Dustin Rudolph, PharmD, is a repeat guest on the podcast. As one of the only pharmacists in the world who favors a plant-based treatment approach, he shared his “coming of age” story and his take on the world of doctors, drugs, and health care.
Today he's back to talk about two specific conditions: high blood pressure (hypertension) and type 2 (insulin resistant) diabetes.
Both are epidemics in the US (and increasingly around the world), with two-thirds of Americans diabetic or prediabetic, and roughly half of us hypertensive or prehypertensive.
So combined, these two conditions afflict 133% of us. (Or is that not how statistics works?)
For each condition, we talked about the classes of pharmaceutical treatments, their mechanisms of action, their effectiveness, and their safety. We also covered root causes, as well as the effects of appropriate diet and lifestyle modifications.
- hypertension as a “silent” killer (no physical symptoms like a toothache)
- how hypertension compromises health
- the “water pills”
- the crucial and not-at-all-understood-by-doctors difference between relative and absolute risk, and why it matters so much
- the ACE inhibitors and ARBs – and why doctors choose one over the other
- the fact that angioedema, which is potentially life-threatening, is considered an “extremely rare” side effect, yet occurs about as third as often as a beneficial outcome (that's relative risk messing with our minds again)
- how calcium channel blockers work, and why they need to “fight” against the muscles' natural role
- when beta blockers might be a good idea
- Dr McDougall's blood pressure reductions in hypertensive patients through a low-fat, whole food, plant-based diet
- Dr Goldhamer's startling results using water-only fasting followed by a plant-based diet
- the true cause of type 2 diabetes – intramyocellular fat – and how doctors and pharmacists have never been told this (and have never thought to ask)
- insulin sensitizers
- drugs to delay carbohydrate absorption (and their very unpleasant side effects)
- liver glycogen inhibitors
- how the fancy new drugs (Farxiga and Jardiance) work, and why they're probably a terrible idea
- “looking for diabetes management under the lamppost” – treating what we can test easily rather than what matters
- metformin, the best of the bunch (with a 5-10% rate of risk reduction over 10 years)
- the power of exogenous insulin (to reduce A1C by about 3%)
- Dr Barnard's studies proving that type 2 diabetes can be reversed through diet
- the surprisingly high compliance rates of patients on a “restrictive” diet, and why
- and much more…
Enjoy, add your voice to the conversation via the comment box below, and please share – that's how we spread our message and spread our roots.
The Empty Medicine Cabinet on amazon
HOWARD: So, my consulting practice helps people make informed decisions about their health care. I do research for them and with them, and show them how to understand it. And we look at drugs, surgeries, lifestyle changes, alternatives, and with all the evidence of risk and benefit, they make up their minds. That's the easy part.
The harder part is helping people change their habits, change their behaviors, adopt a plant-based lifestyle, start exercising, do stress reduction, get some cognitive-behavioral therapy, change their thinking, that sort of thing.
But, I wasn't prepared for the really hard part, which is getting people to talk to their doctors in an assertive way and say, “I don't think I should be on this med. I don't think this is helping me. I've looked at the research.”
They can do the research. They can understand the research. They can make the decision. And yet they're scared of having this conversation with an authority figure. That's why I wanted to bring back a second-time Plant Yourself Podcast guest, Dustin Rudolph, the Plant-based Pharmacist, author of The Empty Medicine Cabinet.
We talked before, in general, about the relationship between pharmaceuticals and disease and diet and disease. And I want to talk to him about 2 of the most common conditions that I see in my practice: hypertension and type 2 diabetes. So, for each of these conditions, we talked about the different classes of pharmaceutical treatments, their mechanisms of action, their effectiveness, and their safety.
And, I think, if you have type 2 diabetes and/or hypertension, or you know someone who does, this conversation can help shake you loose, a little bit, from thinking that these meds are always and definitely necessary. So, without further ado, Dustin Rudolph, welcome back to the Plant Yourself Podcast.
DUSTIN RUDOLPH: Well, thanks for having me. It was a joy being on the first time.
HOWARD: Yeah, well, now I've got more specific questions. You know, you sent me your book. I read through it. I've been doing a lot of other studying. And today I wanted to talk with you about 2 common conditions: high blood pressure and type 2 diabetes.
So, first of all, let's give us a sense of, like, how prevalent these are, you know, in your practice and in your reading. Like, how big a deal are these 2, respectively, in the United States?
DUSTIN: Well, they definitely are 2 of the most common chronic medical conditions that are out there. Hypertension, or high blood pressure, is very common, actually. Up to about 30% or about 1/3 of people have high blood pressure, diagnosed high blood pressure.
And then about another 35%, 36%, 37% have a condition known as pre-hypertension, which is, kind of, you don't have normal blood pressure, but you don't officially have high blood pressure. You're, kind of, in that gray zone in between.
So, you know, if you put those 2 numbers together, you're looking at, you know, 65-70% of people out in the United States there have high blood pressure or pre-hypertension. So, that's, you know, 2 out of every 3 people, basically. That's an enormous amount. And the same really goes for diabetes.
And as the obesity epidemic rises, so does our diabetes epidemic.
And right now, well, the latest data that I have is official data from 2012, and there's 29 million people that were diagnosed with diabetes in the United States. It's about 9% of the population.
And there's a condition known as (kind of like blood pressure with pre-hypertension), there's a condition known as pre-diabetes. So, you're not officially diabetic, but you're, kind of, on your way. And 86 million people have pre-diabetes.
That's about 37% of adults. So, that's roughly, you know, (if you look at those 2 numbers), that's about 45-50% of the US population that has diabetes or pre-diabetes.
So, if you really look at these things, 2 out of every 3 adults have some form of high blood pressure or blood pressure problem, and about half of Americans have some sort of diabetes or irregular blood glucose problem. And that's just an enormous amount of the population.
HOWARD: Wow, so that's pretty much all - everyone knows a bunch of people who are at risk here.
DUSTIN: Yeah, absolutely, if not so themselves.
HOWARD: Sure. All right, so, let's take them one at a time. I think that would be the easiest way to navigate. Let's start with hypertension. First of all, it's a number. It's not a condition. It's not a disease. I mean, what's the big deal if people have high blood pressure?
DUSTIN: Yeah, I really call it, like, a silent killer, a silent medical condition. Because nobody really goes about their day and goes, “My, I have high blood pressure. I can feel it. Like, I know exactly what my numbers are.”
You actually have to measure it, you know. Because people can't feel it. It's not like having a headache or a toothache or something like that. You can't feel what your high blood pressure, what your numbers are. So, high blood pressure's, basically, just a high amount of pressure forced against your artery walls as your heart pumps.
And there's supposed to be a normal pressure there of about 120/80 or less. And so, high blood pressure is just anything elevated above that. You know - a little bit elevated above that: pre-hypertension or pre-high blood pressure - And then, about 140/90 is where they officially diagnose you.
If you're that or above, that's high blood pressure - officially high blood pressure.
