Dr. Paul Mason - 'Treating and preventing dementia - how diet can work when drugs fail'

[Music] hi i'm dr paul mason and today i'm going to present on dementia and i'm going to try and convince you of a few things that if you have dementia or alzheimer's disease you can improve your symptoms by following a ketogenic diet and by following a diet low in sugar and low in vegetable oils you can probably even help prevent it in the first place even if you happen to carry the so-called alzheimer's gene the apoe4 now while there are multiple chronic diseases afflicting modern society none is more feared than dementia in fact one survey from the uk found that dementia was the top health concern for 68 of those over 50 seven times more than cancer and dementia itself is something of an umbrella term comprising several different conditions the most common one being alzheimer's disease which causes about 70 percent of cases of dementia and those with alzheimer's disease ultimately deteriorate they end up not being able to perform even the most simple of tasks independently their muscles wither away eventually leaving them bedridden and unable to feed themselves in fact following diagnosis patients typically only survive for three to nine years a truly awful disease and it's also far more common with age the risk of developing alzheimer's doubles every five years after the age of 65 so it's no wonder that alzheimer's is a prime candidate for drug research in fact funding for alzheimer's research in the us alone this year is estimated to top 2.8 billion us dollars the problem is despite years of research costing billions of dollars there's still no treatment drug candidate after drug candidate have failed more than 200 promising leads have fallen through in the past decade alone and as a result modern medicine is no more capable of providing assistance to the patient with alzheimer's disease today than was dr alois alzheimer when he first described it in 1906 to this day doctors are incapable of curing preventing or even just slowing down the progression of this awful disease and to add further insult to injury despite the billions of dollars spent on research is becoming even more common with numbers predicted to double over the next 20 years in australia alone by 2050 there will be about 1 million sufferers but there is a glimmer of hope you see well drugs can't help i believe lifestyle can alzheimer's is not inevitable it is not a part of normal aging remember that dementia was rare in antiquity with no recorded cases until 1906 it is an aberrance caused by our modern lifestyles and the answer lies not in a small pill so much as it lies on our plate because what we eat dramatically impacts on our metabolic health and alzheimer's disease have no doubt is a metabolic disease of the brain and it makes sense that the brain would be vulnerable to metabolic disease because while it constitutes only two percent of the body's volume it consumes over 20 percent of its energy and no condition typifies poor metabolic health more so than does type 2 diabetes and most of the consequences of type 2 diabetes such as heart disease and kidney failure are directly caused by the high glucose and insulin levels in the blood the very same blood that circulates throughout the brain and this is why alzheimer's is increasingly being referred to as type 3 diabetes indeed type 2 diabetics have between 2 and 5 times the risk of alzheimer's disease with poorly controlled and long-term diabetics varying the worst and diabetes is not the only metabolic marker associated with alzheimer's disease soto is obesity this study measured the abdominal diameter of six and a half thousand subjects and followed them for over 30 years and they found a significant increase in alzheimer's risk with rising abdominal diameter triple the risk in the most overweight compared to the leanest subjects in fact several studies have now found a reliable connection between increasing obesity and reduced brain volume and not just for the elderly this can also occur in people in their 40s so if alzheimer's is driven by metabolic disease in the brain can we do anything to avoid metabolic disease the answer is yes and low carbohydrate diets low in seed oils play a big role recall that type 2 diabetes is the prototypical metabolic disease well this large scale study demonstrated reversal of diabetes on low carb diets in fact at two years 53 percent of the low carb subjects no longer had diabetes and as for weight loss there is no doubt that low carbohydrate diets are best between 2003 and 2018 there were 62 control trials which is the gold standard of research comparing low-fat diets to low carbohydrate diets in terms of weight loss and 31 of these trials found a statistically significant result and here i have charted all 31. no cherry picking the blue bars represent the amount of weight loss on the low carb group and the adjacent red bar the amount of weight lost in the low fat group and if you look at each pair of results you'll see that the low carb arms lost more weight in every single one of them so it would seem that as far as brain size goes a low-carb diet is the way to go now alzheimer's disease leads to destruction of brain tissue but even before there's this destruction of brain tissue often decades before there's prominent cognitive decline seen and that is associated with disturbed energy metabolism within the brain when it comes to using glucose for energy many brain cells can freely utilize whatever glucose is available brain cells in some areas however require insulin to use the glucose and neurons with insulin receptors requiring insulin stained in green on this slide are densely populated in certain parts of the brain like the hippocampus which is especially important for memory without insulin these cells would be unable to access glucose for energy