In this video Dr. Ashley Frazee challenges the conventional amyloid‑tau view of dementia, arguing that neurodegeneration is driven primarily by chronic systemic inflammation, metabolic dysfunction, mitochondrial breakdown, and insulin resistance—essentially a whole‑body problem that manifests in the brain later. She explains the "type 3 diabetes" concept, describing how brain insulin resistance creates a metabolic traffic jam that accelerates plaque and tangle formation. Frazee then reviews emerging therapeutic avenues: GLP‑1 receptor agonists (semaglutide, tirzepatide, retatrutide) currently being studied for dementia, and several experimental peptides—dihexa (potent neuroplasticity via HGF‑C‑Met), SS31 (mitochondrial membrane stabilizer), humanin (cell‑death blocker), and MOTS‑c (exercise‑mimetic that improves mitochondrial quality control). She emphasizes that these are still in gray‑area research. The bulk of the talk shifts to a practical supplement stack aimed at supporting metabolism, mitochondria, and neuroplasticity: NAD⁺ precursors (NMN/NR), high‑dose DHA/EPA omega‑3s, CoQ10, magnesium threonate, highly bioavailable curcumin, alpha‑lipoic acid, lion’s mane, B‑vitamins (especially B12 and homocysteine‑lowering), and vitamin D. Frazee repeatedly cautions that supplements are not a substitute for sleep, exercise, and nutrition, and that her statements are not medical advice. She concludes by noting she runs a direct primary‑care clinic in Mesa, Arizona, and invites viewers to like and subscribe.
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What I'm about to share with you should change how you think about dementia forever. For a long time now, the medical community has thought of dementia and Alzheimer's disease as tau proteins and amyloid plaques, like they've been the whole story. And we've focused on treating these plaques and tangles, but unfortunately, the treatments we have, they're just not good. But here's the thing, dementia, not just Alzheimer's dementia, is Neurodegeneration. It's neurons literally failing to operate, and that failure starts years before plaques and tangles ever show up. So, okay, what drives the failure of neurons? It's this: chronic inflammation, metabolic dysfunction, mitochondrial breakdown, and insulin resistance. See, it's not just a brain problem, it's a whole body metabolic breakdown that shows up in the brain last. So if dementia starts with inflammation in the body and brain, you'd think our treatments would treat those things, but they're not, not even close. And to be completely honest with you, and this is just my experience, not that of all doctors, but if you've ever had a job selling something that you couldn't get behind, you just felt like you were having to fake it in order to sell the product. That's kind of how I've felt prescribing these drugs. I just haven't seen them make real change, and it's hard for me to convince people that they're worth taking. Now, please don't stop taking any medication or convince somebody else that they should stop taking a medication because you're watching this video. I am just a doctor on YouTube. I am not your doctor, and none of this is meant to be medical advice from me to you. All right, so let's get rid of the negative talk here and focus on some more positive things, because I've come across a lot. I'm going to share with you some research that is very promising and also some of my top suggestions of supplements that in theory can give you a fighting chance of avoiding dementia. Basically, we're just gonna go upstream from the brain problem. Okay, have you heard of Alzheimer's disease being called type 3 diabetes? Interesting, right? Well, here's why they say that. So research is actually showing that just like how the body becomes insulin resistant in type 2 diabetes, the brain is actually becoming insulin resistant as well. Insulin resistance, in a grand scheme of things, is where the messaging of insulin— where you're supposed to be able to take sugar from point A to point B inside the cells, the messaging of that gets all gummed up and it just doesn't work right. So sugar doesn't go from point A to point B. So imagine having like a big old traffic jam in your brain's metabolism and things just aren't working right. I don't know if that was— I tried, but that's what I'm talking about. See, with insulin resistance, the brain can feel like it's starving for sugar when it's swimming in a sea of blood sugar. It just can't use it because the messaging to get it to use it is not Working right. And it's been shown that that chronic starvation leads to more amyloid plaques, more tau proteins, weaker synapses, chronic