And then the reason why that's important is because, if you have pressures that are elevated (with your blood pressure readings) for, you know, more than just that one single moment, but over a period of time (days, weeks, months, years, decades), then that road puts you at risk for a lot of different things.
And one of the most scariest things is strokes. Those who have really high blood pressure are most at risk for strokes and heart attacks, but especially strokes. And when you have a stroke, some people die immediately. They don't even make it to the hospital.
Some people who do make it to the hospital (make it through it) are now disabled. They have to learn how to talk again. They may even have to learn how to walk again, how to dress themselves, all this stuff.
Because, the stroke, you know, reduces the amount or stops the blood flow to their brain - parts of their brain - and then they have, you know - Your brain affects your whole body.
So, there's heart attacks, strokes, anything, basically, any of the organs that get a blood supply, which is basically all your major organs.
If there's high blood pressure, that can lead to organ damage. So, you know, your eyes - you can go blind or partially blind, if you don't get the right blood flow or you have problems with high blood pressure.
Your brain - you can get dementia. Your heart can fail. You can get peripheral vascular disease, where you have blood flow problems in your extremities, especially your legs. You can, you know, like I say, you can get strokes, your kidneys can fail, eventually, because you're putting a lot of stress on your kidneys.
There's a lot of different things that can go wrong if you have high blood pressure for a long period of time.
HOWARD: Gotcha. So, one of the debates, I guess, is between, sort of, a medical approach and a lifestyle approach is really looking at, like, what's - Is high blood pressure itself the disease or is it a symptom?
You know, is it a marker for the other things that are going wrong? Does the high blood pressure itself contribute?
DUSTIN: Well, I call it a symptom, because, you know, with a lot of these diseases,
what I care about, and what I think most patients care about is are you going to die, or are you going to have some kind of disability hamper you in your lifestyle that impedes you, you know, to live a long, healthy life?
People don't want to be disabled and they don't want to die. And so, really, high blood pressure, like I said, is a silent killer, because you can't exactly feel that (unless it's a rare case and it's so high that it's causing headaches and all kinds of other stuff going on).
But, for the most part, people can't feel high blood pressure. So, it's really a warning sign, or a symptom of a failing cardiovascular system, of a heart system, a cardiovascular circulatory system that has a lot of work load on it that has really been induced by our diet and our lifestyle, and it can't keep up with that.
So, I call it a symptom.
I mean, some people might, you know, call it a disease out there, but I really think that it is a symptom. And, if you can get on top of it (if you can get on top of the symptom), you won't end up with heart disease or with stokes or with some of these other, you know, target end organ damages like kidney disease or blindness or all these other effects.
So, I call it a symptom (a red flag).
HOWARD: A red flag. OK, which brings us to, you know, your area of expertise, pharmacology. So, that there's a whole bunch - there's a bunch of different classes of drugs that are out there to treat high blood pressure.
And the question is if the cause is an overworked cardiovascular system due to diet and lifestyle, do these drugs address that cause? Do they simply lower blood pressure in some other way?
And how effective are they both in lowering blood pressure and in the outcomes that you say people care about (which is not to be disabled, not to die young)?
DUSTIN RUDOLPH: Well, the medications are there, and they are an option. And what I always try to tell people is that, you know, I'm not here to tell you to take a medication or not take a medication.
I'm not here to tell you to eat a certain way or not eat a certain way. I think the important thing is to, you know, properly educate and inform our patients, you know, how the medications work, how, you know, maybe diet and lifestyle work.
And then that way, when you can see the effectiveness or how these approaches work, you can make that decision on which path you take, or if you want to use both of them or just one or the other or whatever you choose.
And when it comes to medications to treat high blood pressure or hypertension, you know, the medications for this medical condition are much like the medications for many medical - chronic medical conditions and chronic diseases.
They're there to help you manage the disease. So, the key word is manage. And manage the disease means that you still have the disease. You're going to have to take these medications for the rest of your life, but it will help you prevent, hopefully, you know, death or disability, and it will help you manage your blood pressure numbers, so to speak, if you choose to take this approach.
There are quite a few drug classes that are used to treat high blood pressure. There's probably at least 10 or 12 of them, but there's really only 4 or 5 main ones (of classes of drugs) that they use to treat high blood pressure.
And I'll, kind of, run through them here, because you had asked, like, how effective are these drugs.
HOWARD: Sure, yeah, let's go through the classes and then talk about each one.
DUSTIN: OK, so, the first one is the one - it's called thiazide diuretics (thiazide type diuretics). So that includes, some people might have heard of hydrochlorothiazide or the abbreviation for it is HCTZ. Another medication in that group is chlorthalidone.
And there's chlorothiazide. There's metolazone. There's a couple other medications in this group. But hydrochlorothiazide is the most common one that's used in the United States, and prescribed in the United States.
And these drugs - they're diuretics, so they're basically - some people will just call them their water pill. Sometimes patients don't actually know the names of their drugs that they're on, but they know they're on a water pill, you know, for their blood pressure.
And, basically, what they do is they just, they work in the kidney to help you excrete more sodium and more water. Now, wherever sodium goes, water follows. So, basically, in your kidney, these drugs help take sodium out of your blood, you know.
And your blood flow goes to your kidney, and then it filters out water and toxic waste and electrolytes and stuff like that. And then it reabsorbs some of that back into the bloodstream, so that you don't lose everything. Because if you filtered out all of your water in your blood, you would have no volume left in your blood. So, you do need to reabsorb some of it.
So the thought is, if you give a diuretic to lose extra water out of your blood supply, then that's less volume of blood that your heart has to pump around, and that should lower the pressure, which it does. So, that's how these things work.
That's how this class of medication works.
And, whenever I look at success rates for any medication (whether it's a blood pressure pill or a diabetic pill or whatever medication it is), I always try to find, if I can, the absolute risk reduction instead of the relative risk reduction.
HOWARD: Oh, you just made me shiver. This is one of the drums that I beat all the time, so let's talk about that. What's the difference and why is it so important?
DUSTIN: OK. So, relative risk reduction is what you see on TV advertisements and magazine ads and radio ads. It's somebody coming on and saying, “This new drug to treat your high blood pressure will, you know, lower your chances of a heart attack by, you know, 30% or 40%”, or, “This statin medication will lower your cholesterol and lower your chance of death by, you know, 45%”. So, that's relative risk reduction.
Absolute risk reduction is getting down to the raw data. So, what I like to explain is, if I come up with a new drug (a new thing - a blood pressure drug), first of all, I have to do clinical trials.
Because I have to submit this to the FDA so that they can approve my drug so that I can sell my drug.
So, I'm going to get a bunch of people rounded up, and I'm going to put them on my new drug for blood pressure. And I'm going to split these people up into a couple different groups.
So, one group is going to get the drug. And one group is not going to get the drug. They're going to get, like, a sugar pill or a placebo.
