Transcription
There is only one species of animal on planet Earth, or on any planet that I know of, that is confused about what foods they should eat and what foods they should avoid. It seems that every other creature on planet Earth knows exactly what they should eat; they know how much they should eat; they know when they should eat; and they know when they should stop eating. Only human beings seem to have a problem understanding what a proper human diet is.
I've got a great guest with me today, and we're going to be talking about a proper human diet, and no telling where this conversation's going to go. Uh, my guest is… is a bit of a reel like me, so there's no telling what we'll wind up talking about before this interview is over. Welcome, Dr. Paul Mason, from the other side of the earth.
Good day, Ken. It's absolutely wonderful to be here. We've had a couple of false starts here getting this done, and I'm really grateful to be on your program.
Absolutely. Now, uh, it's actually tomorrow morning where Dr. Mason is, compared to where I am. Uh, I'm about to wind my day down, and he's just getting his day started. So Dr. Mason, welcome. Uh, before we get started, give us just a brief 30-60 second bio of about you, and why… why did you become interested in a proper human diet?
Well, basically… well, for my own health. So I used to have metabolic syndrome in my 20s and 30s. I'm now in my 40s, and I no longer have metabolic syndrome, so that's a bit of a win. I'm a sports medicine physician, so uh, we've got a natural interest in human performance. So we deal with elite athletes, Olympians, and the like. So it's kind of useful if we can put them in a… their body and running the way it's meant to run. And uh, there's also a rich heritage of uh, proper human nutrition in sports medicine. We've got Dr. Timothy Noakes, Professor Timothy Noakes, and Professor Peter Brookner, who are uh, both uh, leaders in the field as well.
Absolutely. And now this is being recorded live in our private community, and so one of the benefits of being in our tribe is that you get to ask questions of uh, some of the world's leading thinkers on health, medicine, nutrition, sports medicine. And so uh, we might entertain some questions as I see them go by in the comments. Uh, doc, first of all, I've seen you talk lately… recently I was doing my research about you to make sure legit… you were talking about hemoglobin A1c measurements and plant sterols, and the effect that that eating some plants, at least some of the time, can have on the health and viability of uh, erythrocytes, red blood cells, and how that can affect hemoglobin A1c measurements. Uh, and I've actually… about in about 5% of the carnivores in our community, we see that they get this falsely elevated A1C of uh… and so I'll be using different numbers than you in… in… in the United States. A 5.6 or lower is considered completely normal, uh, but we'll see carnivores get a 5.7, 5.8, and they've been strict carnivore for six months or 12 months. And so we know that that's not coming from glycation events coming from their diet; there must be some other cause. Uh, tell me what you've learned about A1C, plant sterols, and how they can affect reticulocytes and erythrocytes.
Well, first of all, let's have a think about what Hb1c is. Yeah, so you've got a red blood cell, and it's swimming along in a soup. And when we talk about blood glucose, when you do the finger prick and you say, "Oh, there's glucose in my blood," you're physically talking about glucose molecules that are swimming along in this soup. So these red blood cells, also in your blood, they're in contact with the glucose. Now, now these glucose molecules can actually non-enzymatically, which means it's just a passive process, can attach together. And when the glucose attaches to the… to the red blood cell, we call that glycated; we call that Hb1c, glycated hemoglobin. Now, the more sugar that attaches, the bigger the number. So there's two factors that can actually increase the HbA1c. So Factor number one is how much sugar is there. So that's why people with diabetes have greater HbA1c's, because this soup… it's… it's a thick, viscous soup of sugar; it might as well be honey for blood. But number two, the duration of exposure. So if that… those red blood cells are in that soup for longer, then there's going to be naturally more time for things to attach. And that's what happens in carnivores. You see, we talk about red blood cells like they've got a life of 120 days, but not in everybody. Some people's red blood cells… cells just aren't that healthy; they don't live as long; they… they suffer more oxidation stress; they're not as resilient; they're not as deformable. Myriad of reasons why, but they… if their red blood cells are not lasting for very long, then what will actually happen is you'll get an artificially low HbA1c reading. So people who are sick, I'll often see people with an HbA1c of 4.5 or something like that, and I'm just saying, uh-uh, that's not real; there's… we're got to look at a reason why you're red blood cells turning over excessively. But on carnivores, they put their body into a physiological state where the red blood cells can actually live for longer; their survivability is improved. And in that situation, what actually happens is that because they're in contact with the sugar for longer, they're able to actually have an elevated Hb1c. And fortunately, there is a way we can actually assess for this in the blood. So we've got a… when we do a full blood count, we get hemoglobin, you know, red cell counts, on and so forth. And we can also get, although we don't always ask for it, something called reticulocytes. Now, a reticulocyte is a new red blood cell. Now, I'd call it a baby red blood cell, but they're actually bigger. Yep. So we'll go with a new red blood cell. And the idea is that if you're in a steady state, if your… if your red cell count is stable between two blood tests, then the rate of red sub… blood cell production should be a pretty good surrogate marker, a proxy marker, for the rate of red blood cell destruction or turnover. So what we can actually see is that in carnivores, their blood cell… now amount is staying stable; their reticulocytes, their new red blood cells are going down; and at the same time, the HbA1c is going up. So that gives us an insight that the increased HbA1c is actually a consequence of improved red blood cell survivability. So how on God's green earth does this come about? So we heard of cholesterol, this molecule which is absolutely essential for life, but have you heard of fake plant… fraudulent cholesterol… imposter cholesterol… phytosterol? So this is what's in seed oils and plant foods, and this is molecularly very, very similar to actual real cholesterol; it's just got a bit of a tweaking on molecular side chains. And it can actually be absorbed in small quantities by the body, but because it is different, it doesn't have the same biological function, and it gets incorporated into red blood cells, which… by the way, the highest concentration of cholesterol in any cell membrane in the body is in red blood cells… is in red blood cells. So red blood cells take it up, and if red blood cells take up this fake plant cholesterol because you're consuming too many plant… you know, seed oil, so on and so forth, it actually damages them. There's clear evidence, and this has been studied, that when you increase the phytosterol content of red blood cells, they become fragile, less deformable; they turn over quicker. So that's why if you had a diet high in seed oils, you could actually see a paradoxical lowering of your HbA1c. Now, I know not part of your question here, but just why we're talking about… so if you have a HbA1c, what do we do?
