia is a growing area of health and also one that we can do much to prevent if we look after our cognitive health early on. In this article I have made a simple checklist of a few things for you to consider that will make a difference. It doesn't take much to turn down the "drivers" of cognitive decline.

* Tweak your food choices
Choose meals with plenty of different coloured vegetables, including some raw in a little salad. These foods will provide vital antioxidants that help protect cells from oxidative damage.
Instead of sugary treats choose fresh fruit, or choose sweet treats that are sweetened with stevia or monk fruit sweetener. Or ones that contain very low sugar such as my personal favourite organic 85% dark chocolate (fabulous protective antioxidants!). Excess sugar can drive inflammation in the body and may lead to issues with blood glucose metabolism and insulin resistance.

* Buy wild-caught fish and preferably the smaller varieties such as salmon (not farmed), herrings, mackerel, sardines and anchovies for good omega 3s. Small white fish such as whiting, garfish and snapper are also fine but contain less omega 3 fats. Larger fish contain higher levels of mercury which certainly isn't ideal for brain health or general health. Don't go for flake, shark, swordfish or tuna for this reason.

* Buy organic foods as much as possible. And if you can't buy all organic vegetables and fruit, do your best to avoid "the dirty dozen". You can read more here... Also look at that same website in the link for the "clean fifteen". Pesticides and herbicides can add to oxidative stress, damaging cells in the body. In addition, some people due to their genetic influences are slower to metabolise toxins such a pesticides from their body.

* Swap pasta, noodles and rice for konjac substitutes or "zoodles" (noodles made from zucchini using a spiraliser). In my home kitchen, we follow a lower carb diet on week nights and then relax a bit on the weekends particularly during socialising. This way the carbs balance out over the week without adding centimetres to our waistlines. Rather than having bread every day you can lighten the carb load by choosing thin wraps, having wholegrain or seed crispbread, choosing a protein + salad/vegetable, or a hearty chunky low starch vegetable and bean or chicken soup in cooler months. You will feel more alert in the afternoon by limiting the starchy carbs at lunch by going for protein + veggies. This simple diet tweak can make a big difference in preventing insulin resistance. An added bonus is that konjac (pasta, rice and noodles) contains a fabulous fibre that feeds the good microbiome in the gut so it's a win-win situation.

*Move your body
A recent study found that those who had levels of beta amyloid in their brain were still protected against cognitive decline with doing 8,900 steps a day. Beyond the specific effects that exercise has on our brains, it's also reduces the risk for Alzheimer's. It can help maintain a healthy body weight, reduce insulin resistance, reduce inflammation, improve blood pressure, and reduce the risk of heart disease and stroke. It also reduces stress and anxiety, while improving mood and sleep.
What exercise is best? Aerobic exercise takes a slight lead over strengthening exercise, but both are vitally important especially as we age. These two different types of exercise activate different mechanisms, thus protecting against cognitive decline by different routes.

* Look at your lifestyle
If you love a drink then you consider having at least three to four alcohol-free days (AFDs) per week. Alcohol is a neurotoxin and this means it can affect brain cell function over years of drinking. When you do have a drink just have a couple rather than a lot. That can be a big ask for some people I realise however it's a great recommendation for long term good brain health benefits.

*Fast overnight for at least 12 to 14 hours from when you finish eating or drinking any calories at night to when you eat breakfast or calories the next morning. In the morning you can have a black tea or coffee or add just a splash of milk, without breaking the benefits of the fast. For some of my patients with specific genetic influences, I recommend fasting for at least 14-16 hours. This fasting period improves something called autophagy in the brain which essentially is when your body goes into repair mode. I like the analogy of cleaners coming in with the mops, dusters and vacuum cleaner to whiz around cleaning up the brain and body cells.

These just a few of the suggestions I have for you to start with. Let me know how you go!

15/11/2025

Can you catch a heart attack?” A new study suggests hidden bacterial biofilms can lurk silently inside arterial plaque for decades, shielded from the immune system until a viral illness or other trigger awakens them. Once activated, the bacteria fuel inflammation that ruptures vulnerable plaques and blocks blood flow, leading to a heart attack.

Specifically, researchers report that viridans-group streptococci (common oral bacteria) are embedded as biofilms inside human atherosclerotic plaques, where they can hide from immune surveillance. When these biofilms disperse, they appear to trigger local innate-immune activation and inflammation, plausibly weakening the plaque fibrous cap and promoting rupture—the immediate event behind many myocardial infarctions, especially in men. The team detected viridans streptococcal DNA frequently within plaques and outlined a mechanistic model of biofilm-driven, immune-evading persistence with episodic activation that may precipitate rupture.

Prior supporting evidence makes this discovery credible. For example, bacterial DNA was identified in coronary thrombus aspirates from heart attack patients. Also, large reviews highlight the links between periodontitis and cardiovascular disease, detailing plausible pathways (bacteraemia, endotoxins, molecular mimicry etc) and frequent detection of periodontal pathogens within vascular tissue.