And then I'm going to follow them for, let's say - I don't know - a year or 5 years, or whatever it is – whatever the study year period is. And I'm going to follow them for that long.
And then I'm going to see, in the group that got my drug, you know, how many people, you know, suffered a stroke, or cardiovascular related death, and then in the placebo group, how many people suffered a stroke, or cardiovascular related death.
And, after that 5 years, let's say there was 2 people out of 100 in the group that took my drug that had a heart attack or a stroke, and in the placebo group, there was 4 people out of 100 that had a heart attack or a stroke.
So, you can see that the drug did work, because there were only 2 people in my group with the drug that had a problem and 4 people in the placebo group who had a problem.
So, a relative risk reduction is 50% drop in heart attacks and strokes by taking the drug. And how they get that is, you know - they take 2 - and 2 is half of 4 - so 2 is half of 4 - that's 50%.
But the problem is, in that particular example, there's 200 people in the study, because there's 100 people in each group. So, if you forget about 194 people (you only look at the 6 people who had a problem in the study - who had a heart attack or a stroke), then you actually get a 50% reduction in heart attacks and strokes by taking this drug.
The absolute risk reduction is taking all 200 people into account for the study.
So, if you take everybody into account, the drop was really only from 4% (in the one group) that had a heart attack or stroke, to 2% (in the drug group) that had a heart attack or stroke.
So, you really only have a 2% drop in heart attacks and strokes. So, that's why it's important to understand where these numbers come from and what's being reported.
So, what you usually see in advertisements on TV and the radio and stuff is relative risk reduction. It's that 50% reduction, or 40% reduction. But when it comes to absolute risk reduction, usually it's very small. And, when it comes to absolute risk reduction - when it comes to the thiazide diuretic - it's about a 3% reduction in cardiovascular death rate on average when they tested these. They tested chlorthalidone out of this group, and that was over about a 14 year period.
So, you know, do the drugs work? Yes. They definitely work, but, you know, you get about a 3% benefit over about a 14 year period.
And I don't think a lot of people would realize that they're only getting a 3% benefit.
HOWARD: Right, now a 3% benefit might be fine, if there was no down side, right?
DUSTIN: Right. And it would be fine if you knew, if you absolutely knew, that you were going to be in that 3%. But you don't know.
So, you don't know if you're going to be in the 3%. And there's - like with any drugs, there's always side effects. So, with the thiazides, they're actually one of the more safer classes of drugs to take for blood pressure.
But they can still cause, you know, electrolyte disturbances. So, they cause low potassium levels, low sodium levels. They can actually cause high calcium levels. And they can also raise your blood sugar. And, if you have gout, they can increase the risk of gout attacks.
And they've even been shown to increase cholesterol levels and possibly cause erectile dysfunction.
So, probably the most common with those are the electrolyte disturbances. But, you know, if you're a diabetic or if you have gout or problems with your cholesterol already,you know, there's other concerns and other side effects too, with these drugs.
HOWARD: And, just thinking about it, so now, if I've removed water from my blood, my blood's a teeny bit sludgier, isn't it?
DUSTIN: It is sludgier. So, yeah, it is. Now, if you have high blood pressure, and you have an overload of fluid anyway, that your heart's trying to pump out, you know, having less fluid is probably better for you. But, you know, you do run into these other problems. Maybe your cholesterol level goes up a little bit, or now you have erectile dysfunction because your blood flow is altered, as well, down there, if you're a man. So, you know, it's a balancing act.
Are you going to have all of these side effects? No, not everybody has all of these side effects, but some people do. And, you don't get all of the side effects, but some people get more than one.
It's just like anything. You don't know which side effects you're going to get, and you don't know if you're going to be in that 3% that benefit from the drug.
HOWARD: Gotcha. So, before we move on, I have a question. So, I talk to my clients about this stuff sometimes, and I'll mention - like, they all hear, you know - They're all on Lipitor or another statin, and they're all told, you know, “This will reduce your risk of a heart attack or stroke by 36%”. And they're all told that by their doctors. And so, obviously, they're (the medical profession) is trained to speak in terms of relative risk.
As a pharmacist, were you trained to think in terms of absolute risk or relative risk?
DUSTIN: No, it was usually relative risk. It was usually always relative risk. That's what we hear, usually, when we're looking at these studies. The studies almost always report relative risk.
Sometimes it's very, very hard to find studies that report absolute risk.
And then, if they don't report absolute risk, you as the pharmacist or doctor or researcher have to go in and dig through the whole study, and try to find all the raw data and calculate it out yourself.
And sometimes the raw data's provided and sometimes the raw data's not provided at all. So, there's no way to even get the absolute risk reduction. So, it is kind of a balance, a tricky thing, a tricky subject to go at.
HOWARD: So, am I being cynical in thinking that this is all because it's better for marketing? Or is there anyone (any statistician out there) who would argue that relative risk is a useful metric?
DUSTIN: Well, I think it's probably due to marketing. I mean, it's a lot easier to market a drug when you say it's 40% effective as opposed to 3%, you know.
So, I think it comes down to marketing. Now, I don't sit around and do statistics all day. You know, I'm not in the research lab, so I don't know if there's a benefit somewhere, somehow, to a relative risk reduction in certain cases or not.
But, if it were up to me, the only thing that I really care about is absolute risk reduction.
HOWARD: Gotcha. OK. So, we’ve talked about diuretics. What's another common class?
DUSTIN: So, the next one - there's actually 2 classes - and I group them together. They're called the angiotensin converting enzyme inhibitors or ACE inhibitors.
And that's like the Lisinopril, Enalapril, Zanipril, Quinapril, Captopril, all the prils.
And then there is the angiotensin receptor blockers, and those are all the sartans (so, like Valsartan, Losartan, Candesartan, Olmesartan).
And, basically, these 2 classes of drugs - they're not normally used together - meaning that a patient would not normally be on both of them together, but it's not an impossible thing either. I have seen rare instances where a doctor will put them on both together, but most of the time a patient is put on one or the other.
And usually you start on an ACE inhibitor. And how these drugs work is, basically, they dilate the blood vessels, or the arteries. And by dilating and making the blood vessels bigger, you give more area for the blood to flow through, and less resistance.
So, if there's more area for the blood to flow through and less resistance, your blood pressure would naturally - it would come down.
And now the ACE inhibitors are usually (They're the older class, so they've been around longer.) - and that's usually what somebody gets started on.
So, the problem with these drugs (this ACE inhibitor class of drugs), is that about 10 or 20% of people who start on one of these drugs will get a really dry, hacky, just annoying cough that doesn't go away. And it's a side effect of the drug.
And, if you get that, you're probably going to have to stop the ACE inhibitor. And then your doctor would switch you to the angiotensin receptor blocker (the ARB class of drugs). That's the sartans. Because they, basically, they work the same way.
So, the ARBs also dilate the blood vessels (the arterioles). And they reduce the resistance, increase the area for the blood to flow through in the blood vessels.