Well, I… I would recommend cross-referencing it with what I consider to be the gold standard for glucose measurement, glycemic assessment, which is a 24-hour or a continuous glucose monitor. And they are absolutely beautiful. So that's real-time measurement, you know, wirelessly going straight to your phone. You'll see in real time… it's like what we call the election night worm, you know, which political party is winning in that seat. You actually see your sugar trace in response to whatever foods you're eating. And if you've got great glycemic control, you will see this… just a couple of points though that is often overlooked on continuous glucose monitors: they do not measure the concentration of glucose in the blood. So… and this is often… people will say, "Oh, you know, my sugar goes high. I have a shower; when I exercise, my sugar's going way up." And it's like, uh-huh, your sugar's not going way up. Let me explain what's going on. So you've got the little probe from the 24-hour monitor, and that sits in what we call interstitial fluid, not exactly in the blood. So what happens is the blood is flowing around; it's delivering glucose molecules, and some of those glucose molecules are escaping and going into the interstitial fluid. So the interstitial fluid… rating of glucose is dependent also on two factors: one of them is the concentration of glucose; the other one is the speed of blood flow. The greater the blood flow, the greater the delivery of glucose to that sensor, which is why if you have a hot shower, you vasodilate; you open up your blood vessels; you increase the blood flow; it looks like you're getting a spike in sugar; you're getting a spike in blood flow. Same when you exercise; you're increasing your circulation; you're increasing the delivery of glucose to the sensor. And that's why there's not always a direct one-to-one uh, relationship between the finger-prick blood glucose, which is more accurate, and the continuous glucose monitor. But the continuous glucose monitor will tell you if you've got stable sugars, and if you've got stable sugars, you're sitting fairly pretty.
I totally agree, and there's a… a long list of things that can falsely lead to an elevated A1C. There's a… there's a long list of things that can lead to a falsely depressed or lowered A1C. Uh, chronic alcohol intake can actually give you a falsely low A1C. There's a long list that anybody can look up. And so when I see a carnivore, and I don't… I don't see this in… in people eating a ketogenic diet, it's really only in carnivores or… or keroes who are just almost carnivore, 95%, but I'll check either a fructosamine or a glycated albumin. And invariably, even though the A1C is a little bit elevated in these carnivores, the fructosamine or the glycated albumin is stone cold normal, which I think is another good way… and I love your reticulocyte… that's an excellent way of looking at this… to see how many new young blood cells are out there in the circulation. Why are you having to create so many of those? Well, it's because the degraded red blood cells that… that have the plant sterols, they're being uh… preferentially broken down and destroyed by the spleen and other… other parts of the body because they're improperly made. I think that's an excellent insight.
Um, well, just… just one thing there, Ken, though, just on fructosamine. So fructosamine is analogous to HbA1c, and that there's a protein called albumin… or albumin, as we might say down under… from the… an… yes… al… now… now albumin is what we call a negative acute-phase reactant. So now what does that even mean? So basically, in a normal existence, healthy existence, our liver produces lots of proteins, which is good because we need proteins to live. But when we're sick, we have other proteins that the liver produces, like C-reactive protein; that's an inflammatory protein. But there's a finite synthetic capacity in the liver; it can't just say, "Oh, I'm going to produce more CRP now and not subtract away from something else." So your albumin production will actually reduce when you're actually inflamed and chronically inflamed, and the… the change in albumin synthesis uh, rate can actually impact on your fructosamine as well. So fructosamine is not… not removed from having extraneous factors that can impact it in the same way that HbA1c can. So… so absolutely, I… I do use fructosamine from time to time, but I still always come back to the continuous glucose monitor.
I love that. Yeah, 24-hour continuous glucose monitor; it's hard to beat. Now, I always love to point this out because there's a few people in the carnivore community now calling it animal-based diet who eat hundreds of grams of… of carbohydrates a day in the form of fruit and honey. And I actually had a discussion with one of these folks… we won't name any names, but he and I are good friends, but he said uh… that… that the hemoglobin A1c and fructosamine test… they… they absolutely test… test for fructose glycation as well as glucose glycation. And I was like, "I don't think so, my friend; you maybe need to look into that." And so let's be very clear: even though "fruct" is in the name, it only checks for glucose glycation; it does not monitor… and here's the other problem with fructose is that the glycation potential of fructose is 5 to 10 times greater than that of glucose.
Exactly right. And so these people who are eating lots of… and honey are getting a gigantic amount of fructation… or fructose glycation that no test that the doctor's office can detect. And so I always like to make that clear because it's confusing for… for the layman. Say, "Well, it's got… it says fructose… of mean… it's got to measure fruct…" No, it doesn't. And even… and don't feel bad if you're a layman and you thought that, because some doctors don't know that… that it only checks for glucose glycation, as does the glycated albumin; they do not check for fructose glycation. And so that's very important for people to understand. Now, are you a big fruit and honey eater as well, or do you believe that's probably not the best choice?
Look, for me, I don't think it's the best choice, but I'm also… I don't want to be dogmatic about this. So this whole thing about carnivore… it's turned into a bit of a dogma and ideology, if you will. Yes. My personal belief is that people who are metabolically healthy probably can tolerate certain amounts of sugar. And I have a sneaking suspicion, which I think will be borne out in future, that a lot of these plant food intolerances that we're actually seeing that we didn't see in generations gone by is actually a direct consequence of alterations to the way food is produced, namely… to a lesser extent, nutrient deficient, and more significantly, pesticide adulteration. So in Australia… say… here's a pop quiz here for you. So I'm a farmer; I'm growing wheat in Australia; I'm uh… I want to turn it into bread in the future. How many days before I harvest that wheat am I allowed to spray it with Roundup?
I don't know what the regulation is in Australia.
Six days.
And okay. So… and if I spray a crop with Roundup, um… we… we often do it while it's growing. So the… the whole thing about GMO, modified organisms, is not worried about the genetics of it; it's designed to make it resistant to weed killers, so we can spray the crap out of them with weed killers, so that only one thing grows; that's the whole point of a monocrop. And the reason that they would spray it six days before harvest… a lot of people don't know this, Dr. Mason, is that it desiccates… that dries the crop out so that it's easier to harvest.
