The heart is the engine of our system and the biggest reservoir of mitochondria. If we improve mitochondrial health, we improve heart health. Chronic stress increases heart rate but reduces contractility over time. Reduced contractility results in systemic problems over time - specifically the removal of metabolites from the brain. This is due to the effects of gravity and the location of the subarachnoid space in relation to the heart - although it's the first system to benefit from stress because it initially increases the pressure. But if stress is chronic, over time this leads to reduced heart contractility, even though the heart rate remains high. This reduces vascular pressure and pulsation leading to problems.
Hypothesis: Alzheimer’s Disease as a Cardiovascular Condition Driven by Heart Contractility and System Coherence Alzheimer’s disease (AD) is typically regarded as a neurodegenerative condition characterised by the accumulation of tau proteins and amyloid-beta plaques in the brain. However, I propose that Alzheimer’s may also be understood as a cardiovascular condition, fundamentally driven by heart contractility and the body’s overall system coherence. This hypothesis is based on the role that the heart plays in generating sufficient arterial pressure to push cerebrospinal fluid (CSF) through the brain’s perivascular space (PVS), thereby clearing neurotoxic waste products. The studies attached to this hypothesis-the BALTAZAR study, which explores the effects of caffeine on CSF biomarkers in Alzheimer’s, and the PVS research on CSF flow-are foundational to this argument. Key Mechanisms 1. Heart Contractility and Arterial Pulsations: The heart’s contractility is a key driver of arterial pulsatility, which is critical for generating the necessary pressure to push CSF through the glymphatic system in the brain. The PVS study demonstrates that arterial pressure drives CSF flow, which is essential for clearing metabolic waste, including tau and amyloid-beta proteins. Therefore, when heart contractility is weakened, CSF flow diminishes, resulting in the accumulation of waste products that contribute to Alzheimer’s pathology. 2. Caffeine’s Role in Enhancing Contractility: The BALTAZAR study provides evidence that caffeine consumption is associated with improved CSF biomarker profiles in individuals with mild cognitive impairment. Caffeine increases heart contractility and arterial pressure, which, according to the PVS study, would enhance the flow of CSF through the brain. This suggests that caffeine’s protective effects against Alzheimer’s could stem from its ability to maintain or increase heart contractility, facilitating better clearance of neurotoxic proteins from the brain. 3. System Coherence: Heart contractility is not purely a mechanical phenomenon; it is also influenced by the coherence of the mind-body system. In this context, coherence refers to the harmonious functioning of consciousness, the mind, and the body. Consciousness, though separate from the mind and body, can influence their collaboration. When individuals are mentally engaged and consciously aware, heart rate variability (HRV) tends to be high, indicating a coherent system. This coherence can directly enhance heart contractility, thus maintaining effective arterial pressure and CSF flow. Conversely, when coherence is low (due to mental disengagement or stress), heart contractility weakens, exacerbating the risk of neurodegenerative conditions like Alzheimer’s. Electromagnetic Considerations The heart’s contractility and the body’s overall coherence can be further understood through the lens of electromagnetism. The heart generates a strong electromagnetic field that interacts with the body’s systems, including the brain. In this model: - Electricity represents the physical matter of the body. - Magnetism represents the energy or mental processes. - Electromagnetism represents the conscious coherence that binds the system together. Strong heart contractions generate a more coherent and synchronised electromagnetic field, which helps align both mental coherence and physical coherence. If heart contractility is compromised, the body’s electromagnetic field weakens, reducing overall system coherence and potentially accelerating neurodegenerative processes. Hypothesis Implications for Alzheimer’s Treatment If Alzheimer’s is indeed linked to heart contractility and systemic coherence, future treatments should focus not only on neurological factors but also on improving heart function and enhancing coherence. Such treatments could include: 1. Pharmacological interventions that improve heart contractility, such as rapamycin (please see attached study) or other cardiovascular agents. 2. Lifestyle interventions that enhance mental and physical coherence, including meditation, exercise, and heart-rate variability training. 3. Comprehensive cardiovascular monitoring in Alzheimer’s patients, focusing on contractility and arterial pulsations as key indicators of brain waste clearance efficiency. Conclusion Alzheimer’s disease should be considered, at least in part, a cardiovascular condition where the failure of heart contractility and system coherence leads to the accumulation of waste products in the brain. By addressing heart health and promoting systemic coherence, we may be able to prevent or slow the progression of Alzheimer’s. The attached research on the PVS system and the effects of caffeine on Alzheimer’s biomarkers provides empirical support for this hypothesis, offering a new lens through which to explore both the causes and treatments of neurodegenerative diseases. PVS Research doi.org/10.1073/pnas.2407246121 BALTAZAR cohort study doi.org/10.1002/alz.14169 Rapamycin Study doi.org/10.1111/acel.13086
Very good video! My mother also has Alzheimer's + Levy Body dementia. She can no longer walk or talk. Can I give her NMN? There's an official study that says this treatment is very good! The study was done by the Hungarian University of Szeged in collaboration with the University of Oklahoma.