And they work closely with the kidney. 7
So, the ARBs - you don't get the cough with them. But both of these drug classes can cause other things that happen. A rare side effect is angioedema. You've got to be real careful with that.
That's where, basically, your face, your lips, your tongue, everything swells. It's almost like an allergic reaction. And it can be life threatening. So, it's very rare that that would happen (usually less than 1% of people), but if it happens, you need to get to the ER right away, because it's life threatening.
But these drugs, as far as their success rates go, you're looking at about the same, you know, about 1 to 2, 2½% of people actually reduce their risk of death or hospitalization or chance of having a stroke. And that's absolute risk reduction.
And they haven't studied these over as long of a period of time as the diuretics.
Remember, thiazide diuretics - that absolute risk reduction of 3% - was over 14 years. These drugs, they've studied for a less amount of time, so they've put them in a study for, like, 4 or 5 years, and they found that you get about a 1 or 2% reduction in death rates or disability from hypertension.
HOWARD: So, that's not a lot different than the rate of what you call a very rare event, the angioedema, - right? - at 1%?
HOWARD: So, the very, very rare thing is about half the rate of the thing you're hoping for.
DUSTIN: Right, exactly. And these drugs, in particular - they're used - they can be useful in specific populations, like people with diabetes or heart disease, because in diabetics it kind of helps protect the kidney a little bit.
And one of the complications of diabetes is that you get kidney disease, and your kidneys eventually will fail. And, so, these drugs have been shown to, you know, prolong or delay that from happening and help your kidneys out.
And then in heart failure, it's actually been shown to help reduce death rates over the long period of time with heart failure. And it helps remodel and fix some of that broken cardiac tissue that surrounds your heart - your heart muscle.
HOWARD: So, it sounds like the appropriate med works best in extreme populations, right?
DUSTIN: Yeah, yeah, or for people, I guess, who, I mean, I always, kind of, tell people you, basically, you have, you know, 3 or 4 choices within each disease, and one of those choices is to do nothing, and one of those choices is to go the conventional route and use pills and procedures and surgeries, and then the other choice is, basically, to make diet and lifestyle changes.
So, I guess it would be better than doing nothing, and staying on the standard American diet and not doing anything, but it's certainly not nearly as good as making diet and lifestyle changes.
HOWARD: Right. Ok. So, I'm a fairly simple person when it comes to understanding the ins and outs of biology, but, when I think of, like, blood flow, I think of, like, fluid dynamics.
So, I think about, like, a river that is narrow, and the water's rushing rapidly, and then it opens up. And it looks to me like the water starts going much slower. So, are these ACE inhibitors and angiotensin receptor blockers - aren't they slowing the blood down by dilating the vessels?
DUSTIN: Well, not really, because your heart was - in a normal person you would pump about 5 liters around your whole body. And that's every minute.
So, you're not necessarily reducing the amount of blood that's flowing around your entire body and getting around there. You're just making it so that it's less work on your heart and less taxing on your blood vessel walls, because you're dilating them. So, they have less pressure to work against - you know, less force against the blood vessel walls.
And, just like anything, if you picture a – what's a good example? – maybe a, not like a garden hose, but, I guess, if you had, like, one of those animal balloons, those skinny balloons. And you're trying to flow water through it.
And, well, if you have more blood - if you have more blood volume trying to go in the same space, it's going to weaken the walls, you know, because you've got so much blood volume. So, that's where the diuretics come in.
Now, if you help, kind of, loosen up those walls and dilate them a little bit, and have less pressure (like with the ACE inhibitors or the ARBs), now you have less pressure and less force exerted against those walls.
So, they're not going to wear down as quickly, I guess, you could say, over time. But you're still bringing the same amount of blood through, because it's a closed system. Like, in a river, it's usually an open system.
You know, you're going from the top of the mountain, basically, down into the oceans, where it's just open everywhere. And in the body you're, kind of, working with a closed system, you know.
You're pumping water around a closed system, 'cause the beginning and the end are the same. It just flows in a big circle.
HOWARD: Got it. So, but before we go onto the next class, so, if we're back to the animal balloon, the people who don't have high blood pressure, is it because their blood vessels are always dilated, or because they manage to pull - they don't have excess water?
Like, what's the root cause of the condition?
DUSTIN: Well, it's usually our diet - our diet and our lifestyle. So, it's when years of abuse by, basically, the foods that we eat is very hard on the cardiovascular system.
And the reason why is because, you know, we eat a very high fat, rich diet that's, you know, a lot of fat, a lot of sugar, a lot of oil, and that leads to atherosclerosis, or the lining of the blood vessels of these plaques and these cholesterol, and all this, you know, crap, basically, that shouldn't be in our blood vessels, clogging up the system.
So, whenever you do that, and you have these plaques that line the blood vessels, it starts to make the blood vessels (the walls of the blood vessels) very firm. And they're supposed to be flexible and able to expand and contract, as needed, you know.
Like, a normal person who doesn't have heart disease or high blood pressure, it's supposed to expand and contract on these blood vessel walls so that it can absorb any extra pressure or not.
You know, like, when you go exercise, you're going to have more pressure against those walls, so your blood vessel walls need to be able to relax and expand.
And in the person with high blood pressure, or a person with heart disease, now you have blood vessels walls that are not elastic and are not able to expand and contract as good as they want to. And they're firm and they're rigid. And so, they just, kind of, stay there and they don't move as much.
And so then, you have this force exerted against them, like, you know, if you're up and walking around, or exercising, or just going about your life, the more activity you do, the more that the blood pressure goes up, as compared to just laying in bed.
If you're just laying in bed, it's going to be very low pressure, but once you get up and even walk around the house, your heart has to pump that around and get that blood around. So, if you have firm blood vessel walls, now you've just compounded the situation. You know, now you are at risk for that high blood pressure. And that's from eating all those high fat foods, and meat and dairy that's full of fat, and oils.
And it just lines those blood vessels. It makes them very rigid – the walls of them very rigid.
HOWARD: So, therefore, then the ACE inhibitors and the ARBs are just trying to, sort of, relax those rigid muscles? So, they still, they can't still move in and out, because they're sort of calcified, right? They're encrusted? But at least they're a little bit bigger. They're now stuck in a relaxed state rather than a constricted state?
DUSTIN: Well, they try to undo the damage that we did to them. Now, you know, they can work a little bit. They, you know, the average (Let me find the average. I think I have the average right in front of me here - how much they actually lower your blood pressure.)
Like, the diuretics will lower it about, on average, about 13 over 6, with your numbers. And ACE and ARBs: ACE inhibitors will lower your blood pressure about 5 over 2. And then ARBs will lower it about 8 over 5. So, when I mean 8 over 5, its 8 drops your first number (your systolic number) by 8 points and your bottom number by 5 points for the ARBs.
I mean it does work a little bit, but, you know, there's a lot of years of abuse to your blood pressure, or your blood vessels, that it has to overcome and medication can only do so much.