Exactly. It… it allows for a much more rapid harvest, but often they… they're… they're not just spraying it on… on at the end; they're also spraying on it when it's rapidly growing. Now, what do grains do when they're rapidly growing? They take everything up from their environment. So when you're got a crop that's been sprayed by pesticide, it is actually internalized; you cannot break it down by cooking; you cannot wash it off. The rate of pesticide exposure is increasing exponentially. So a World Health Organization report calculating the worldwide per capita… for every single person in the world… use of pesticides is estimated that in the last 30 years, there's been 11 kilos of Roundup applied to our food for every person on Earth, and 70% of that has been applied in the last 10 years. I mean, this is… and that's just one single pesticide; you know, there's… there's numerous versions. So this whole thing about… and the pesticides has incredibly wide-ranging… I know we probably didn't want to get too much into the weeds on this kind of… but I mean, we have to understand that what this does is it destroys the soil. So the… the… all the… the fungal elements and all the… these uh… protest elements… the things that are necessary for soil structure are destroyed. Now, sure, that doesn't sound like a big deal, but where does the nutrition… how do we release the nutrients from the sand and the stone and the clay from the soil? It's with these complex ecological biological forms, and the pesticides just demolish that, which is why when we perform nutrient analysis on fruits and vegetables today compared to earlier… many nutrients are down by at least half, you know, often up to 3/4.
Yep. And a lot of the data that I've been able to get is still 20-30 years old, which doesn't incorporate the recent massive increases in fertilizers. So when I come back and say, "Look, this is not an ideology about carnivore, plant foods versus, you know, so on and so forth," we have to understand that our very food systems are not the same. So sure, if you want to eat plant foods and they agree with you and you're not Celiac and you're not reacting to gluten, so on and so forth, then there's no ideological reason why you ought not do that. But I would strongly encourage you to make sure that it is organic. And even if you're eating organic foods, that doesn't completely eliminate your exposure to pesticides, but it has been proven by research to reduce it significantly.
Yep. I totally agree, and in many cases, I've actually… I've read all the studies you've read about the decrease in the nutrition in… in uh… plants, in grains, and in actual vegetables as well. And in many cases, when the… when the researchers look at the soil itself and do chemical analysis, the… the vitamins and minerals are in the soil… yes… but all the bacteria and all the fungus… that's… that… that beautiful… currently indescribable… ununderstandable food… that soil web of life… that's how the… the… the minerals get into the vegetables or the wheat. And when you destroy that with fungicide, pesticide, herbicide… it might be in the dirt, but it's not going to get into the… into the plants. And that's a huge problem; that's a huge deal. And I love it that you know that about uh… about raising crops; that's… that's good information; most people don't… aren't aware of that.
Um, you talk a lot about statins; I talk a lot about statins; we talk about cholesterol. Um, I understand that you've got some newish information on statins because one of the main problems I have with statins is that the drug companies will not release the raw data from their studies. We just have to finally trust them that… that… that the study was properly designed, that it was properly conducted, and that they got the numbers they actually said they got. And I understand that you've got a little bit of insight on that situation.
I mean, this is a complete debacle. I mean, the fact is that you and I, as independent doctors, independent researchers, do not have access to the raw, participant-level data on statins is… is just astonishing that we have to accept at face value what these pharmaceutical companies, who have this uh… obviously desire to increase their profit… so if we go back to… we all know about the uh… the Oxford University and Sir Rory Collins and you know all of that. But in 2013, there was a… the Cochrane Collaboration did what's called a systematic review on statins, and they said, "Oh, we found in some benefit," but they acknowledged the possibility that perhaps if they had access to the full data, that unpublished data, that perhaps their results might change. So in 2012, there was an agreement with drug companies around the world for them to provide access to unpublished data. So two authors from the Cochrane Collaboration, they actually approached drug companies, and they made 10 submissions using these convoluted um… approaches to drug companies to say, "Look, can you please give us your unpublished data?" So obviously, you know, statins are a wonderful drug, you know… you know that… we know that… um… if you give us the unpublished data, we'll be able to tell the world the convincing truth. So of these 10 submissions, two companies didn't respond; flat-out didn't respond. So much for an agreement. Then we had AstraZeneca; they declined on the basis of their internal company policies, which makes me wonder how the company was able to make this agreement. Pfizer… we may have heard of Pfizer, too… um… they said, "I would love to, but we actually didn't collect any data on the side effects of our drugs… of the statins," sorry… I'm not talking across their whole product range; that would be speaking out of turn. Um… other companies, they said uh… that the… the statin data was collected before they formed the agreement, therefore it doesn't form part of the agreement. Uh… in another situation, the company said, "Oh, the period where we're required to retain the data for the statin has lapsed." So presumably, they just burnt the data rather than having it be released transparently. Um… a Japanese company… now this is very interesting… the one that was researching the very first statin, Sankyo, they actually specifically excluded statin data from the… the drug-sharing agreement, almost like they had something to hide. Now, the really interesting thing is that this company was actually in a race with Merck to develop the first statin back in the 1970s, and it's on record… there is some documentary evidence that they stopped researching the first statin because it was causing too many cases of cancer in their test animals. And gee, it would be wonderful if they hadn't excluded that data from this uh… this data-sharing agreement, wouldn't it?
Yes, that would be very nice. I mean, wouldn't you love to have your hands on this data? But the simple fact is… you know, we… we say we've got all of this data, and this information was something that unfortunately I didn't have room for in my lecture, but I probably should talk about… I'm glad that you've given me the opportunity to talk about it publicly today. But the fact is that the drug companies do not give us access to all the data on side effects. And even when they do give us data, the data that they curate, that they want us to see… the benefits on statins are marginal at best. Now, that they're technically… they are there… in the matter of… you know, it might increase your life expectancy by three or four days… um… but you know, would those benefits vanish if we had access to the full data? And that… that's a question we don't have the answer to, but in my head, I think I know what the outcome would be.