and the state of insulin resistance which occurs with metabolic disease means insulin is not able to effectively do its job and if insulin can't work properly it's effectively the same as a deficiency even if there's plenty of insulin around and here on this pet scan we can see how the insulin resistance in alzheimer's disease impairs the ability of brain cells to take up glucose you can see much more glucose is able to be used by the brain cells in the healthy brain on the left than the alzheimer's disease affected brain on the right now one way around this would be to infuse the brain with even larger amounts of insulin on top of the already elevated amounts and this study showed that indeed infusing very high levels of insulin was able to improve memory in patients with alzheimer's disease the problem is infusing high levels of insulin is not without significant side effects and so this is not a feasible or a safe option so then we come to another strategy what if we had a source of energy which did not require insulin something like ketones ketones are able to enter neurons without the need for insulin meaning it can fuel the brain even in a state of insulin resistance ketones can be produced following fat metabolism which release fatty acids which are then converted into ketones by the liver these ketones can then enter the bloodstream and travel around the body including to the brain and because of their accessibility to the brain whenever the supplier ketones in the blood increases the amount used by the brain also increases and conversely increasing ketones also reduces the use of glucose by the brain that is ketones are used preferentially over glucose as a source of energy by brain cells as ketone metabolism increases glucose utilization drops it simply isn't needed so the brain will preferentially use ketones when both glucose and ketones are available and the main determinant of whether we produce ketones or not is our insulin levels and if you understand that carbohydrates cause our bodies to release far more insulin than either fat or protein it's clear that a diet low in carbohydrates can also be ketogenic meaning we have ketones circulating in our bloodstream so then if we put someone on a low carbohydrate ketogenic diet we would expect to see an increase in ketone utilization by their brain and indeed we do here you can see that in the brain of someone who's on a very high carbohydrate diet there is a very low uptake of ketones but when we put them on a ketogenic diet the brain literally becomes a ketone sink a massive increase in ketone metabolism by the brain and we see this ability to metabolize ketones in brains affected by patients with alzheimer's as well even with significantly damaged brain tissue and as we've already seen healthy brains are able to function quite well with glucose but the brain with alzheimer's down the bottom here is not you can see the reduced capacity for glucose metabolism but when it comes to ketone uptake store is completely different the alzheimer's brain is even more efficient at taking up ketones than the control brain which makes sense given the impairment of glucose metabolism in the alzheimer's brain and this recent study demonstrated clear benefit of a ketogenic diet on brain activity in those at risk of alzheimer's here we can see baseline brain metabolism before starting a ketogenic diet and afterwards an improvement in brain metabolism of three times now compare this improvement to the changes that we see before and after starting the american heart association diet the before the after clearly the ketogenic diet is far superior and this also translates into the real world this randomized control trial found improved memory in patients on a ketogenic diet so a ketogenic diet is clearly beneficial when it comes to improving cognitive function in someone with alzheimer's and they're also useful in preventing alzheimer's in the first place let's take a closer look at how a diet low in sugar and low in seed oils might stop you from pickling your brain you may have heard about the apo e4 gene the so-called alzheimer's gene having two copies of this gene one from each parent is said to increase your risk of alzheimer's by up to 20 times the truth is though it only does this if you have poor metabolic health that is your genes don't necessarily equal your fate let's start by looking at this study which compared two genetically similar populations in two very different parts of the world a population with the highest carrier rate of this apo e4 allele in the world and what this study found was that those living in nigeria were two and a half times less likely to suffer from alzheimer's than their genetic counterparts living in the u.s now consider for a moment that only 2.1 percent of u.s adults over 60 are considered metabolically healthy and it becomes obvious that the difference in rates of alzheimer's was most likely due to poorer metabolic health in the us population and we have very good science that can explain why this is the case let's take a closer look at how sugar and seed oils can increase your risk of alzheimer's disease a key feature of the pathology of alzheimer's is the deposits within the brain tissue of something called beta amyloid plaques and here we can see a pet scan demonstrating low levels of beta amyloid in a young brain now compare this to the brain of a patient with alzheimer's disease and you can see there's a significant burden of beta-amyloid deposits and it's these beta-amyloid deposits that are thought to lead to the death of brain cells that is they are neurotoxic and if we were to examine the brain of an alzheimer's disease patient under a microscope we would see something like this these circular deposits are the beta amyloid plaques you've just seen on the pet scan and they're made from clumps of protein let's take