HOWARD: Right. All right. So, let's maybe let's cover one more class and then move on to type II diabetes?
DUSTIN: Yeah, so, the 4th choice would be calcium channel blockers. And those are, like, Amlodipine, Diltiazem, Verapamil, Nifedipine, Nisoldipine.
Maybe some people have heard of those drugs. And, basically, what these drugs do is they're calcium channel blockers. So, they block calcium from moving, you know, in and out of the cell like it needs to.
And the reason why that's important is because your cells (your muscle cells, including your cells that line the walls of your blood vessels, which are smooth muscle cells, and the muscle cells in your heart, which are cardiac muscle cells) - all of those muscle cells need calcium in them to help contract the muscle.
So, if you don't have a nice influx and eflux of calcium in and out of the cells to help you contract and relax your muscles, then the muscles don't work very well. And what these do is - calcium channel blockers - so they block, not all of the calcium, but some of the calcium from, you know, going inside the cell where it needs to be.
Now, when that happens, if you don't have calcium inside your muscle cells, then the muscles can't contract and they can't work properly. So then, again, the thought is, if you prevent calcium from going into the cells so that your muscles can't contract, then they'll stay dilated.
Those smooth muscles around your blood vessels will stay dilated and loosened up a little bit so that it helps your blood vessels stay bigger. So, it will reduce the resistance that the blood has to flow against and be easier on your heart that way. And that's basically how these work.
Success rates are about the same. You know, you're getting about 1½ to 3% success rates in reducing strokes. And that's over about a 5 year period. So you're getting about the same success rates.
HOWARD: Gotcha, you know, you said that the muscles of the heart and the blood vessels need calcium to work properly. So, you're taking a drug that prevents your muscles from working properly.
DUSTIN: Exactly. You're trying to keep your muscles in a more relaxed state so that they don't contract and constrict. 'Cause that's the problem with your blood vessels, is they're stiff and they're constricted, and that forces more resistance against blood flow.
So you want to try to undo that process.
HOWARD: Gotcha. So are there any down sides to the calcium channel blockers?
DUSTIN: Yes, and actually one of the down sides with these drugs is that - and each - There's different nuances with them. 'Cause there's some, like Diltiazem and Verapamil, that are considered like a subclass of calcium channel blockers. Those are non-dihydropyridine.
And then there's the dihydropyridine portion of the calcium channel blocker. That's like Amlodipine and Isradipine (all the pines). And the Diltiazem and the Verapamil - you can't use those in people who have heart failure. 'Cause it can make their heart failure worse. You want to be very careful on who you use these in.
And then Verapamil can also cause constipation. And that's specific to Verapamil that can cause constipation.
Some of the other calcium channel blockers, like the dihydropyridine (Amlodipine - that's the most common one - you know, Norvasc), those can usually cause low blood pressure. Sometimes it can drop too low, and they'll have low blood pressure. So, they get dizzy, you know, maybe feel a little faint.
They can also cause headaches and flushing, peripheral edema (swelling in the extremities), and then sometimes - it's rare - but some people can get gingival hyperplagia. So, they can get overgrowth of their gums in their mouth.
And those are the main side effects of the calcium channel blockers.
HOWARD: Ok, and before we move on, do you see beta blockers used a lot these days?
DUSTIN: Not as much. Beta blockers are used, but, usually, after you've already put somebody on a diuretic or an ACE or an ARB or calcium channel blockers, or, if they can't use those drugs ('cause maybe they're in a specific part of the patient population like the heart failure patients who can't have those Diltiazem and Verapamil).
Or if they're allergic to one of these drugs, then sometimes you put somebody on a beta blocker. And beta blockers, they don't work quite as well to lower the blood pressure. They work better to, basically, reduce the heart rate (so, reduce the amount of times your heart pumps every minute).
And they also work to, basically - some of them have cardiac remodeling features.
So, if you're in heart failure and you're a chronic heart failure patient, they'll put you on a beta blocker.
Or, if you've just had a heart attack, they'll put you on a beta blocker, 'cause that kind of helps remodel some of the heart tissue.
So, those are the patient populations that usually benefit from beta blockers. But it does work to lower blood pressure, but not as well as the other classes.
HOWARD: Gotcha. So, we're roughly (with all of these) in the 1-3% range of benefit?
DUSTIN: Exactly. And the beta blockers are the same. They're about a 3% benefit.
HOWARD: So, before we move on, compare that – you know, you're the plant-based pharmacist –compare that to a fairly rigorous comprehensive plant-based diet.
DUSTIN: Well, if you go on a well constructed plant-based diet, which is low in fat, and also comprised of whole foods (so foods that are as close to nature as you can get - the fruits, the veggies, the legumes, the whole grains).
If you go on that kind of a diet, and you get rid of the junk foods and the processed foods and the meats and the dairy and the eggs, then, there's a pretty good chance that you might not even have to go on medication. Or, if you are on high blood pressure medication, you can get off of it and still have normal blood pressure.
John McDougall and Alan Goldhamer, out in California there, have published the best studies that I have seen at doing this (putting people on this diet, and, basically, reversing the hypertension, or the high blood pressure).
And, you know, when I talked about the meds - how they reduce blood pressure by maybe 8 over 5 or 13 over 6 with the diuretics - these diets here that McDougall and Goldhamer used, they are reducing blood pressure.
McDougall had a drop in his patients' blood pressure of 17 over 13 and then 18 over 11 in a second study.
And Goldhamer had a drop in blood pressure of up to 60 over 17 in some of his patients. But he also did a water only fast. So, he put people on nothing but water, and medically supervised them for a period of several days - maybe a week or two. And then he switched them to a whole-foods plant-based diet.
So, it really goes to show you, that once you do this, and you take away the cause of the disease, which is the food, then the condition or the disease goes away, when it comes to high blood pressure.
Diets have also been shown, as you know, to reverse heart disease (you know, coronary heart disease), and diabetes, and all kinds of other chronic diseases.
HOWARD: Awesome. Cool. Well, we have less time left than I thought for diabetes, but maybe we can, kind of, go through, in a similar fashion.
So, what causes type 2 diabetes? And the people who come to me for counseling and for coaching pretty much assume that it's something that struck them. Right? It happened to them. Is that accurate?
DUSTIN: Yeah. A lot of people think that. They think that, “Oh, it's in my genes. I have bad genes - a family history of it.”
Or, another thing I hear is, “Oh, it's all those carbs I'm eating. It's all those carbs. And actually, I give a talk on diabetes, and my main point that I want people to leave with is diabetes is not (type 2 diabetes) is not caused by carbs. And it's not genetic.
Type 2 diabetes is caused by fat. It's excess fat inside the muscle cells and inside the body. And this fat interferes with insulin and how insulin works in the body, 'cause your body needs insulin to utilize the glucose that you're eating.
And the glucose is just, basically, the simplest form of a carbohydrate. And you use glucose to make energy. So, your body needs to make energy to live and work and go about its day.