Yeah, me… me as well. And so the 10 companies that were responsible for the majority of statins on the market either just didn't reply at all or said, "No, you can't have that," or "We… we've destroyed that data," uh… even though much of this data… much of these… many of these studies were actually paid for with government dollars… AKA… on public…
Yes, exactly right. But yet somehow they own the data, even though it was paid for by the people. And… and not only that… understand that we're wanting data on personal, individual side effects. We want to know what happened to Mr… you know, Joe and Mary when they took the statin. Did they get muscle aches? Did they start weeing blood? You know, did their liver start, you know, cooking itself? You know, so these are… this is individual…
Yeah, it's… it's crazy. And speaking of drugs, statins are very often part of a… of a pharmaceutical soup that patients, especially over the age of 50, they're going to be on a statin, two blood pressure medications, two diabetic medications, a medication for restless leg, a medication to help them get to sleep, a medication to help them stay awake… polypharmacy. I know you have some rather strong opinions about this, and… and most of them align very closely with my beliefs. Uh… I'm… I… and I… listen, I used to be guilty of this, Dr. Mason. Let me be the first to… to fess up. Early in my career, when somebody would come to me on 5, 10, 15, 20 different prescriptions, and they'd be like, "Yeah, I'm just here to get labs and get my refills," I would refill every single medication. I never went down line by line, "Do you still need this? Do you still need this?" I never did that. It never occurred to me to do that. I thought my job was just to refill everything. I'm not joking; I'm serious. And now I would never in a million… do that. If somebody came in on 20 medicines, they would walk out with at least nine, if not 15, of those medicines cancelled. Right. And so if we were to sit down together and say, "Well, let… let's… let's take a root-cause approach to medicine," now what does root cause mean? It's saying, "Find out the cause of disease and address the root cause." We've either got a root-cause approach, or we've got a Band-Aid approach, which we call a… a pill for every ill. Oh, you got a headache? Oh, you don't sleep well? You know what… have you… now if we… if you and I were to sit down and put our heads together and come up with a list of medicines that would genuinely be root-cause medicines, it would be less than 20 medications; I would imagine… would have anti-infective agents; you might have hormonal therapies for people who have had a damaged gland, like a thyroid gland might have cooked itself, and they need thyroid hormone, or they might need testosterone or something like that. Um… they might even need insulin. But the list would be far, far shorter than what we're actually able to prescribe. Most drugs actually just treat symptoms. So… so what I presented on recently in a lecture called "Fixing Medicine" was a case of egregious polypharmacy. So there was a 71-year-old lady, and she was found to have slightly high blood pressure, um… which… by the way, have you ever gone looking for the all-cause mortality benefit of blood pressure medication… like for evidence that they actually make people live longer? Well, for… for minimally elevated blood pressure, it's infinitesimally small; it's… it's an unsatisfying search. So anyway, so this… this lady was started on a… she had blood pressure that was elevated, so she'll started on a blood pressure drug. Now, this particular drug is called a calcium channel blocker, amlodipine, and it is known to have a side effect of ankle swelling. And as you know, ankle swelling can also be a sign of heart disease… but… or… or a drug side effect… surprise, surprise. So she ended up seeing another doctor who said, "Oh, you've got swelling of your ankles; well, you must have too much fluid in your body; let's give you some fluid tablets." These are called diuretics; they… they force the kidneys to expel extra water from the body, basically leading to a state of dehydration. Now, if you put an old lady on two diuretics, you can reliably predict she's going to start peeing, and guess what she did. So she was diagnosed with urinary incontinence, so she was put on another drug for the urinary incontinence. Now, this drug has what we call an anticholinergic side effect, which leads to the sense of a dry mouth, and that was bothering her quite a lot, so she was given a drug to treat this, which is lovely. Um… but eventually, she ended up being on 17 separate drugs, including all these ones that were commencing in rapid succession, including two antidepressants and an antipsychotic drug, most of them which have falls risk as a side effect. Can you guess what happened? She fell over in her bathroom, struck her head on the basin as she went down, and fractured her spine. Now, the interesting thing was that two days ago I was seeing a gentleman who was in quite a pickle. Uh… last year he came to see me, and he was in quite significant heart failure; his lungs were full of fluid; his legs… he had, you know, fluid pitting edema up to his… woo… he really wasn't in a good state. And he embarked on what you and I might call a proper human diet; he's lost 20 or 30 kilograms in the last few months, and he's in a much healthier state. And I just saw him a couple of days ago; I said, "How you going?" He goes, "I had a fall." I said, "You tripped over…"
Like, no. I fell. I, I just fainted. I had a look at his drugs, and he was on two diuretics and two different blood pressure medications, and I just, oh no. And it's like, once you get healthier, you know, we need to take you off of these drugs. These drugs are causing side effects. And he, he went to an emergency department; they gave him a full cardiovascular workup. They said, "Sorry, buddy, we don't know why you fall; see you later." Um, did nothing. And it's very clear that he's on multiple drugs that are causing increased risk of falls. And I suspect that if we appropriately change his drugs, as in deprescribe—which, as you know, we're never taught how to do—always makes us feel uncomfortable because we're never told to deprescribe, we're never taught how to do it. But if he goes through an appropriate process of deprescribing, his chance of having another fall will be way down, absolutely. And my heart goes out to the poor woman on 17 different medications. People think, well, that's probably a special case, probably very rare. That is so common in people over the age of 50 or 60 or older. That is so common that now doctors are actually writing books about pharmacology and pre-deprescribing, finally. But it's hotter than you think it is; it's not easy. Then, especially for some drugs, it, it's a very touchy thing to do it too quickly. And so I'm glad there are books about it, but you're right, as a young doctor, I never thought about stopping a medication. I didn't think that was my job.
Well, what—let's take proton pump inhibitors, so an acid reflux medication, right? So incredibly commonly prescribed. So when I was in medical school, we basically got told, "Safe as houses, as long as you want." Rest the natural acid secretion in the stomach, that you can risk becoming deficient in uh, a lot of electrolytes—calcium, magnesium, so on and so forth—which is why you have an increased risk of osteoporosis, increased risk of community-acquired pneumonia because of aspiration risk, increased risk of dementia because you, you reduced absorption of B12. In the United States, this would be Nexium, Prilosec, Pariet; those are the probably the biggest three, and there's a couple more. Go ahead, doctor.