Professor Pekka Karhunen, the study’s lead author, explains that until now it was widely believed that coronary artery disease was primarily driven by oxidised low-density lipoprotein (LDL), which the body identifies as a foreign substance.

The study was conducted by Tampere and Oulu Universities, Finnish Institute for Health and Welfare and the University of Oxford. Tissue samples were obtained from individuals who had died from sudden cardiac death, as well as from patients with atherosclerosis who were undergoing surgery to cleanse carotid and peripheral arteries.

“Bacterial involvement in coronary artery disease has long been suspected, but direct and convincing evidence has been lacking. Our study demonstrated the presence of genetic material – DNA – from several oral bacteria inside atherosclerotic plaques,” Karhunen explains.

This study provides a mechanistic link to oral health and periodontitis management as a key cardiovascular risk-modifying strategy. See my recent posting on licorice.

It should be kept in mind that while the ‘biofilm → dispersal → rupture’ model is compelling, direct real-time observation in human plaques is impossible.

Specifically, bacterial dispersal might be a consequence rather than a cause of fibrous cap weakening.

For more information see: https://scitechdaily.com/heart-attacks-may-be-infectious-and-vaccines-could-prevent-them/
and
https://pubmed.ncbi.nlm.nih.gov/40767295/

05/11/2025

Micro plastics are very troubling and yet we can do something about it right now which is great news. Read on...

https://www.facebook.com/share/p/1BRzozhSM8/

Two recent online articles have highlighted the need for a greater awareness of the potential health benefits of reducing micro- and nanoplastic exposure. The emergence of microplastics (1 µm to 5 mm) and nanoplastics (less than 1 µm) has raised alarms about their harmful effects on human health. Nanoplastics are especially hazardous due to their smaller size and enhanced ability to infiltrate the human body.

The first article reviews a recent paper by Sarah Sajedi and colleagues, published in the Journal of Hazardous Materials, which examines the science around the health risks posed by single-use plastic water bottles. They are serious, she says, and seriously understudied.

In her analysis of more than 140 scientific papers, Sajedi reports that people ingest an estimated 39,000 to 52,000 microplastic particles each year. For those who rely on bottled water, that number climbs even higher, about 90,000 additional particles compared to people who primarily drink tap water.

According to Sajedi, the health risks are significant. Once inside the body, these small plastics can pass through biological barriers, enter the bloodstream and reach major organs. Their presence may contribute to chronic inflammation, cellular oxidative stress, hormone disruption, reproductive issues, neurological damage, and some cancers. Still, their long-term impacts are not fully understood, largely because of limited testing and the absence of standardised ways to measure and track them.

Sajedi says: “Drinking water from plastic bottles is fine in an emergency but it is not something that should be used in daily life. People need to understand that the issue is not acute toxicity—it is chronic toxicity.”

The second article in MedPage Today highlights the ubiquitous and insidious nature of micro- and nanoplastics. One of the authors (Meyer) is an emergency physician who believes it is now time to be warning patients about reducing exposure.

Teasing out the health impacts of micro- and nanoplastics requires some nuance. There is never going to be a randomised controlled trial: it is hard to conceive of a control group with no plastics exposure (given their ubiquity) and unethical to deliberately expose an experimental group to high-dose plastics. But waiting for perfect data risks ignoring an escalating health threat. Hence, much of what we know is by necessity extrapolated from animal studies and observational trials -- and there are multiple red flags.

In humans, studies are slowly emerging. In 2024, researchers followed patients undergoing carotid endarterectomy and found that those with microplastics in their plaque had a significantly higher rate of myocardial infarction, stroke or death 34 months later. More recently, decedent human brains from 2016 and 2024 were evaluated for microplastics: concentrations were significantly higher among individuals diagnosed with dementia compared to those without dementia (and plastic concentrations increased 50% from 2016 brains to 2024 brains, consistent with increasing environmental exposure). Last year, researchers at University of California San Francisco (UCSF) reviewed existing human and animal studies and found a suggestion of harm to reproductive, digestive and respiratory health in humans, as well as a possible link with colon and lung cancer.

All of this has been enough to convince Meyer that it is now time to start warning patients about microplastics. Although it would be impossible to avoid plastics altogether, there are some practical steps people can take to decrease their exposure.

To start (as per the first article), it makes sense to give up single-use plastic water bottles in favour of reusable steel or glass bottles. The water in plastic bottles has been found to contain 20 times more microplastics than tap water.

It is also a good idea to limit plastic in the kitchen, since we acquire many of our microplastics by eating and drinking them. This means using wooden cooking utensils and cutting boards over plastic ones, foil over plastic wrap, and glass food storage over plastic. If possible, avoid nonstick and plastic cookware. In situations where plastic containers are unavoidable, don't microwave food in them. And wash them by hand instead of the dishwasher, since heating plastic hastens its breakdown and chemical leaching.