So, it needs insulin to get that glucose into the muscle cells to make the energy. And, if it can't do that, then you have insulin resistance and type 2 diabetes that develops, and all kinds of issues that develop after that. But it's not from the carbs. It's from the excess fat and oils, and saturated fat, and trans fat that's in the diet.
HOWARD: Gotcha. And just to be clear, 'cause earlier you mentioned with the rising obesity epidemic there's a rising diabetes epidemic. So, now you've made that connection clear.
I have people come to see me who are - they may be chubby. They have a belly, but they're not fat. They're not obese. How does that work?
DUSTIN: Well, you still have the problem of this excess fat ending up in the muscle cells causing insulin resistance. So, you know, I have actually seen people and known people myself that are actually, I guess, what you would call “skinny” type 2 diabetics. And it's not that, you know, most people that are type 2 diabetic are overweight or obese, but you don't have to be, you know?
As long as you have a problem with metabolizing all that fat, some of this can end up in your muscle cells, and that's where the problem is.
So, you can't necessarily see the fat that's stored inside of your muscle cells, all this excess fat that's inside your muscle cells. I mean, you can see the fat that's stored on your butt, or your thighs, or your arms, or your chin, but you can't see the stuff that's inside (the microscopic, little bitty parts of fat that are inside your muscle cells).
And that's the fat that's ruining, basically, the whole body's process of using insulin to get glucose inside the muscle cell and use it to make energy.
That's what's impeding that whole process right there. So, it's the fat inside the muscle cell.
HOWARD: I see. So, it's like me having all my drawers be really messy and packed full, but I don't look like a hoarder, because I don't have stacks of magazines on the kitchen counter.
DUSTIN: Exactly. As long as it's out of sight, out of mind, right?
HOWARD: Gotcha. Ok, so it's really, really clear to see the connection between diet and type 2 diabetes, if the cause is intramyocellular fat (fat inside the muscle cells that's blocking insulin from allowing glucose in). So, then the glucose is stuck in the bloodstream, where it goes too high and -
So, what are the drugs that are used to treat type 2 diabetes, and do they deal with the insulin resistance in the fat cells, or are they just dealing with the symptom, again, of the high blood glucose?
DUSTIN: Well, there's several classes of drugs to treat diabetes, and none of them actually target the root cause of the disease, which is these excess fats (intramyocellular lipids) that are stuck inside the muscle cells.
So, none of them target that. You can only target that by changing your diet and your lifestyle.
And so, what these various, different classes of diabetic drugs do is, some of them will help your muscle cells be a little bit more sensitive to insulin, so that it uses the insulin that's available a little bit better, but it doesn't make it perfect.
Some of them will help you, maybe, delay absorption of carbohydrates in the gut. And then you get all kinds of GI effects, like excess gas and bloatiness and uncomfortableness and crampiness down there.
Some of the drugs will tell your liver to not dump out glucose into the blood. Because your liver is like a big storage tank. So, what your liver does is it, when you eat, you're not going to use every single bit of carbohydrate in food that you consume at that very moment.
You're going to have periods of time throughout the day where you're not eating, and yet you still need energy. You still need nutrients to make energy. So, your liver stores up any excess glucose inside of it in the form of glycogen. It puts a lot of little glucoses together and it calls it a glycogen.
And it stores that glycogen, so that when you're not eating (you know, in the middle of the afternoon), and you do need some more glucose, it goes, here's some, here's some from the liver. We'll let it go out into the bloodstream. So, there's some drugs that will tell your liver to stop pouring the glucose out into the bloodstream.
And then there's the new class of drugs for diabetes.
And they're the ones that are advertised on TV now all the time (Forxiga, Jardiance and Invokana). And they, basically, make you pee out extra glucose in your urine.
And glucose should never be in the urine. Your urine should never have glucose in it. So, they're, basically, making everybody do something that's unnatural - to, basically, pee out the glucose, instead of it staying in your bloodstream.
HOWARD: Gotcha. So, the fact that they're measuring blood glucose (that's the number that they're looking at daily and, you know, quarterly with the A1C), and that's what leads to this idea that it's carbs and sugar, because carbs and sugar is the presenting symptom?
DUSTIN: Right. Because it's really easy to test your blood sugar, and it's fairly easy to go to your doctor and get a test for the A1C, like you mentioned, which is, basically, your 90 day average for your blood sugar.
But it's not easy at all to test somebody for the amount of intramyocellular lipid. In fact, I think I've only seen that in a couple of research studies. And it's not something that's readily available for your doctor to order or for you to just to buy some kind of a kit or a tool, you know, over the counter, to test in your body.
So, that's what we really should be testing, is the amount of intramyocellular lipids inside of type 2 diabetics, because if we can reduce those, then we know that we're getting on top of this disease.
HOWARD: Hmm, do you think if we had that sort of test, that then pharmaceutical companies would come out with drugs that would reduce it, or, like, is there always going to be a pharmaceutical blow back if it's not dealing with lifestyle and diet?
DUSTIN: Well, maybe they would come up with a drug to reduce that, but I don't see how they would really make any headway, because, if you have a patient who's still eating the standard American diet and consuming all this excess fat, you still have, you know, fuel coming and adding to the fire even if you're trying to put the fire out.
So, you can try to put the fire out, but if you keep putting fuel on it, I mean, it's a no win situation.
HOWARD: Right. So, how well do these drugs work? And first let's talk about what are the outcome measures that we're looking at. Obviously, you know, diabetics want to know that their numbers are good and are controlled by the meds, but what are the long-term outcomes, and is there a correlation between taking the drugs and having better long-term outcomes?
DUSTIN RUDOLPH: Well, the only drug that I know of, off the top of my head, that I have absolute risk reduction numbers for, in terms of death and disability, is Metformin (or Glucophage is the brand name). And Metformin, basically, primarily works by telling your liver not to dump glucose back into the bloodstream.
It also improves insulin sensitivity in your muscle cells, as well.
But with Metformin, over about a 10 year period, you're going to get anywhere from about a 5-10% benefit in terms of absolute risk reduction in disability from diabetes and in preventing deaths from diabetes.
So, you know, a little bit better than those blood pressure meds when treating hypertension, but still, you know, it's relatively low when you look at the grand scheme of things. And normally - you had asked what we normally keep track of when using these drugs as far as measurements. Normally, it's not your absolute risk reduction in terms of death and disability.
Most of the clinicians and the drug companies out there will target lower blood sugar levels and lower A1C levels. So, basically, we're just looking at, what can we do to lower your numbers, not necessarily, what can we do to lower your rates of death and disability to the disease.
HOWARD: Right. So, again the metaphor that I think of here – help me understand if it's accurate or misguided like the river one – is that your cells need glucose in order to function. Right?
That's, like, one of the only things I remember from high school biology is the Krebs cycle and the mitochondria.