So they're just awful drugs long-term. Yes. And we, and if you have a look at the prescribing information, and the thing about prescribing information is that by law that has to be accurate, otherwise those execs could go off to jail. So the prescrib—that little leaflet inside the drug box—that's the Holy Grail, yeah, for accurate drug company prescribed information, which is, I love sometimes, which is why when you look up on Crestor, you'll see it causes diabetes and so on and so forth. But that's a, that's another side tale. But these side effects of these proton pump inhibitors are huge. And the problem is that if you suddenly stop them, you will get a side effect. So they took a bunch of volunteers, and they said, "Here, take this drug," and then they suddenly—and these volunteers were healthy; they had no reflux before they started—then they stopped. 40% of them developed symptoms of reflux. So this is called rebound acid hypersecretion. So what happens is, by taking this drug, you, you suppress the natural acid secretion of the body, and the body says, "I need the acid," so it dials up the acid production to counteract the drug. So if you suddenly take the drug away, you take off that break, you're going to have a lot more acid being produced. And this is why when people inappropriately—well, they may appropriate, but usually inappropriately—get prescribed one of these proton pump inhibitors, when they try to stop it, they get the reflux. "Oh, I still need to take it." They end it indefinitely. So you actually have to wean off these drugs quite slowly. You, you know, start half, half, half it again, do it second daily, however you want. And I usually, you know, have a protocol over, you know, two to six weeks, depending on how long they've been on it, where we actually get to wean them off. But you think we're taught how to do this in medical school? No. Not in your life. Nope.
And for many people, when they begin a proper human diet—whether that's low-carb, real whole food, or ketogenic, real whole food, or ketovore, or carnivore, wherever, wherever you fall on the proper human diet spectrum—most people with chronic heartburn, their heartburn gets substantially less severe. And so we've had so many people in the private community be able to come off of these. But if they come off them too quickly, they're like, "Oh, I, I just stopped it cold turkey; I had the worst heartburn I've ever had in my life." I got back on it. Then I have to have this conversation with them: You got to do it slowly, so you don't have the rebound uh, acid reflux.
Well, do you know Dr. W. Eric Westman? Sure. So I believe he did a study—it's a bit of an older study, and I don't think enough is made of it—where they actually did aophageal probes—I think it was Eric, I hope it is—a esophageal probes, and they were measuring the acidity in the food pipe. There's not meant to be acidity in the food pipe, and they actually found that when people went on low-carb diets, they had a significant reduction in the, the acid levels of the food pipe, the esophagus, within six days. Why? And interestingly, I've actually delved into the, the mechanisms of this, and a lot of it is not so much the low-carbohydrate element, but the low-grain element. Because with the grains, you can get what we call lectin cross-linking of IG, which leads to histamine release, which leads to acid secretion. So it's actually—there is a mechanism by which grains, because they contain these uh, carbohydrate-binding proteins called lectins, that will actually specifically induce acid secretion. So it's nice, we've got the, we've got the biological mechanism, and we've got the experimental proof that when you go on a low-carb diet or you cut some of that crap out of your diet very, very rapidly, you get improvements. Yeah. And we see that all the time. One of our uh, community members has a question: What are your thoughts about the uh, PCSK9 inhibitors? In the United States, this would be Praluent and Repatha are the two most common brands, right?
Well, they're very effective at lowering cholesterol. Yeah, damned effective. Here's the thing: Is cholesterol essential for life? I don't know. Okay. Well, that's one conversation. Here's another question: Have they ever been proven to statistically significantly extend lifespan? So I ask patients—when patients come in on a drug, I like to ask them why. And they usually have no idea what I'm getting at. And I say, well, they say, well, "I'm taking it because my doctor told me to," but why? Why are you taking it? And we get there—what I want them to say is, "I'm taking it because I think it will make me healthier; I think it will help me live longer; I can enjoy a longer retirement and see the grandkids grow up. You know, I want a mortality benefit." So mortality is one of those fabulous markers that is very difficult to fudge. Even a disingenuous, dishonest researcher has a hard time saying that somebody's alive when they're under six feet of dirt. Yes. So it, it's, it's a brilliant end point because it's accurate; it's objective. So if we actually use—we don't worry about surrogate markers like cholesterol—but we say, well, you know, when we give you this drug, do you actually live longer? That's proof that that will be offering you some benefit. And to my knowledge, there's not been a single study that's proved any mortality benefit for the PCSK9 inhibitors.
Now this probably segues—if I may hijack this a little bit—into a conversation on cholesterol. And I often see this—there's two schools of thoughts in the carnivore community. Yes. One that says, "Cholesterol, it can be as high as you like; it's never going to be a problem." And there's this other school says, "Oh, I want to have a bet in each camp." Look, I don't think cholesterol is bad, but everybody else says it is, so I'm still want to take a statin and I want to lower it. And I think the truth is somewhere in the middle. Now what do I mean by that? So if you've got high cholesterol, we can determine whether you're likely to derive a mortality benefit or a survival benefit from taking a statin by looking at something called your triglyceride-to-HDL ratio. And if you got a good triglyceride-to-HDL ratio—that means low triglycerides, higher HDL—then the data very clearly indicates—and this is drug company-owned data, which in an article with Ben Bikman and um, David Diamond, we, we did a couple of years ago, we, we very clearly made this, demonstrated this using drug company-owned data—that you don't get a mortality benefit from taking a statin. So we can assess high cholesterol level. First thing to do is to assess the triglyceride-to-HDL ratio, you know. And if you've got a good ratio, then there's really no reason on God's green earth why you would need to take a statin. But that doesn't mean that the cholesterol is fine, because there are—if we actually have a look at the all-cause mortality curves, we see this little U-shape, and we know that when people's cholesterol goes too low, their chance of dying significantly increases. But also—and to a lesser degree, lower gradient, but still exists—when the cholesterol is very high, there does appear to be a statistically significant increased risk of death. Then I believe the reason for this is because cholesterol production does associate with other health-related parameters, such as nutrient deficiencies and chronic inflammation. For example, if any of your listeners out there want to do a quick uh, internet search, just type in "B12 deficiency and cholesterol," and you'll see that there's very clear evidence that B12 deficiency increases the biosynthesis of cholesterol. There's other factors that can increase cholesterol as well: a folate deficiency, what about an underactive thyroid, what about a condition we call it hemochromatosis—a genetic tendency to overabsorb iron. It doesn't have to be full-blown hemochromatosis where you've got two affected genes; you could be heterozygous and just have one affected gene that also will affect your cholesterol levels. So there's multiple aspects to health that we're starting to have more visibility of that can consequently lead to an elevated cholesterol level. So in my patients, if they're coming in with a very high cholesterol, I do two things. So first of all, we have a look at the triglyceride-to-HDL ratio; we want to determine is this atherogenic, you know, artery-clogging or non-atherogenic. And number two, I still want to find out why it's high. Is there some underlying pathology that we're missing that we, we don't have visibility of? For example, I've seen high cholesterol in people with mold exposure, you know, not what you expect. But when we actually have a look for antibodies against mold in the blood, we see that their sky high. And when we address the mold issues and we say, "Oh, okay, well, I've been exposed, you know, had a water leak in my car; I just ignored that moldy smell," get a new car, and over a period of months, the cholesterol, without doing anything else, would just come back to normal. So there's multiple possibilities, multiple potential causes for these things. And I think rather than being in one camp where saying, "Oh, all cholesterol is fine," or, you know, you know, "all cholesterol is bad; everybody needs a statin," I think the truth is somewhere closer to the middle.