a closer look at these beta-amyloid deposits these plaques are made up of multiple peptides known as beta-amyloid monomers and each one of these is a fragment of a large apparent protein known as amyloid precursor protein an amyloid precursor protein is embedded in the outer membrane of several different types of cells in our brain and amyloid precursor protein is essential for several functions in the brain including forming connections between and repairing our brain cells now if amyloid precursor protein gets snipped up in just the right places it leaves this beta-amyloid peptide behind now what a lot of people don't realize is that these beta-amyloid monomers are actually useful for instance they've been shown to act as antioxidants and protect nearby neurons but if they are damaged they can clump together and form these plaques and these plaques are the hallmarks of alzheimer's disease and are toxic to nearby neurons remember though that unclumped beta-amyloid the single monomers actually serve an important role in the brain and they can actually be neuroprotective take for instance this graft plotting neuron survival and culture you can see that by day three all the neurons are dead but when beta-amyloid is added about 90 of the neurons are still alive at day four the question is then how do sugar and carbohydrate and oxidized seed oils contribute to these beta-amyloid monomers turning from their neuroprotective normal self into these toxic clumps so understand that carbohydrates are essentially chains of the sugar glucose and once ingested these glucose molecules enter the circulation where they come in contact with various proteins and this includes bitter amyloid monomers which are types of proteins the sugars can then covalently bind to these proteins and form what is known as an early glycation product and some sugars are far more potent at doing this than others take fructose which forms up 50 of sucrose commonly known as table sugar or indeed 55 of the sugar found in high fructose corn syrup fructose can generate up to 10 times more glycation stress than the same amount of glucose and after glycation there's one more step which leads to the formation of something called an advanced glycated end product which makes proteins prone to forming cross links between them and clamping together hence the clumping of better amyloid which we see in alzheimer's disease and this is the step where seed oils come in you see the progression from the early glycation products in the middle to advanced glycated end products on the right is strongly driven by oxidation and seed oils deliver large amounts of oxidation stress when we ingest them and this is due to their chemical structure which makes them very prone themselves to oxidation have a look at the amount of toxic compounds following heating of sunflower oil and compare that to olive oil and indeed then have a look at butter and lard it's clear that as fats become more saturated as we move to the left they have less oxidation potential and seed oils are readily oxidized even when they're not heated here you can see that the oxidation products in walnut oil build up in a matter of days and that oil in your cupboard is almost certainly months old and if you ingest seed oil the oxidation products will be absorbed even more so if you have poor blood sugar levels take a look at the absorption of oxidation products in subjects with good blood sugar levels and compare it to the oxidation absorption in somebody with bad blood sugar levels there is a massive increase in oxidative stress with oil ingestion if you have bad blood sugars and so the combined stresses of sugar causing glycation and oxidation stress from seed oils can lead to proteins such as beta beta-amyloid being affected by advanced glycated end products and as i've already mentioned these advanced glycated end product affected proteins have a tendency to clump together and that is effectively what these senile plaques or beta amyloid deposits that we see in alzheimer's disease are advanced glycated end product affected beta-amyloid monomers and advanced glycated end products are much more common in the brain with alzheimer's disease compare the control brain on the left to the alzheimer's disease brain on the right and these images show the relationship of advanced glycated end products to beta amyloid plaques which are now shaded you can see that whenever a plaque is existing immediately advanced glycated end products are adjacent and here's a close-up view of a beta-amyloid aggregate through an electron microscope and in this state beta-amyloid is no longer the neuroprotector it once was but it now seems to become a neurotoxin this study looked at the viability of bone neurons in the hippocampus the main memory area of the brain and you can see that compared to neurons cultured with healthy normal beta-amyloid monomers neurons exposed to glycated beta-amyloid had reduced survival and when neutralizing antibodies to advance glycated end products were added there was clear evidence that this reversed so we can see that glycation of beta amyloid is what leads to its neurotoxicity and this was demonstrated nicely in this study here you can see a normal sensory neuron and here is a neuron when a glycating agent was at it it basically withers away so let's now circle back to the apoe4 genetic allele which in a metabolically unhealthy state can increase the risk of alzheimer's by up to 20 times i'm now going to show how this is largely dependent on glycation and oxidation stress the apoe gene provides a recipe if you will for this protein that sits in the membrane of hdl particles and the apoe gene comes in three flavors each one leading to this membrane protein having a slightly different structure and these slight structural variations can make the surface apoe protein more or less vulnerable to