HOWARD: The mitochondria, ATP, and it uses glucose. And so, if the glucose can't get in, or it can't get in sufficiently, and the drugs are basically lowering your blood sugar (they're not lowering your blood sugar by sending it into the cells where it's needed), aren't your cells still starving for energy?
DUSTIN: Yes, in a way, and it depends. Some of the classes of drugs, they do help improve insulin resistance. So they help make the insulin work better to get the glucose into the cell, but still, even at their best, they still don't work as well as changing your diet.
So, you know, your cells are still starving, basically.
HOWARD: Gotcha. So, Metformin is the best of the bunch, and that's been around for a long time. Right? That's a generic at this point?
DUSTIN: Yeah, it's been around for decades. It's been around for probably 4, 5, or 6 decades.
HOWARD: So, the new ones, are doing something, it sounds like, quite unnatural.
DUSTIN: Yes, by trying to make you, basically, pee out the extra glucose. Yeah, that's the newest class of drugs.
HOWARD: In that case, it's definitely not going anywhere useful, unless you're an ant on the sidewalk, and that's where you decide to pee.
DUSTIN: Ha ha, exactly, exactly. And then it creates an environment in your urinary system, where it's, you know - there's a lot of water in your urinary system. Now you're adding - and it's a warm environment, 'cause it's inside your body. -
And now you're adding glucose or sugar in there, so bacteria and yeast love it.
HOWARD: Sounds like a recipe for beer making.
DUSTIN: Yeah, exactly, exactly. So, it's a great place to form yeast infections and bacterial infections.
HOWARD: Gotcha. So, as you said, I know you don't have numbers, exact numbers, for the other classes of drugs. Do you have, sort of, a general sense? If Metformin is the best of the best at 5-10% risk reduction, where are the others?
DUSTIN: That I'm not sure of, because I haven't actually looked, but I do know the A1C reductions for a lot of these drugs. And usually it's around ½ to 1% for most of the drugs. Like, if you actually give a type 2 diabetic insulin (which is the most powerful medication that you can give for a diabetic), you might see a reduction of up to 3% in your A1C.
So, if you're doing that, you know, hopefully you would be preventing death and disability or delaying it. I'm not sure that you are by using some of these drugs.
But again, you know, it's just testing the numbers. It's not actually testing death and disability rates. And some of those numbers might be out there, with reducing death and disability, but, like I said, some of these studies are very hard to find, that actually report this stuff. Most of them report the reduction in either your blood glucose level or your A1C level.
HOWARD: Right. Well, that's because we're looking for our keys under the lamppost.
DUSTIN: Exactly, yup. You've got that right.
HOWARD: All right, so let's quickly compare that to diet. So, somebody taking these meds - they're never going to not be type 2 diabetic, right? So, again, this is going to manage the disease. It will hopefully give them extra years. It will reduce their symptomatology. Have you seen diet actually work better?
DUSTIN: Yeah, and you're exactly right. The medications, in this case, are just like the blood pressure medications were. If you don't change your diet and your lifestyle, you're going to be on them for the rest of your life, and at best will just help you manage the disease. So, you know, again, it's probably better than doing absolutely nothing (and continuing to eat the standard American diet).
But, you know, if you actually change your diet and your lifestyle to the same approach that treats hypertension (which is the low-fat, whole-foods, plant-based diet), there is actually a review study that looked at this.
And they looked at over a 10 year period different patterns of diet. And low-fat plant-based diets were more effective than any of the other common diets used to treat type 2 diabetes. They lowered the A1C the most, blood glucose the most, and they actually had very good compliance rates ('cause people think that this way of eating is so restrictive).
But they had just as good or better compliance rates eating this way, because it actually gets results. And you can come off a lot of your medications when you do this. And you can even prevent the disease itself and reverse type 2 diabetes by doing this.
I think Dr. Neal Barnard has published many of the studies showing that you can reverse type 2 diabetes this way.
HOWARD: Gotcha. But we wouldn't be complete if we didn't talk about the side effects of this diet.
DUSTIN: Oh yeah, like, lost weight and more energy, and less heart disease or no heart disease at all, less cancer, all that good stuff?
HOWARD: Yeah. 'Cause I have doctor friends and some of them are very data driven, they're not, you know, ignorant of studies, but they look at it very reductionistically. So that, ok, well, this study - they looked at the Adventists - and maybe, you know, they had a 5% lower risk of something from the ones - the vegans (and, of course, we're not talking about a low-fat, whole-food, plant-based diet, but something to some extent, possibly, approximating it).
But, when you look at all of those (you know, 3% here, 5% here, 4% there, 9% there), and then you realize that the side effects of that diet is those percentage points for all the other conditions. You know, it's a hard sell to someone who's just looking at individual dots, but, when you look at the big picture, it's pretty compelling, isn't it?
DUSTIN: It is. It is. And part of the problem is that we're taught, right from the time we start going through school, is to look at just maybe one thing, with a very narrow focus on what we're looking at and what we're studying with a different medical intervention, whether it be a pill, or procedure, or surgery.
We're just looking at, basically, that one thing, and, kind of, ignoring all the rest of the things. And that's how we're, kind of, trained and taught to think. So, it's very hard, coming out of that sort of educational style and then into a system that thinks that same way, to break apart from that and to think big. And that's a hard leap to make for a lot of clinicians.
HOWARD: Right. I think of the negative connotations attached to the word “panacea” - right? - a cure all.
DUSTIN: Yup, yup, 'cause it sounds too good to be true.
HOWARD: Right. I think that was one of the criteria for the American Cancer Society's Committee on quackery. If anyone says that their treatment can solve a lot of problems, then you know they're a quack.
DUSTIN: Ha ha, yeah, but fortunately, eating this way and living this way, with a whole-foods, plant-based diet, it really has panned out. And, I think, more and more information and more and more validated studies are coming out, as time goes on. And it's catching on.
HOWARD: Right on. So, your book came out, I think, a year and a half ago now. What are you up to now?
DUSTIN: Right now, I'm actually buried in pharmacy literature and material, because I'm studying to take my board certification exams in pharmacy. So, I'll be a board certified pharmacal therapy specialist, which is - I'm in the hospital arena. So, I work in hospitals as a clinical pharmacist.
And direction of medical care is going that way - where pharmacists need to really become board certified and become more specialized in what they do. 'Cause, otherwise, you're going to get left behind.
DUSTIN: So, that's what I'm working on now.
HOWARD: And how is the plant-based part, or, I would say, the evidence-based part playing in? Are you getting more of a chance to talk about diet and lifestyle - root causes?
DUSTIN: Yeah, since my book came out, I have went around and spoken at several spots - different areas. I'm giving a speech on diabetes, actually, on type 2 diabetes, this Saturday at one of our local gyms here. I've been there quite a few times. We always have a good turn out.
And, you know, I've gotten around. I've been fortunate to go to Hawaii and talk to the vegetarian society of Hawaii up there, and then up to Michigan and Detroit with the plant-based nutrition support group up there, and, of course, the Tampa veg fest and Orlando veg fest in Florida here, and a number of other local and other smaller events.