Yeah, I totally agree. And can you see—I hope the viewers can see this—this concept: When a doctor's got a pill for every ill, it actually actively discourages them from looking for root causes. Because when somebody comes in with really high cholesterol, the doc—does the doctor say, "I wonder if they have undiagnosed hypothyroidism? I wonder if they have folate or B12 deficiency? I wonder if they have mold?" No. They say, "Oh, you need a statin." They put them on the statin; that's the end of the matter. None of the root causes that actually might make the patient die sooner—it never occurred to the doctor to look for any of that. He, he can fix that problem: just put them on a statin or or a PCSK9 inhibitor. Same goes for heartburn, reflux. If somebody is—if if a relatively healthy person is having reflux, it's either from their diet or they've got some underlying condition that needs to be diagnosed. But when the, when the, the physician has his prescription pad, "Oh, I'll just put you on Prilosec or Nexium. Boom, heartburn's gone. Okay, there we go; problem solved." Not, not thinking, "Maybe I need an EGD to look for a gastric ulcer? Maybe I need to look for an esophageal problem or a lower esophageal sphincter problem or any other number of problems." It just, it encourages doctors to be lazy.
I think you're right; it does lead to unthinking doctors. Yes. And, and, and the trouble is with that—so doctors are often being put up on their pedestal. You know, one thing that really annoys me is when you hear stories of these doctors—they're the kind of doctor—they got their cup on their shelf that says, "Don't confuse my medical degree for your Google search." Just, yeah. Anyway. But let's talk about a more positive example. So I had a uh, a patient who I just saw last week, and he told me a story. He had consulted previously with a doc called Bob Atkins; you may have heard of him, Dr. Atkins. And he was way ahead of his time, and he was an incredible thinker. Now we tend to think of him as being, you know, all about nutrition, protein, F-blah. I can tell you he wasn't; he was a real thinking doctor. Because this patient I was chatting to, he said, "Oh, yes, he'd done a test on me, because one of my questionnaires that I give to patients, we asked them, you know, 'Do you have amalgam fillings?'" And he said, "Yeah, I used to have amalgam fillings, but uh, you know, Bob told me about them," and uh, he underwent EDTA chelation therapy to get rid of the, the mercury toxicity that he found in his blood. And I'm sort of thinking, there you go, there's a real thinking doctor. His, his root cause—he was so far ahead of his time. And, you know, and I think you can predict that, you know, would like to hope that most doctors with visibility of nutrition and who understand the impacts of nutrition—they're just not limited to nutrition—that they're able to think about all environmental exposures and think about things across the board. And as you said, they're not just prescribing a pill; they're not just—"You've got a headache; I take—" A pet peeve of mine—well, there's two pet peeves—is menopause. And I don't know if I should say this, but menopause is the, the scapegoat used by the diagnostically incompetent. You, you have a female, "What's wrong with you?" "Oh, I, I have trouble sleeping." "It's menopause." "What's wrong with you?" "I have sweats." "Oh, it's menopause." And, and too often we use these symptoms as diagnoses when they're not—they're symptoms. So if we take sleep disturbance—a standard doctor says, "Okay, what—you have sleep disturbance?" "I have a sleeping pill." No. Sleep disturbance is a symptom; it's not a disease by itself; it's not a diagnosis by itself. Did you know that 75% of people with inflammatory bowel disease have pathological sleep disturbance? How much sleep disturbance you think people are taking these Z-class drugs for when they've actually got undiagnosed autoimmune inflammation? And it's really obvious when you think about it. So if you drink two liters of water before you go to bed, what's going to happen? You're going to get up; you're going to pee in the middle of the night; you're going to have a broken sleep. And when we actually—funny story from the Australian Institute of Sport—they were focused on, "Oh, you have to have light straw-colored urine, otherwise you're dehydrated." So they were having athletes drink so much that when they woke up in the morning, their, their urine would be light straw-colored. Now, as you know, a working kidney—the job of a kidney is to concentrate the urine. One of the first signs of a failing kidney—I do a urine osmolality test first thing in the morning—and when that starts to get dilute, that's a first sign of a failing kidney. So anyway, these athletes having terrible, terrible sleep disturbance. And then that in short order, they said, "Okay, that's a failed experiment; okay, you know, go back to not drinking before bed because, you know, you best want your sleep." But why do you wake up? Because you get this visceral stretch on your bladder; you get visceral irritation. So if you're getting any—and viscera is basically anything contained within this part of your body—so if you're getting any irritation, or that say, with inflammatory bowel disease or reflux or something like that, it is going to disturb your sleep. So when people are sort of treating sleep disturbance as a symptom and they're not thinking deeper about what the underlying cause is—those people with inflammatory bowel disease, they can do as much sleep hygiene as they want; they can wear all the bloody blue light filters and earplugs and eye masks and all that—and it's not going to help unless you deal with the root of the problem. And like yourself, I try and get to the root of the problem.
Yep. How would you recommend that a patient—I saw a question here from one of our tribe members—uh, how would you recommend a patient go about talking to their doctor if they think that they're taking prescription medications that may not be giving them any benefit? Uh, let's talk about that, and then also let's, let's segue into patient rights and, and the right, the rights that patients should have in the doctor's office.