It's interesting to see more mechanistically how the Rapamycin might effect the deterioration of the membrane potential of the mitochondria. This would greatly aid in prevention of apoptosis of neurons.
I watched both videos. It seems that Rapamycin could help in many ways to prevent AD. I workout hard to build muscles. Can Rapamycin compromise the processes of building muscles by interfereing with mTor ?
Please cover Palmitoylethanolamide, PQQ, Pycnogenol vs Alzheimer's as well. Our friends at the FDA approved a $2650/month med for Alz, and it has questionable effects. Also Mg Threonate for dementia and Alz.
Hah, you got me to comment. What would be the insult that would cause the mitochondria to become a target? I will assume others here have a lot more knowledge than, but I am among those who have tried lots of things and had success, and don't quite know why, but among things I've tried, some I've had to stick to, mostly one thing, and others have faded into the past. No seed oils for me, and I have some bias toward the idea that the high omega 6 imbalance, plus any pretense of omega 3 in the form of alpha linolenic acid that converts so slowly to what I have found to be more beneficial DHA/EPA, maybe even DPA... but one element of seed oils I am probably persuaded on, if I am informed correctly, is how the mitochondria isn't very adaptable to metabolizing fats of different saturations. It appears to be somewhat fixed in its electron hand off system, and it can be made to appear at least for a moment that a saturated fat has a predictable chemical formula that runs through cleanly, and as it starts to try generating energy from these polyunsaturated fats, that there are extra and missing hydrogens and oxygens that end up causing it to create more by-products as they produce energy, in the form of free radicals, that then insult the cell. If I'm wrong I still can't go back to the seed oils. Avocado, olive, coconut, butter, if there are always trade offs and no elixir of immortality, that is where I am leaning my imbalances for now. My favorite helpful supplements in those days were coenzyme active B vitamins, NAD, alpha lipoic acid, CoQ10, PQQ, all at the end of the day supporting maybe many things, but for my perception of my success in hindsight, metabolic function and clean up. Whatever changed, I still supplement, but not like a junkie, and miss a lot of days. Before if I missed a day I knew and getting the right mix fixed a lot of things. Something changed, and above is my opinion of what it was. If I'm wrong I have still succeeded sufficiently for it to count for me. It is easy for me to imagine mitochondria making more diesel exhaust than clean energy under different situations. If you try it there will be a strange mix of instant relief and nothing at all for 2-5 years. Maybe other microbiome work I did at the time helped in ways I can't as easily tell too. I have not had to maintains any strictness of those protocols and can't quite tell if they helped.
The microscopy images look weird. I skimmed through the paper and couldn't find the methods part about how they acquired those images/what kind of microscope they used. The DAPI signal looks more than just oversaturated (i.e. more like thresholded and binarized) in 1g, 1i and 31and in 3i I don't quite understand why they used MitoTracker to measure the membrane potential. If I understand that figure correctly they are showing 2D cells, so why didn't they use JC-1 or some other mitochondrial membrane potential dye? I do understand that they wanted to counterstain with TOMM20 (iirc TOMM20 is the name of the gene and TOM20 is the protein btw) but afaik you can't really measure membrane potential using MitoTracker. n=5 for single cells is not great imo and I don't quite understand how they calculate 3j (i.e. how do they determine the fluorescence intensity?). 3k doesn't make any sense whatsoever. You need subcellular resolution if you want to determine the mitochondrial membrane potential of individual mitochondria. I guess the MitoTracker can tell you which mitochondria are active/don't have a membrane potential, but it's extremely inacurate imo. Just think about incubation time: a short difference in incubation time could make a difference in MitoTracker accumulation. And I think n = 5 are technical replicates (maybe even same well?) and not biological replicates.. I guess you could say that the ratio of MitoTracker+ & TOM20+ mitochondria / TOM20+ mitochondria can give you an idea of how many active mitochondria you have per cell, but then you need a better resolution to count individual mitochondria, just intensity over the whole cell is a rough estimate. The next problem I see is whether 3i is a single slice or stack. And I'd like to see some brightfield images of the cells to see if there are morphological differences.