So, it is kind of nice to get out there and get this message out there, especially coming from a pharmacist. 'Cause a lot of people have heard it from, you know, maybe a physician or dietitians and stuff. And there's only a couple of us pharmacists out there who are educating others on this lifestyle. And I think it really opens eyes when it comes from pharmacy too.
HOWARD: Yeah. Have you had any opportunities to speak to pharmacy students?
DUSTIN: I have, actually. I went to the local university here, the University of Southern Florida, and USF over in Tampa there. And I spoke to a big group of their pharmacy students there, and gave them this talk that I do on diabetes (type 2 diabetes), about, you know, basically, I talked about Metformin, and, you know, the absolute risk reduction with that.
And then I get into the disease process and the intramyocellular lipids and a couple other aspects of type 2 diabetes. And it was really good. You know, it was well received, and it really opened some of those students' eyes.
Because we're not really taught about intramyocellular lipids in school, even though it's the root cause of the disease. It doesn't really make its way into the curriculum. So, when people hear that for the first time, you know, you get the deer in the headlights look. Like, what are you talking about? But, when you start to explain it, I think it starts to sink in, especially with students, you know, who are scientifically driven and are interested in biology and stuff. They really take to it.
HOWARD: Hmm. That confuses me, though. If they hear the causal mechanism of the disease, and they're deer in the headlights, was there an alternative causal mechanism that they were taught, or is that simply not part of the conversation?
DUSTIN: Well, it's not part of the conversation. So, the conversation ends at insulin resistance. Everybody is taught about insulin resistance, but nobody's taught about what causes insulin resistance, which is those excess fats inside the muscle cells (those intramyocellular lipids).
So, when the conversation stops at insulin resistance, we just, kind of, take it for granted, that - I mean, if you don't know this other stuff - we just, kind of, take it for granted in the medical community that, “Well, that's the cause of diabetes - it's insulin resistance. And we don't really know how to make that go away, so we'll just - we have these drugs that can treat it and try to improve it just a little bit, but we don't really have anything that makes it go away.”
HOWARD: Wow. So, we've got a lot of work ahead of us, huh?
DUSTIN: We do. Yeah, we have a lot of work ahead of us. But, you know, I think there's a lot of people that are listening up - both patients and clinicians. And I see more and more people (more and more medical professionals) taking light to this. So, it's encouraging, but there's a lot more that has to be taught.
HOWARD: Gotcha. Well, I can just see the new, the new TV ads, you know, “Ask your doctor about intramyocellular lipids.”
DUSTIN: Yes, that would be great. I'd love to see that.
You know, I was mentioning to - one of my texts to coworkers (another pharmacist) the other day - I go, “You know, these hospitals all over the nation, they charge a lot of people to be here. I think a requirement for all these hospitals should be to give a complimentary copy of Forks Over Knives to every patient that comes through the door.” I think we could afford that.
HOWARD: Yeah, right. That's like asking me to put my competitor's literature in my waiting room.
DUSTIN: Yeah, I guess so, if you look at it that way. That's true.
HOWARD: You're catching me at a cynical incarnation.
DUSTIN: Yup, exactly. We can try.
HOWARD: All right, well, Dustin Rudolph, thank you so much for your work.
Thank you for this wonderful book, The Empty Medicine Cabinet.
Thanks for all your guidance, and for all you do in the world, and for taking the time today.
DUSTIN: Oh, I appreciate you having me, Howard. It's been a pleasure.
HOWARD: All right, be well.
DUSTIN: All right, take care
This transcript has been donated in memory of Brenda and Russell McVaugh.
Download the PDF transcript here (courtesy of Beth Hillman, donated in memory of Brenda and Russell McVaugh)
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It can be found on his first CD, titled Will Ridenour.
You can learn about Will, listen to more tracks, and buy music on his website, WillRidenour.com.
Thanks to Plant Yourself podcast patrons – Kim Harrison – Lynn McLellan – Brittany Porter – Dominic Marro – Barbara Whitney – Tammy Black – Amy Good – Amanda Hatherly – Mary Jane Wheeler – Ellen Kennelly – Melissa Cobb – Rachel Behrens – Tina Scharf – Tina Ahern – Jen Vilkinofsky – David Byczek – Michele X – Elspeth Feldman – Leah Stolar – Allan Kristensen – Colleen Peck – Michele Landry – Jozina – Sara Durkacs – Kelly Cameron – Janet Selby – Claire Adams – Tom Fronczak – Jeannette Benham – Gila Lacerte – David Donohue – Blair Seibert – Doron Avizov – Gio and Carolyn Argentati – Jodi Friesner – RuthAnn Funderburk – Mischa Rosen – Michael Worobiec – AvIvA Lael – Alicia Lemus – Val Linnemann – Nick Harper – Bandana Chawla – Martha Bergner – Molly Levine – The Inscrutable Harry R – Susan Laverty the Panda Vegan – Craig Covic – Adam Scharf – Karen Bury – Heather Morgan – Bonnie Lynch of Plant Happy Oregon – Sabine Kurtzhals – Nigel Davies – Marian Blum – Teresa Kopel – Julian Watkins – Brid O'Connell – Shannon Herschman – Linda Ayotte – Holm Hedegaard – Isa Tousignant – Connie Haneline – Erin Greer – Alicia Davis – Heather O'Connor – Carollynne Jensen – Sheri Orlekoski of Plant Powered for Health – Karen Smith – Scott Mirani – Karen and Joe Crabtree – Kirby Burton – Theresa Carrell – Kevin Macaulay – Elizabeth Rothschild – Ann Jesse – Sheryl Dwyer – Jenny Hazelton – Peter W Evans – Justine Divett – Joshua Sommermeyer – Dennis Bird – Darby Kelly – Lori Fanney – Linnea Lundquist – Valarie Hummel – Emily Iaconelli – Levi Wallach – Rosamonde McAtee – Dan Pokorney – Stephen Leinin – Patty DeMartino – Mike and Donna Kartz – Deanne Bishop – Bilberry Elf – Marjorie Lewis – Tricia Adams – Ian Cramer – Nancy Sheldon – Lindsey Bashore – Gunn Marit Hagen – Tracey Gulledge – Lara Hedin – Meg from Mamasezz – Stacey Stokes – Ben Savage – Michael K – David Hughes -Coni Rodgers – Claire England – Sally Robertson – Parham Ganchi – Amy Dailey – Brian Tourville – Mark Jeffrey Johnson – Josie Dempsey – Caryn Schmitt – Pamela Hayden – Emily Perryman – Allison Corbett – Richard Stone – Lauren Vaught of Edible Musings – Erin Hastey – Sean Owens – Sagar Naik – Erika Piedra – Danielle Roberts – Michael Leuchten – Sarah Johnson – for your generous support of the podcast.
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