inflammation, and faster cognitive decline. So dementia isn't just plaques and tangles, it's metabolic failure in the brain. So now you can see why diabetes, chronic inflammation, and insulin resistance increase dementia risk years before it ever shows up. And in my opinion, our treatments should be aimed at fighting those problems. In fact, this is why the GLP drugs, semaglutide, tirzepatide, retatrutide, are literally being studied for dementia right now, because they have the power to fix inflammation and insulin resistance. You know, everybody's been terrified of overusing the GLP drugs, but in my opinion, and I might regret saying this in 10 years, but I've seen them do more good than harm. The GLP drugs are just one type of peptide therapy showing huge promise in the world of dementia. And this is a perfect opportunity to talk about other peptides that work even more directly on the brain's ability to repair itself. This is where it gets really interesting. There's a peptide called dihexa. It's known for its ability to increase neuroplasticity. And here's the research on dihexa. The dihexa has been shown to cross the blood-brain barrier and it activates the strongest neuroplasticity pathway we have, the HGF-6 C-Met, or hepatocyte growth factor to C-Met receptor pathway. In animal studies, dihexa has been shown to be up to a million times more potent than BDNF, or brain-derived neurotrophic factor, which is basically the brain's master switch for neuroplasticity. This means that dihexa has the ability to drive synaptic growth at levels we've never seen from a natural molecule. Dihexa has been shown to reverse cognitive deficits in Alzheimer's models and motor deficits in Parkinson's models. Now, these are animal studies, they're not human studies, and I have to say that there's some hesitancy in researching dihexa on humans, and that's because the HGF-C-Met pathway is also very heavily involved in cancer growth. So there's a huge theoretical risk of using it and promoting tumor growth. So dihexa kind of sits in this place of potentially revolutionary and potentially dangerous. We just don't know. Now, if you're like me, risk versus benefit might pop into question here, and you might ask yourselves the question, okay, what's worse, having cancer or losing your mind? And I'm not going to answer that here. It's just a personal opinion, and feel free to start a war about it in the comments. Just giving you something to chew on. Now, dihexa was potentially the most potent neuroplasticity peptide that I could come up with, but let me give you a quicker rundown of some Serious contenders. This is SS31. It's a mitochondrial membrane stabilizer. It's a peptide that travels into the inner mitochondrial membrane where all of your ATP production happens, and it stabilizes that membrane from getting unfolded, which it tends to do with inflammation and oxidative stress. And so it helps preserve ATP production, brain-derived neurotrophic factor signaling, and it protects synapses from breaking down. That's what's been shown in the research. It literally has been shown to improve memory and and inflammation in animal studies. Honestly, it's one of the most promising mitochondrial therapies that we've seen, and the FDA has approved it for human use, even just not for this purpose. Another one is humanin. Humanin is a peptide that your mitochondria make, and its entire job is to protect cells from dying. And get this, it was first discovered in the brain of an Alzheimer's patient. It was found to be the thing keeping neurons alive when everything else around them was starting to fail. In a nutshell, research shows that That humanin blocks cell death pathways, defends neurons from amyloid beta damage, reduces mitochondrial damage by reducing oxidative damage, improves insulin sensitivity, and improves cognitive function and memory in mice with Alzheimer's disease. MOTS-c, this is another mitochondrial peptide that you make, and its job is completely different from humanin. If humanin is preventing cells from dying, MOTS-c basically helps keep the entire system functioning in the first place. Now here's the wild part. MOTS-c is basically an exercise mimetic. It turns on the things that also get turned on when you exercise, all the good things like mitochondrial biogenesis, fatty acid oxidation. And considering how protective exercise is for the brain, well, you understand how this could be a big deal in relation to dementia. Here's what the research shows on MOTS-c. It improves mitochondrial quality control, meaning your neurons can repair their power systems instead of letting them fail. It activates key metabolic pathways that reduce