glycation depending on the particular amino acid sequence and the apoe4 protein is three times more susceptible than the more common apo e3 allele and this is clearly shown in this paper here you can see the amount of advanced glycated end product binding to apoe3 compared to the amount binding to the apoe4 protein about three times more binding to the apoe4 and this binding can defunction the proteins effectively rendering them useless in terms of their normal role and the apo e protein which you saw embedded in the membrane of the hdl particle has a very important role in helping prevent alzheimer's disease this is because hdl like particles can remove beta amyloid deposits from brain tissue and it requires a functioning apo e protein to do so if this apo e protein is damaged by glycation which it's particularly prone to do as we've seen with the e4 variant it can't function and this study demonstrates exactly that here you can see the amount of beta-amyloid deposited in tissue without hdl and then with hdl added we can see adding hdl dramatically reduces tissue deposition and that finding was also shared by this study and when we look at blood levels of hdl versus the severity of alzheimer's disease we find a clear association between cognitive performance and hdl the higher the hdl the better the cognitive performance and it also seems that high levels of hdl also protect against alzheimer's disease in the first place in fact a hdl level of 55 milligrams of deciliter or about 1.4 millimoles a liter is associated with a 60 reduction in the risk of alzheimer's disease and this overall has implications if the mechanism of beta-amyloid removal by hdl is due to the apoe4 protein and glycation can damage this apoe4 protein then this has implications regarding the interaction between genetics and environment so while we understand that the apo e4 variant is more prone to glycation it doesn't have to be so remember that nigerians had a two and a half times less risk of alzheimer's disease than their genetically similar counterparts in the us and this paper looked at things in terms of brain health from a slightly different angle and still came to the same conclusion that low carb diets are best for brain health not only did they find that low carb diets could prevent brain damage they also found that some reversal of brain damage may in fact be possible so these researchers perform brain scans looking at neural pathway stability which is a reliable indicator of brain age in this arm of the study subjects were fed either a standard or a ketogenic diet for one week and they then had a repeat brain scan assessing for changes in network instability and as you can see the network instability was significantly higher on this carb heavy diet in effect the researchers found that the damage to neural pathways accelerated when the brain was reliant on glucose for energy and reduced when ketones were used for energy so far we've established that carbs especially sugar and oxidized oils can both contribute to the development of alzheimer's disease and you may be wondering how to translate this practically well the first thing you can do is consider purchasing a continuous glucose monitor these can talk wisely with your phone and provide real-time feedback on which foods cause your blood sugar levels to rise and then once you've identified which foods cause your sugar levels to rise it's a simple matter of eliminating them from your diet and the elegance of this device is that it takes your personal metabolism into account there's no guesswork a spike of blood sugar means that you've exceeded your threshold and while it's important to avoid oxidized oils please understand that polyunsaturated fats are essential for good health this includes both omega-6s and omega-3s so the safest way to consume these fats is contained within fresh foods such as eggs fish or meat as a rule if the food is fresh the fat it contains will not be oxidized else the food would be rancid oxidation of fats is actually what leads foods to golf so stick with fresh foods and you'll be better off getting adequate sleep is also important in reducing the risk of alzheimer's with very clear evidence of a heightened risk with chronic sleep deprivation even short-term sleep deprivation can be problematic take this study where they use scans to detect beta amyloid deposits and after a single night of sleep deprivation there was a significant increase in beta amyloid deposition in the brain shown here in red furthermore sleep deprivation also worsens insulin resistance which as we have already seen is a major contributor to alzheimer's elevated blood sugar levels on waking often referred to as the dawn phenomenon was shown to be four times greater when sleep was disturbed now we don't have to take this whole process that leads to the formation of advanced glocated end products lying down for example there's a supplement that has the capacity to reverse this first step and the same supplement can also inhibit the second step through its antioxidant action and that supplement is carnosine a small peptide made from two amino acids and carnosine has been shown to lower both glycation and improve memory this double-blinded randomized control trial assessed memory in subjects who were supplemented with carnosine and a closely related compound answering and they found that when they were assessed using the wesler memory scale there was a significant improvement in memory in the supplemented group but there's more to this story you see the root of the word karnazine khan actually means flesh and as its name alludes to it is found in meat flesh foods in fact there is no known plant source of carnosine and this is likely to be one reason why vegetarians have higher levels of advanced glycated end products in their bodies and there's a suggestion in the literature