Okay. So in terms of talking to your doctor—so doctors are evil. So I, and I've been criticized in the past, so I, I don't think doctors are deliberately making people sick. I think doctors are ignorant, for the most part. I think it's more negligence than anything else. They—so look up the list of the side effects on the medications you're taking and present them to your doctor. Your doctor may have no visibility of these side effects; they may just be blindly, you know, mindlessly prescribing them. Also, number two: Ask your doctor, "Why am I taking this drug?" All too often, I ask my patients, "Why are you on this drug?" and they can't tell me. Their doctors haven't explained to them, or it was started by an old doctor who they're no longer seeing, and their current doctor just continues on status quo. So I think those two—bring to your doctor's attention what the side effects of the drug are, and bring to your doctor's attention why you might need that drug, or more importantly, why—when you're on a healthy diet—why you may no longer need the drug. So if you used to have high blood pressure of 160, and you went on a healthy diet and your blood pressure would naturally fall to 120, if you still keep taking the drug, it'll go down to 100. So, you know, you—when you improve your physiology with diet, you're no longer the same person, and the drugs that no longer—that may not have had terrible side effects—their side effects can increase in the same way that if you have a diabetic who's injecting insulin and they go on a ketogenic or a carnivore diet, if they keep injecting that same dose of insulin, there's every chance they could enter a hypoglycemic coma, which could kill them. So, so uh, yeah, just make sure your doctor's got visibility of those two things.
Then you're talking about what rights patients have, and I think you and I are absolutely on the same page here. So in my consultations, I open my consultations by saying, "Just to let you know, you can record this consultation." Usually, there's—first time I see a patient, there's a bit of a stunned silence; it's like, "Why would I?" "Oh, okay, yes, thank you, please," because they've never been told that—in their—given permission for that—never. But I think it's really important. So I don't—I like my patients educated. This kind of, you know, if you're the patient up there who's doing your Google searching that that doctor's mug is talking about, you're my kind of patient. I want my patients empowered, and that also empowers me as a doctor. And so here's the thing: If you come in on 12 different drugs, I don't want to put my medical registration at risk by saying, "Oh, your doctor's a bit silly; I think you shouldn't be taking this drug." No. Well, I rely on something called informed consent. So if I educate you as a patient to what the science is, you are then in a position to make the decision that is right for you. That's called informed consent. You've been given all the information, and you're the only person who truly understands your particular circumstances; you make the decision right for you. So I think the number one unyielding patient right is to be provided with factual, unbiased information. Absolutely. And to not be then pressured into doing something. So as doctors, we, we gaslight our patients all the bloody time. You hear about cardiologists, "Well, if you're not going to take this statin, you're no patient of mine; you might as well die. You know, you could die at any time." We scare patients without any evidence for it. Y. So I would like to take this opportunity to encourage everybody listening to this video—from this day forward—anytime—go to a doctor's appointment—your family doctor or a specialist—I want you to pull out your, your cell phone and say, "You won't mind if I record this, doctor, because I want to listen to it later because I might miss something." I encourage all you guys to do that. And if the doctor has a problem with that—because first thing's going to happen is the doctor's going to be on much better behavior when they're being recorded; I promise you—it's just human nature; they're going to be much nicer; they're going to be much more thorough, much more complete, and they'll actually answer your questions if you're recording the conversation. But also, what's not going to happen is the gaslighting that he was just saying, because he knows he's being recorded; he's not gonna say, "Well, you'll die within a week or two if you don't take this statin," because he'll know that you could play that for who knows who. You'll play that for, right? But you're going to preface it with, "I, I, I want to listen to this because I don't want to miss anything; my health is very important, so I'm going to record this if that's okay with you." And if they have a problem with that, that's a huge red flag that you might need to find another doctor.
Absolutely. I, I, I've found my—I've not had a single bad reaction from a patient in doing this. And some patients—so what I also do is, at the conclusion of each consultation, I email the patients a complete copy of my notes. And when I order testing, I copy the patients in on those test results. So we try and have as much openness and transparency. And I say to my patients, "If you have any questions about anything that I've said, you're entitled to question why I've made that recommendation." Looks like I've just lost my camera. I can still hear you. Will—okay. Well, we'll keep going. So I, that, that was a bit distracting there. So yeah, so I tell the patients that they're entitled to question any bit of advice that I offer, and, and if I can't point to peer-reviewed science, then they should question what I'm saying. I also explain to patients that they can—the person they should trust the most is themselves. Nobody cares about them more than them. And even though I try and be an unbiased, transparent doctor, the simple fact is there's still conflicts of interest; there's still—if I tell—if I see somebody on a certain drug that I think is inappropriate, but that was prescribed by uh, a high-ranking professor at a, you know, top Sydney hospital, um, I know that if I go—if I give explicit advice and say, "Well, that's dissily," then that's not very professional, number one, and it's not necessarily good for my career. So I don't—I do not directly contradict other doctors. What I do is I say, "Here's more information; you can make your own decision." But what I recommend you do is you approach your other doctor, and in the same way that I've provided you with evidence of a certain effect, I'd like you to approach this other doctor and request that they provide you with evidence to support their basis for their strategy. Nobody—no other doctor has ever taken the patients up on that.
That's a brilliant strategy. Here in the United States, we're very good at getting informed consent for any surgical procedure, even a minor surgical procedure—an excision of a mole or implantation of a, of a birth control device—but when it comes to prescribing pharmaceuticals and then also vaccines, we are terrible at giving and getting informed consent. So doctors will say something about a statin drug—Zocor, Lipitor, Crestor—"Well, you just need to take this; you, you just need to listen to me." Uh, that's not informed consent; that's not even close to informed consent. And so I, I don't know what the solution to this is. I love your solution—have the patient record the conversation and ask as many questions as they can—but many doctors are just not going to allow that, and they don't want to—they don't want to be required to give informed consent when it comes to pharmaceuticals. And I, I can hear the argument, "Oh, it would take—this person's on 15 medications; it would take me an hour and a half to get informed consent on each one." Then maybe you should revisit that medication list, doctor, and get them off some of those medications, right? Uh, but that's a huge problem in the United States. I'm not sure how it is in Australia. Do you have to get informed consent before prescribing a pharmaceutical, or can you just say, "Here, you need this; take this?" I don't do a hell of a lot of prescribing, but, but we—I don't think we have enough of a focus on informed consent. All too often, I see patients, and they have side effects from a drug, and I say, "Did you know this drug causes this side effect?" "No." "What about this side effect? What about this drug? What about this drug?" And it's complete ignorance. So one can only assume whether or not there's a requirement for informed consent. I think it's fair to say that it, that that standard is not met in day-to-day practice, not routinely anyway.