inflammation in the brain, actually strengthens the blood-brain barrier, which is huge because barrier breakdown is actually something that we see in dementia, and it reduces neuroinflammatory conditions and stress responses. In animal studies, MOTS-c has been shown to improve cognitive function and memory. Now, we aren't prescribing these things. They're in a very gray area in research and medicine, but the science is fascinating. Okay, so those were my favorite things to talk about, but I can't ignore supplements. Keep in mind, supplements are not substitutes for good sleep, exercise, and nutrition. Oh, and somebody told me that I should probably mention on a video that I have a degree in nutrition science. A lot of biochem as it applies to the body, actually. But anyway, if I were worried about my brain, here's what I would consider supplementing with: NAD or its precursors, the NMN or NR. I've actually said this many times in videos, but NAD is like a battery charger to your mitochondria. You need it to make energy, and levels of it fall as we get older. You see, over time, as we age, we have less NAD, and stress and inflammation actually use more of it than we tend to replace it. Research has literally shown that very low levels of NAD correlate with Alzheimer's dementia. And I feel like that's all you need to know. Omega-3s. If you want a no-brainer brain supplement, take omega-3s, especially ones with high DHA. DHA is brain-building material packed in your neurons and synapses. High DHA intake is associated with lower risk for dementia. I would look for a supplement that's got 1,000 milligrams of DHA and EPA, with DHA being prioritized. CoQ10. CoQ10 is essential for energy production and mitochondrial function. It also acts as an antioxidant in cells. Levels also tend to drop with age, and they really drop with statin use. And so if you have an older person on a statin, you're worried about their memory, put them on CoQ10. Magnesium threonate. Most people are actually low in magnesium, and threonate is the version that can cross the blood-brain barrier. It is thought to support synaptic plasticity and memory. Fun fact, I have nightmares when I take this supplement, so I tend to stay away from it. Let me know if you do too. Curcumin. This is a potent anti-inflammatory and antioxidant with multiple brain-relevant pathways. Now, regular curcumin actually absorbs terribly, so you have to get a highly bioavailable type. Alpha lipoic acid, or ALA. ALA is also an antioxidant, but it's also an antioxidant recycler. It's kind of like a cleanup crew inside your neurons. You can think of ALA as something that reduces Oxidative stress, supports energy production, and supports other antioxidant functioning. It's actually one of the few supplements that's been shown to have a possible cognitive decline slowing effect. Lion's Mane. Lion's Mane is something that people swear by for nerve growth. It contains compounds that may boost something called nerve growth factor. It's basically the brain's please grow new neurons signal. Early studies on this are showing mild cognitive improvement. Um, just know that this is not a treatment, it's just a supplement. And here's something that we don't talk about enough— B vitamins. B12 deficiency can show up as cognitive impairment, and so it's important to get your B12 levels checked if you're having memory issues. You can also check levels of homocysteine in your blood. High homocysteine is a huge risk factor for brain function decline, and B vitamins can help bring that down. Vitamin D. If I ran labs on 100 people with brain fog or cognition issues, many of them would have a vitamin D deficiency. People with low vitamin D show lower mood, poor cognitive function, fatigue, worse executive function, and higher risk of developing dementia. These are showing up as correlations time and time again in research. Okay, so I hope that showed you that dementia is not just a disease in the brain itself. It's stemming from inflammation, a whole body problem that just manifests lastly up here. But these new strategies coming out of the woodworks are something that I'm getting on board with. You know, fix metabolism, fix inflammation, fix the mitochondria, and support neuroplasticity. And we're stepping outside the box because staying inside of it has just not worked. I'm Dr. Ashley Frazee. I run a direct primary care clinic in Mesa, Arizona. It's just where my patients pay me directly instead of using insurance, and I like it better that way. If you like this video, please hit like for me, subscribe to my channel, and I'll keep making videos that should have some relevance to you. You have the best day.