At the supermarket, pack groceries in reusable cloth or paper bags, and try to avoid fruits and vegetables wrapped or packaged in plastic (admittedly challenging). And finally, limit ultraprocessed foods. Not only are they associated with increased mortality, obesity, chronic disease and malignancy, but they also come coated in plastic.

Could the demise of modern civilisation be caused by something we cannot even see?

For more information see: https://scitechdaily.com/scientists-warn-bottled-water-may-pose-serious-long-term-health-risks/
and
https://bit.ly/47TCyO3

25/05/2025

This is really helpful for everyone to have a realistic view of what is possible in reversing cognitive decline. You can see that it is well worth pursuing the help of a ReCode practitioner.

Let’s be clear about the current best outcomes in preventing and reversing cognitive decline.

- Cognitive decline is reversible. Peer-reviewed studies confirm it. (See the research: https://journals.sagepub.com/doi/10.3233/JAD-215707)

- Gains can last for years—sometimes over a decade. This isn’t a short-term fix. It’s a new way forward. (See the evidence: https://www.mdpi.com/2227-9059/12/8/1776)

- In contrast, the “breakthrough” anti-amyloid antibody drugs do not improve cognition at all, they simply slow decline modestly, while exerting side effects that include brain hemorrhage, brain swelling, and death.

- We’re not just improving memory scores — we’re reversing the disease process. Brain scans show increased volume, improved blood flow, healthier brain waves, and better biomarkers. This is actually reducing pathophysiology, not simply boosting cognition.

- Not every case is successful, especially when treatment begins too late or the full protocol isn’t followed. But this is true of any medical intervention — from antibiotics to surgeries. That’s why early intervention is critical.

- Here’s the new reality: dementia is quickly becoming optional. With the right tools, no one needs to wait for symptoms to spiral. We now have the ability to detect risk early — and act in time to prevent cognitive decline altogether.

We recommend that everyone over 35 get screened and begin a prevention program.

This chart is what we typically see based on when treatment begins. This is not speculation. This is data-driven proof. This is hope grounded in science.

22/04/2025

Excellent video for headache and migraine sufferers.

22/04/2025

Absolutely! I have dark chocolate every day.

Dark chocolate isn’t just a treat—it’s brain food. Studies show that cocoa flavanols support cognitive function, reduce inflammation, and even boost mood. That said, quality matters!

I recommend choosing dark chocolate that’s at least 70% cocoa to maximize benefits while keeping sugar intake in check.

In my latest blog, I break down the science behind cocoa, how it differs from chocolate and cacao, and how to choose the best option to support your brain health.

Read it here: https://drperlmutter.com/brain-wants-cocoa/

16/02/2025

Very soothing sound healing session this morning with
The good news is if you’re not in Perth she also does online programs. Rachel@is a Sound Healing Academy practitioner.
I can’t wait to book into a session with her again! 🤩

12/12/2024

No surprises here but good to see it's a recognised "thing" now.

"Chronic exposure to glyphosate — the most widely used herbicide globally — may be a risk factor for Alzheimer’s disease (AD), new research showed.

Researchers found that glyphosate exposure even at regulated levels was associated with increased neuroinflammation and accelerated AD-like pathology in mice — an effect that persisted 6 months after a recovery period when exposure was stopped.

“More research is needed to understand the consequences of glyphosate exposure to the brain in humans and to understand the appropriate dose of exposure to limit detrimental outcomes,” co-senior author Ramon Velazquez, PhD, with Arizona State University in Tempe, told Medscape Medical News"

Exposure to glyphosate, the most widely used herbicide, exacerbates neuroinflammation and AD-like pathology in mice, with effect lasting even after a significant pause from exposure.

08/11/2024

This is new information and pretty helpful.

According to a surprising recent paper, aging is not steady, but rather accelerates in two major bursts around 44 and 60, perhaps giving us two time periods in which we can optimize our health routines to improve outcomes. https://med.stanford.edu/news/all-news/2024/08/massive-biomolecular-shifts-occur-in-our-40s-and-60s--stanford-m.html

03/08/2024

Such a good take on what style of eating is best.

Recently, I was in Brazil with colleagues at dinner, and they asked me "how I ate." They talked about themselves as following a vegan, vegetarian, and plant-based approach, with a few of them eating more fish and meat. I responded by saying, "I'm a diversitarian." They looked at me quizzically. I said, "Because I travel so much, I want to experience the culture through their foods and gut microbiome. I want to experience life through the varieties of foods."

Unless I'm truly allergic or intolerant to something, I try to broaden and diversify my intake. The research on dietary diversity is extensive, indicating that it is associated with better nutritional status, gut microbiome adaptability, cognitive function, visual and auditory sustained attention, and less risk for mental health issues, allergic symptoms, and even fractures and falls.

Over the years, as I've worked with people and their food intake, I've seen that people get into food ruts. Sometimes, we need to shake things up. Aiming for at least 30-50 unique foods weekly is a general guideline, with the premise that everyone's gut is different and may need a gradual increase.

Diversity is Nature's principle. It can help people thrive and be more resilient in body and mind.