If I understand correctly autophagy is critical in this matter, and then one of the best way to induced autophagy is through fasting. Hmm, that means intermittent fasting for example has the potential to repair/replace these mitochondria thus prevent dementia 🤔
You got your fancy doctorate and now you think you’re in charge of sick notes 😂 Seriously though, as soon as I get the down payment for my house squared away, Insiders is my very next stop.
Drugs? Or just do it the natural way through ketosis and/or fasting; promotes mitochondrial biogenesis and autophagy. All our modern diseases are thanks to us being told that we are omnivores, when we are in fact carnivores. A bit like with dogs and cats; they can eat plants/carbs, but just like us, they develop human diseases.
That makes no sense, Ketosis more than likely induces Senescence, given the body thinks it's in food scarcity mode. Not to mention the long-term effects on Kidney and Heart Function are shown to be overall negative. Fasting might be ok but there's not much data on that so far.
Just discovered this today-what an incredible body of work! Truly impressive.
The heart is the engine of our system and the biggest reservoir of mitochondria. If we improve mitochondrial health, we improve heart health. Chronic stress increases heart rate but reduces contractility over time. Reduced contractility results in systemic problems over time - specifically the removal of metabolites from the brain. This is due to the effects of gravity and the location of the subarachnoid space in relation to the heart - although it's the first system to benefit from stress because it initially increases the pressure. But if stress is chronic, over time this leads to reduced heart contractility, even though the heart rate remains high. This reduces vascular pressure and pulsation leading to problems.
lol. You are awesome. Making learning fun
Thanks! :)
😂😂the reason I clicked on this so fast is because I WATCHED the first video and was waiting eagerly for class.😅
Do a video talking about Capsaicin fighting against Cancer stuides! there are dozens of amazing spicy food studys out there!
Thank you for all your work.
What about an upload about the power house of the cell mitochondria ???
Good morning
Morning
Lovely. Thank you!
Thanks for this interesting and important information!
Thanks for tuning in
Hypothesis: Alzheimer’s Disease as a Cardiovascular Condition Driven by Heart Contractility and System Coherence
Alzheimer’s disease (AD) is typically regarded as a neurodegenerative condition characterised by the accumulation of tau proteins and amyloid-beta plaques in the brain. However, I propose that Alzheimer’s may also be understood as a cardiovascular condition, fundamentally driven by heart contractility and the body’s overall system coherence. This hypothesis is based on the role that the heart plays in generating sufficient arterial pressure to push cerebrospinal fluid (CSF) through the brain’s perivascular space (PVS), thereby clearing neurotoxic waste products. The studies attached to this hypothesis-the BALTAZAR study, which explores the effects of caffeine on CSF biomarkers in Alzheimer’s, and the PVS research on CSF flow-are foundational to this argument.
Key Mechanisms
1. Heart Contractility and Arterial Pulsations:
The heart’s contractility is a key driver of arterial pulsatility, which is critical for generating the necessary pressure to push CSF through the glymphatic system in the brain. The PVS study demonstrates that arterial pressure drives CSF flow, which is essential for clearing metabolic waste, including tau and amyloid-beta proteins. Therefore, when heart contractility is weakened, CSF flow diminishes, resulting in the accumulation of waste products that contribute to Alzheimer’s pathology.
2. Caffeine’s Role in Enhancing Contractility:
The BALTAZAR study provides evidence that caffeine consumption is associated with improved CSF biomarker profiles in individuals with mild cognitive impairment. Caffeine increases heart contractility and arterial pressure, which, according to the PVS study, would enhance the flow of CSF through the brain. This suggests that caffeine’s protective effects against Alzheimer’s could stem from its ability to maintain or increase heart contractility, facilitating better clearance of neurotoxic proteins from the brain.
3. System Coherence:
Heart contractility is not purely a mechanical phenomenon; it is also influenced by the coherence of the mind-body system. In this context, coherence refers to the harmonious functioning of consciousness, the mind, and the body. Consciousness, though separate from the mind and body, can influence their collaboration. When individuals are mentally engaged and consciously aware, heart rate variability (HRV) tends to be high, indicating a coherent system. This coherence can directly enhance heart contractility, thus maintaining effective arterial pressure and CSF flow. Conversely, when coherence is low (due to mental disengagement or stress), heart contractility weakens, exacerbating the risk of neurodegenerative conditions like Alzheimer’s.