I totally agree. One final question that I want—I want to ask you—I, I'm a primary care physician. One of the things I'm looking for when I see patients is signal. I'm looking for signal. So when I used to tell people who are overweight and had type 2 diabetes, "Hey, join the gym and join Weight Watchers; that's what you need—need to do," when they would come back in three months or six months, I would see zero signal that that had helped them at all. And so I became completely disillusioned with recommending diet and exercise because it didn't ever help, right? So one thing I—one signal I keep hearing from the carnivore community—and I've actually experienced this myself—so full disclosure—is that back when I was eating the diet filled with vegetable seed oils and grains and junk, I was almost allergic to, to the sun. If I were—if I was out in the sun—I'm very fair, Northern latitude DNA—I would burn within 10 minutes, especially at the beach in just full sunlight in the summer—10 minutes, I was going to have a sunburn. And now, since I've been a carnivore, I can stay in the sun three or four times longer without getting a sunburn. And also, I can actually get a tan now. As you can tell, I'm quite ruddy; I've, I've been ruddy all my life; that's my, my heritage, my DNA. So don't make fun of my skin color; it's insensitive. But I can actually get a tan now, whereas before I could not get a tan at all. Do you have an explanation—a physiological explanation? Really interesting. Phytoplankton—500 million years old—they're very vulnerable to the UVB radiation, which, which is just the right wavelength to damage DNA. So they actually synthesize vitamin D, and the vitamin D molecule is just the right size molecule to absorb the wavelength of UVB radiation and protect phytoplankton from the damage. So basically, vitamin—
Vitamin D throughout history has had a role as a sunscreen, and it appears to be that in humans today we still have that role. So, why do people with dark skin not secrete much vitamin D on exposure to the sun? Because the melanin serves the same purpose as the vitamin D, absorbing the UVB wavelengths and protecting their skin; they don't need to secrete much vitamin D. Why do pale-skinned people secrete vitamin D? Well, because we need to; otherwise, we will burn. But it's only from the UVB radiation, which is more found when the sun is closer to being overhead. Because of the wavelength of UV, it's uh, it gets attenuated when the sun's coming in on an angle; it gets attenuated through the thicker, massive atmosphere that it has to pass through. So UVB is actually absolutely associated with skin cancers and I don't believe offers any major benefits.
Now, the interesting thing is that what's vitamin D made from? What's the substrate for it? It's cholesterol. Yeah, so if you're having a whole lot of seed oils and stuff like that, that will affect your normal biological functioning of cholesterol, then you won't be able to produce as much vitamin D. You will burn much easier. Ancel Keys, he actually did a study, and they actually, people in England looking at uh how much time they were exposed to the sun, and they found that when you were exposed to more sun, your cholesterol level actually fell. Why? Because the cholesterol was then needed to synthesize vitamin D. So it's actually the ability to synthesize vitamin D from cholesterol which can actually improve your natural protection from the sun.
Then the question is, do you actually need to be exposed to the sun for vitamin D levels? And historically, not well. The Inuit, they never had low vitamin D levels, did they? Because vitamin D, being a fat-soluble vitamin, is in food. So if you're eating, you know, whale blubber and all these other foods, seafoods that are very rich in saturated fat, you're also getting all the vitamin D you need there. So in a natural diet, we can actually get all the vitamin D we need, and our modern diet is so far removed; the standard American and Australian diets are so far removed from what is an appropriate diet that we now consider you can't get vitamin D from diet. Well, you can't get it from a modern diet, but you can get it from a proper human diet, absolutely.
Now, the other interesting thing is that the vitamin D level in your blood, the reason it associates with health is because, remember, we said it's fat-soluble. So if you're big and fat, you've got this massive reservoir or sink for vitamin D, and it will actually absorb the vitamin D from your blood, leading to lower levels of vitamin D in the blood. And this has been shown by research that when we give people vitamin D supplements or expose them to UV radiation, that if they're overweight, their level, the vitamin D levels in their blood don't increase by as much because a lot of the vitamin D is taken up in fat stores. And that's the connection between metabolic health and lower vitamin D levels. So, one, you can get all the vitamin D you need from a healthy diet. Number two, if you're overweight, your vitamin D level will read lower, but that's a correlation and not a causation.
Now, one other thing is, this is not me saying I don't think sunlight is healthy. Sunlight is incredibly healthy because there's another UV that we get called UVA, and that stimulates the release of something called nitric oxide, which has been shown to lower blood pressure. It also lowers Hb1c; UVA exposure lowers the level of glycated hemoglobin. Um, so UVA does a lot of good things, and you get exposed predominantly to UVA when the sun is passing through a thick, massive atmosphere; it's coming in on an angle. And that's because UVA is a longer wavelength; it doesn't get attenuated the same as the shorter wavelength UVB does. So if you have a look at your shadow, uh, that will give you an idea of how the angle the sun's coming in; if your shadow's at least as tall as you are, you're getting predominant UVA exposure with less UVB exposure; you're generating the nitric oxide, which is why people, even people with skin cancer, they've actually been shown, for squamous cell carcinoma and basal cell carcinoma, to live longer, almost 10 years longer. The magnitude of effect of exposure to sun in terms of life mortality benefit is equivalent in reverse to the magnitude of detriment that you have when you're a smoker; it is absolutely huge. Population-based data shows that people with squamous cell carcinomas and basal cell carcinomas live longer, and I believe the reason for that is because sure they're getting skin cancer from UVB damage, but they're getting the UVA, the nitric oxide exposure, which is hugely important to health; it's got immune regulation properties, blood vasoactive properties, so on and so forth.
So, in my world, the, to get the best of both worlds is to expose yourself to the sun when you're getting predominantly UVA. You reduce your risk of uh getting sunburn and skin damage from UVB radiation, and if you've got high cholesterol levels and you're on a healthy diet and you're producing a good amount of vitamin D, that will provide another layer of protection from the UVB radiation. So yeah, that would be my take on it. I love it; I love it, Dr. Paul Mason. Thank you so much for doing this; it's always a pleasure chatting with you. Tell, tell people watching where they can find you if they really resonated with your message. Well, I, I do a few lectures from, from time to time, and they go on to the Low Carb Down Under YouTube channel, which, and you've got videos on there too, I believe. So I'm in illustrious company. Um, I've got a Twitter handle, and from time to time when I have the chance, I'll uh, I'll do a bit of tweeting, uh, but for the most part, uh, it's a Low Carb Down Under YouTube channel, and uh, I'm hoping that I uh, in future, I can be a guest on your show again. Hey, I think we need to do round three in the near future. Thank you so much, Dr. Mason. Have a good day. Please; all thank you so much, so.