that vegetarian diets can impair cognition this study found cognition scores increased with increased fish intake and dropped with increased bean consumption that is the more beans eaten the worse the mental impairment and the likely reason eating beans was associated with impaired memory is that beans like many plant foods contain anti-nutrients chemicals which impair nutrient absorption nutrients such as iron and zinc take for example the amount of zinc being absorbed from the circulation after consuming 120 grams of oysters and see what happens when black beans added to the very same meal still the same amount of zinc in the oysters as just now the body can't absorb it and the story is even worse for corn tortillas so deficiencies of these nutrients can actually impair the production and transport of neurotransmitters which are the chemicals which communicate between brain cells hence the mental clouding commonly seen in iron deficiency and other nutrient deficient states now all this talk about avoiding seed oils and consuming animal foods might leave some of you feeling uneasy because to make these changes to your diet your saturated fat intake would have to increase taking your ldl levels with it well have no fear this systematic review from 2016 looked at 19 cohort studies with over 68 000 participants and of those 19 studies 16 of them found an inverse relationship between ldl cholesterol and all-cause mortality that is the higher your ldl the lower your mortality in fact the medical evidence is clear that solid saturated fats are healthier than unsaturated oils today there's been more than 10 systematic reviews and meta-analysis on this topic and on balance i find in favor of saturated fat but the real issue is that even when good quality studies looking at vegetable oils and saturated fat have been performed the results haven't always been openly disclosed let's have a look at how the scientific process has been distorted by looking at three large randomized control trials and have a look at how researcher bias impacted the communication of their very important findings the sydney diet heart study was conducted from 1966 to 1973 and was a randomized control trial examining the effect of replacing saturated fat with polyunsaturated fat in men who'd had a recent heart attack but despite being finished in 1973 the data on mortality wasn't published until 2013 some 40 years later and the only reason the data was eventually published was that an intrepid researcher by the name of chris ramsden was able to locate and decode the findings from inch magnetic tapes and what were the findings well displacing saturated fat from the diet with polyunsaturated fats led to a 62 increase in mortality also of the same era was this study which ran between 1968 to 1973 this was a double-blinded randomised control trial on more than 9 000 men and women comparing high saturated fat diets with high unsaturated fat diets and it should be noted that ansel keyes father of the lipid heart hypothesis was an investigator in this study and 16 years later when some of the results were finally published key information regarding mortality was missing and again it was christopher ramsden who recovered the original study data from magnetic tapes and punch cards who finally published the full results in 2016. so why the delay in publishing the results well in the words of the now deceased lead author it was because the findings were disappointing that is they didn't get the results they wanted and what were those results well they found lowering cholesterol with vegetable oil increased mortality plain and simple and this kind of behavior is not just an artifact of the last century we also have the woman's health initiative study published in 2016 a massive study of over 48 000 females who were randomized to either a low fat or a controlled diet this costs 700 million us dollars and the findings well according to the study conclusion there was no significant finding and nor would you have found any significant findings in the results table for it seems that the only statistically significant finding of the whole study was one which the study's authors wanted to keep out a public view something which they were largely successful at for the only reference to this finding could be found on page 661 of the journal buried in obscure text it was found that females with a history of cardiovascular issues did worse on the low-fat diet their risk of complications like heart attacks actually increased on the low-fat diet by 26 percent and what all of these three studies show is that researchers even when they themselves perform the research often cannot accept their favorite idea in this case the lipid heart hypothesis might be wrong and the result is distortion of the scientific process which affects all of us so at the end of the day the lifestyle that keeps your body healthy is also the lifestyle that will keep your brain healthy and that means restricting your sugar intake and restricting your seed oil intake eating healthy nutritious animal foods sleeping well and exercising regularly and if you can do that may you age gracefully thank you paul fascinating talk as always um now i'm sure with all the research you were doing there are a few little extra tidbits that you'd like to share with us that you couldn't quite squeeze into that talk well as is always the case that's true and uh i have to thank you for staying awake i suspect now it's probably your nap time so uh i'm uh doubly appreciative and uh but yeah really um as you know there's always an immense amount of data but whenever we do a lecture and it all can't fit in and i was particularly struck by a few things that i learned relating to brain function and females in particular i guess one of them was that a pre-menstrual syndrome appears to be a state of an increase in a transient