Electromagnetic Considerations
The heart’s contractility and the body’s overall coherence can be further understood through the lens of electromagnetism. The heart generates a strong electromagnetic field that interacts with the body’s systems, including the brain. In this model:
- Electricity represents the physical matter of the body.
- Magnetism represents the energy or mental processes.
- Electromagnetism represents the conscious coherence that binds the system together.
Strong heart contractions generate a more coherent and synchronised electromagnetic field, which helps align both mental coherence and physical coherence. If heart contractility is compromised, the body’s electromagnetic field weakens, reducing overall system coherence and potentially accelerating neurodegenerative processes.
Hypothesis Implications for Alzheimer’s Treatment
If Alzheimer’s is indeed linked to heart contractility and systemic coherence, future treatments should focus not only on neurological factors but also on improving heart function and enhancing coherence. Such treatments could include:
1. Pharmacological interventions that improve heart contractility, such as rapamycin (please see attached study) or other cardiovascular agents.
2. Lifestyle interventions that enhance mental and physical coherence, including meditation, exercise, and heart-rate variability training.
3. Comprehensive cardiovascular monitoring in Alzheimer’s patients, focusing on contractility and arterial pulsations as key indicators of brain waste clearance efficiency.
Conclusion
Alzheimer’s disease should be considered, at least in part, a cardiovascular condition where the failure of heart contractility and system coherence leads to the accumulation of waste products in the brain. By addressing heart health and promoting systemic coherence, we may be able to prevent or slow the progression of Alzheimer’s. The attached research on the PVS system and the effects of caffeine on Alzheimer’s biomarkers provides empirical support for this hypothesis, offering a new lens through which to explore both the causes and treatments of neurodegenerative diseases.
PVS Research doi.org/10.1073/pnas.2407246121
BALTAZAR cohort study
doi.org/10.1002/alz.14169
Rapamycin Study
doi.org/10.1111/acel.13086
Very good video! My mother also has Alzheimer's + Levy Body dementia. She can no longer walk or talk. Can I give her NMN? There's an official study that says this treatment is very good! The study was done by the Hungarian University of Szeged in collaboration with the University of Oklahoma.
Nic can we buy it as a supplement in the EU?
*THE SEQUESTOSOM-M-M-E* yes, booming & slight reverb at the end. [edited because I learned the spelling😊]
Sequestosome is pretty good but I was chuckling over ‘ubiquitin”. Like, “Hey, this stuff is everywhere…what should we call it? Wait, I know!”
You and Dr. Greger posting simultaneously a video about Rapamycin :o
It's interesting to see more mechanistically how the Rapamycin might effect the deterioration of the membrane potential of the mitochondria. This would greatly aid in prevention of apoptosis of neurons.
Or you can exercise, it will tremendously benefit your brain.
Thanks for the awesome video as always Nic.
I dont know if I missed it but do those benefits work with intermittent dosing of Rapamycin or continous?
I watched both videos. It seems that Rapamycin could help in many ways to prevent AD. I workout hard to build muscles. Can Rapamycin compromise the processes of building muscles by interfereing with mTor ?
nice. so are we safe to take it? if so what mg. I got a lot of mito to fix.
Please cover Palmitoylethanolamide, PQQ, Pycnogenol vs Alzheimer's as well. Our friends at the FDA approved a $2650/month med for Alz, and it has questionable effects. Also Mg Threonate for dementia and Alz.
do one on interleukine 11 and telomir please
Maybe you can investigate klotho?
Already on it. I have two videos planned.
Rod Serling--
"There's a signpost up ahead. Next stop: The Sequestosome."
Vitamin k-2 is supposed to be anti cancerous and nearly no one is talking about.
Hah, you got me to comment.
What would be the insult that would cause the mitochondria to become a target? I will assume others here have a lot more knowledge than, but I am among those who have tried lots of things and had success, and don't quite know why, but among things I've tried, some I've had to stick to, mostly one thing, and others have faded into the past.
No seed oils for me, and I have some bias toward the idea that the high omega 6 imbalance, plus any pretense of omega 3 in the form of alpha linolenic acid that converts so slowly to what I have found to be more beneficial DHA/EPA, maybe even DPA... but one element of seed oils I am probably persuaded on, if I am informed correctly, is how the mitochondria isn't very adaptable to metabolizing fats of different saturations. It appears to be somewhat fixed in its electron hand off system, and it can be made to appear at least for a moment that a saturated fat has a predictable chemical formula that runs through cleanly, and as it starts to try generating energy from these polyunsaturated fats, that there are extra and missing hydrogens and oxygens that end up causing it to create more by-products as they produce energy, in the form of free radicals, that then insult the cell.
