Insights
Functional medicine and chronic diseases

Agetech World spoke to Pete Williams, founder of Functional Medicine Associates, on how functional medicine can address cognitive decline and chronic diseases, and support optimal ageing
What is functional medicine in a nutshell and what is its role in addressing chronic diseases?
Conventional medicine represents one problem solved by one answer, which the majority of the time is pharmaceutically led. This can work to an extent, but most chronic diseases are multifactorial with numerous things going on at the same time.
Functional medicine gives you a different way to look at chronic diseases as it looks at the ones that have multifactorial consequences. For this reason, trying to treat a disease with one medication isn’t going to work and so, it’s important not only to deal with the symptoms but to actually deal with the reasons why the symptoms are there in the first place.
What does it offer that conventional medicine can’t?
Chronic diseases are multifactorial. If you look at drug trials and interventions proposed and used for Alzheimer’s disease so far, none of them have worked and the ones that are still available don’t work that well.
Professor Dale Bredesen always uses this summary to explain why this happens: you might be looking at an object that has a hundred holes and you have to try to plug all of those holes before you truly get to solving Alzheimer’s disease. A drug may plug a hole but there are still 99 more.
That’s when you have to think: what else do we need to know? And what else do we need to do to try to plug as many holes as possible? The more holes that we plug the more likely we are going to see a reduction or a slowing down of symptoms.
You often use the Bredesen Protocol, what is it and how does it work?
The Bredesen Protocol gives you a really good instruction booklet which is a multifactorial way of looking at Alzheimer’s, rather than the usual ‘here’s the medication to use’.
Alzheimer is not a disease that you suddenly get, it’s a disease that develops over many decades. There are some genes that predispose the patient who needs an understanding of what else predispose them or accelerate their risk of Alzheimer’s disease.
The Bredesen Protocol gives you a robust starting point to look at an individual from a multifactorial way. When using the Bredesen Protocol the number one thing to look at is if the patients are genetically predisposed. The key gene that you would look at is the APOE e4 e4, the most common genetic variant associated with Alzheimer’s disease. If you have an understanding that you have the APOE e4 e4 or that you are family predisposed, you might want to start doing something about it decades before there’s any risk.
This means understanding what you can do from a lifestyle perspective that is going to reduce your risk: not drinking, not smoking and doing consistent physical exercise.

Pete Williams is the founder of Functional Medicine Associates (FMA). He is a medical scientist with over 20 years of experience applying Functional Medicine in clinical practice. His work is based on the Functional Medicine approach to treatment of the root cause rather than the symptoms. Pete is also an advisor to nutraceutical and lab testing companies.
News
USC funds AI projects for Alzheimer’s trials

The USC Clinical Trial Recruitment Lab will fund four projects testing how AI can strengthen recruitment for Alzheimer’s trials.
The initiative, dedicated to accelerating and improving Alzheimer’s clinical trials, selected the projects from more than 30 applicants to explore digital approaches.
Alzheimer’s clinical trials are more complex, costlier and take longer than those in other therapeutic areas, despite the pressing need for new treatments.
The lab evaluates innovative recruitment strategies to improve access and representation in trials, with the goal of identifying scalable evidence-based recruitment practices.
The USC Clinical Trial Recruitment Lab is a collaboration between the USC Schaeffer Center for Health Policy and Economics and the USC Epstein Family Alzheimer’s Therapeutic Research Institute.
The four projects will explore the following strategies.
- Miriam Ashford at University of California, San Francisco will develop and test a generative AI voice agent to support remote informed consent and assess patient capacity for Alzheimer’s clinical trials.
- Erika Cottrell at OCHIN, a national network of community health centres, and Vijaya Kolachalama at Cognimark will integrate an AI-enabled diagnostic platform into primary care electronic health record workflows to support earlier identification and referral of patients.
- Andrew Kiselica at University of Georgia will establish a digitally enabled, trial-ready cohort of rural older adults to improve recruitment, participant selection and engagement.
- Raeanne Moore at University of California, San Diego will leverage electronic health record portals and digital cognitive assessments to accelerate prescreening and better match potential participants.
An estimated 5.6 million Americans are living with Alzheimer’s and related dementias, a number expected to increase dramatically in the coming decades as the population ages.
An extensive therapeutic development pipeline and new early-detection approaches, such as diagnostic blood tests and advanced digital tools, have the potential to reduce the burden of the disease.
However, fewer than one per cent of eligible individuals participate in Alzheimer’s therapeutic trials due to barriers that include limited patient awareness, health system resource constraints and lack of access to diagnostics, according to research from USC Schaeffer.
Certain populations at higher risk for the disease, including Black and Hispanic patients, remain underrepresented.
“We can only innovate as quickly as we can test new therapies,” said Dana Goldman, founding director of the USC Schaeffer Institute.
“That’s why it’s crucial we keep expanding the toolkit of evidence-based recruitment strategies for running faster, better trials.”
The lab previously funded six pilots, some of which have already yielded insights.
For example, one found remote blood collection could help identify potential participants, while another showed that offering a small gift card significantly increased enrolment in an online memory concerns registry.
“Faster and more effective recruitment is essential, and we’re excited to incorporate these solutions in an integrated way as part of our clinical trials,” said Paul Aisen, founding director of the USC Epstein Family Alzheimer’s Therapeutic Research Institute.
“As studies move earlier into pre-symptomatic disease, this opens the door to new recruitment paradigms, and continuing to push forward the science of recruitment will be critical to what comes next in Alzheimer’s research.”
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News
Blood sugar spike after meals may increase Alzheimer’s risk

Sharp rises in blood sugar after meals may raise Alzheimer’s risk, according to genetic analysis of more than 350,000 adults.
The findings point to after-meal glucose, rather than overall blood sugar, as a possible factor in long-term brain health.
Researchers examined genetic and health data from over 350,000 UK Biobank participants aged 40 to 69, focusing on fasting glucose, insulin, and blood sugar measured two hours after eating.
The team used Mendelian randomisation, a genetic method that helps test whether biological traits may play a direct role in disease risk.
People with higher after-meal glucose had a 69 per cent higher risk of Alzheimer’s disease.
This pattern, known as postprandial hyperglycaemia (elevated blood sugar after eating), stood out as a key factor.
The increased risk was not explained by overall brain shrinkage (atrophy) or white matter damage, suggesting after-meal glucose may affect the brain through other pathways not yet fully understood.
Dr Andrew Mason, lead author, said: “This finding could help shape future prevention strategies, highlighting the importance of managing blood sugar not just overall, but specifically after meals.”
Dr Vicky Garfield, senior author, added: “We first need to replicate these results in other populations and ancestries to confirm the link and better understand the underlying biology.
“If validated, the study could pave the way for new approaches to reduce dementia risk in people with diabetes.”
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