increase in insulin resistance and certainly i've had several patients who have mentioned to me that their pre-menstrual symptoms improve significantly on a ketogenic diet and i suspect that really what it's doing it's uh leading to basically an impairment in the ability of the brain to metabolize glucose and basically leading to cognitive dysfunction and when we actually have a look at some of the data on glucose metabolism i've actually come across some data that actually demonstrates there's glucose hypometabolism basically a defect in glucose metabolism seen in females as young as 24 years old so certainly if anybody's struggling with premenstrual symptoms a ketogenic diet is likely going to be able to offer some benefit and i think the one of the other interesting things is uh with regards to estrogen and estrogen has the capacity to also worsen uh insulin resistance especially if it's what we call exogenous which means it comes from outside the body and there seems to be a differential effect of estrogen depending on whether it's taken orally or whether it's taken through another source such as transdermally or intravaginally and when it's taken orally the metabolism of the estrogen by the liver actually is uh the process that generates a degree of insulin resistance and certainly for females with problems so for athletes who are trying to maintain a particular type of body composition at the elite level it's uh having uh the oral contraceptive pill is certainly can cause some of them problems with maintaining their weight and i've seen a few athletes where it's been good for three or four kilograms of weight loss simply by stopping the oral contraceptive pill but um that's all sort of by the by because one of the things that i discovered struck me more than anything else and it's perhaps quite controversial and i'm not sure if you've ever come across the supposed link between gestational diabetes and autism no don't tell me more well it's absolutely fascinating i was able to come across about uh you know more than 10 separate articles that uh and most of them epidemiological for obvious reasons but there seems to be a very strong association between maternal gestational diabetes and the risk of autism in offspring and i think given that autism likely does represent a a a a problem with the the function of the brain obviously and it's not unreasonable to think that that might actually be a metabolic limitation and i've just find it's uh i i think it certainly bears further research because if this relationship does hold up i think we have a very powerful intervention um obviously we know that the rate of autism appears to be increasing exponentially over the last couple of decades and we're not really sure why there's some argument that we're just better at diagnosing it but that really doesn't hold a lot of weight when we have a look at the severity of a lot of the cases and the increasing frequency and i think that this could actually potentially explain that link and i think if this does hold up then it makes it even more important that we maintain good maternal health throughout the whole life span including pregnancy now that's that's i mean why don't we know about this uh you know you said there were what 10 papers and so on and yet you know obviously certainly never been talked about in in public well i'm not exactly sure why but it's not unreasonable we know that metabolic defects within the brain are strongly implicated in most um disorders uh neurological disorders such as schizophrenia or parkinson's disease they all play a role with certainly in my lecture we've seen how strong it is in alzheimer's disease and then i didn't touch on vascular dementias and those kind of things but certainly across the board um insulin resistance in the brain contributes to cognitive dysfunction so i don't think it ought be much of a surprise even if we have a look at a condition chronic traumatic encephalopathy which as a sports physician you're aware of you get bumped in the head too many times and that can lead to problems well head injury absolutely leads to disturbed energy metabolism as well so there's some promising animal research that the state of ketosis could actually be beneficial for managing perhaps improving the symptoms of chronic traumatic encephalopathy as well so i think uh sure this is going to be controversial but it's it's backed up by reasonably solid data and i think it's certainly worthy of further investigation and study interesting not just chronic conditions either there's some interesting work on the role of a ketogenic diet in the management concussion or mild traumatic brain injury as well which is quite quite exciting so uh well i'm sure you'll uh tell us all about that uh in the future paul but uh once again it's been fascinating uh hearing you uh you speak and uh congratulations again on organizing this this fabulous conference my absolute pleasure thanks peter [Music]

Channel: Low Carb Down Under

Views: 161,426

Keywords: Low Carb Down Under, LCDU, www.lowcarbdownunder.com.au, Low Carb International All-Stars, Paul Mason, Low Carb Doctors, dementia, alzheimers, ketogenic diet, brain health, nutrition science, Type 3 Diabetes, insulin, obesity and dementia, ketosis and memory, cognitive function, APOE4, glucose vs ketones

Id: O36CNNdgDGQ

Length: 40min 7sec (2407 seconds)

Published: Wed Sep 09 2020

Reddit Comments

[u/DavidNipondeCarlos]

I personally believe dementia begins decades earlier so prevention should begin early. I can’t prove 40-50 years old have it because they seem fine, we also adapt for smaller losses.

[u/Mike456R]

Excellent presentation. Quick and does not waist any time give loads of info and studies.

Imagine that. Too much sugar and not enough fat causing dementia and Alzheimer's. And what do these idiot doctors prescribe? a low fat diet.