If I'm wrong I still can't go back to the seed oils. Avocado, olive, coconut, butter, if there are always trade offs and no elixir of immortality, that is where I am leaning my imbalances for now. My favorite helpful supplements in those days were coenzyme active B vitamins, NAD, alpha lipoic acid, CoQ10, PQQ, all at the end of the day supporting maybe many things, but for my perception of my success in hindsight, metabolic function and clean up. Whatever changed, I still supplement, but not like a junkie, and miss a lot of days. Before if I missed a day I knew and getting the right mix fixed a lot of things. Something changed, and above is my opinion of what it was. If I'm wrong I have still succeeded sufficiently for it to count for me. It is easy for me to imagine mitochondria making more diesel exhaust than clean energy under different situations. If you try it there will be a strange mix of instant relief and nothing at all for 2-5 years. Maybe other microbiome work I did at the time helped in ways I can't as easily tell too. I have not had to maintains any strictness of those protocols and can't quite tell if they helped.
The microscopy images look weird. I skimmed through the paper and couldn't find the methods part about how they acquired those images/what kind of microscope they used. The DAPI signal looks more than just oversaturated (i.e. more like thresholded and binarized) in 1g, 1i and 31and in 3i I don't quite understand why they used MitoTracker to measure the membrane potential. If I understand that figure correctly they are showing 2D cells, so why didn't they use JC-1 or some other mitochondrial membrane potential dye? I do understand that they wanted to counterstain with TOMM20 (iirc TOMM20 is the name of the gene and TOM20 is the protein btw) but afaik you can't really measure membrane potential using MitoTracker. n=5 for single cells is not great imo and I don't quite understand how they calculate 3j (i.e. how do they determine the fluorescence intensity?). 3k doesn't make any sense whatsoever.
You need subcellular resolution if you want to determine the mitochondrial membrane potential of individual mitochondria.
I guess the MitoTracker can tell you which mitochondria are active/don't have a membrane potential, but it's extremely inacurate imo. Just think about incubation time: a short difference in incubation time could make a difference in MitoTracker accumulation. And I think n = 5 are technical replicates (maybe even same well?) and not biological replicates..
I guess you could say that the ratio of MitoTracker+ & TOM20+ mitochondria / TOM20+ mitochondria can give you an idea of how many active mitochondria you have per cell, but then you need a better resolution to count individual mitochondria, just intensity over the whole cell is a rough estimate.
The next problem I see is whether 3i is a single slice or stack. And I'd like to see some brightfield images of the cells to see if there are morphological differences.
If I understand correctly autophagy is critical in this matter, and then one of the best way to induced autophagy is through fasting. Hmm, that means intermittent fasting for example has the potential to repair/replace these mitochondria thus prevent dementia 🤔
You got your fancy doctorate and now you think you’re in charge of sick notes 😂
Seriously though, as soon as I get the down payment for my house squared away, Insiders is my very next stop.
Haha - looking forward to it, Ryan.
I better get that red light therapy
Need a video on what is known of the biological effects of lithium.
Always some thing new to rub two neurons together. Keep that PhD. cooking.
So autophagy cleans out bad mitochondria? Sounds like a win to me. Fast and clean out the damaged cells and mitochondria.
Rapa Nui to the rescue!
Improving autophagy and increasing metabolic rate are suicidal behaviors.
Physionic, are you taking Rapamycin yourself?
I mean is it a “good thing” to cause more neurons to die.
Drugs? Or just do it the natural way through ketosis and/or fasting; promotes mitochondrial biogenesis and autophagy. All our modern diseases are thanks to us being told that we are omnivores, when we are in fact carnivores. A bit like with dogs and cats; they can eat plants/carbs, but just like us, they develop human diseases.
Yep. People are eating themselves to death with plants. Diabetes "type 3".
Nah
Sure ;)
Nope! Humans are omnivores
Carnivore diet = atherosclerotic heart disease = 💀
That makes no sense, Ketosis more than likely induces Senescence, given the body thinks it's in food scarcity mode. Not to mention the long-term effects on Kidney and Heart Function are shown to be overall negative. Fasting might be ok but there's not much data on that so far.