Reshaping Perspectives on Benign Prostatic Hyperplasia and Prostate Cancer with Dr Mark Donohoe

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Reshaping Perspectives on Benign Prostatic Hyperplasia and Prostate Cancer with Dr Mark Donohoe

One in seven males can expect to suffer with a problem with their prostate by age 40, the most common being benign prostatic hyperplasia (BPH), a non-cancerous enlargement of the prostate. However prostate cancer is the most commonly diagnosed cancer and the fourth leading cause of mortality for males in Australia today.

Despite these health issues being exceedingly common they remain chronically under-recognised and in some cases, poorly managed.

Today we are joined by Dr. Mark Donohoe who expertly takes us through the quandary that is the prostate. Dr Donohoe discusses why, in a quest to deliver better screening and diagnosis it may have actually resulted in unnecessary over-treatment and invasive medical intervention. He also shares the simple, modifiable risk factors that everybody can benefit from. 

Covered in this episode

[00:55] Welcoming back Dr Mark Donohoe
[01:39] How common is benign prostatic hyperplasia (BPH)?
[05:39] Hyperplasia vs. Hypertrophy?
[09:22] Can we intervene with lifestyle medicine?
[10:24] Race-related risk factors
[13:33] Looking into family history and genetic factors
[15:48] Modifiable prostate cancer risk factors
[19:01] Diet and the microbiome
[19:40] The importance of Vitamin D and liver health
[27:29] Regular ejaculation: a modifiable risk factor
[31:41] The case for and against zinc supplementation
[34:56] Screening and the usefulness of PSA
[44:00] Preventative, proactive medicine
[49:47] Safety: what do you need to be looking for?

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Andrew: This is FX Medicine, I'm Andrew Whitfield-Cook. Joining us in the studio today again is Dr. Mark Donohoe, who graduated in 1980 from Sydney Uni. He worked around the Central Coast of New South Wales, and this is where his interest in integrative medicine sparked because patients just weren't fitting into the boxes of diagnoses and treatments. He's one of the fathers of integrative medicine in Australia, and he's been the vanguard for patient health throughout his whole career. 

Welcome back to FX Medicine, Mark, how are you? 

Mark: Oh it’s good. I move from father, to grandfather, to uncle, I just shift around in this time...

Andrew: I had a giggle. I thought no, I'll be serious today. 

Mark: Well, it's so appropriate for today the difference between fathers, grandfathers, and...

Andrew: Fathers, grandfathers, very true. And I did want to add a serious spin, even though we jockey about a bit. But you know, we're talking about disorders that causes everything from a little bit of discomfort and potentially embarrassment in men, to devastating effects. Indeed, more men die from what we're going to be talking about today than women die of a similar gonadal-type disease. 

So, the topic today is both benign prostatic hyperplasia, BPH and prostate cancer. So I think Mark, we need to start off with... let's talk about prevalence. BPH, prostatic hyperplasia.

Mark: BPH, if you live long enough is almost 100% of prevalence. There are things... I mean we're going to talk about risk factors and things that can be done to drop it. But basically, as you get older, the prostate gets bigger its uses become less and less necessary, shall we say. And benign prostatic hypertrophy is the ‘norm.’ You can't make it a disease state, when it is so normal that basically if you examine anyone over the age of 70, they've got a big prostate. 

Andrew: Why?

Mark: Were we ever meant to live this long?

Andrew: This goes back to your thing…

Mark: You must recall my daughter's line of what does medicine do? It props up white, privileged, males, way beyond their use-by date, and I love that kind of line. What are males useful for? Inseminating, going out hunting, dying, and we find ways of doing it. We go to wars, we do all kinds of things to make sure males die off early. What does medicine spend 90% of its budget on? Heart attacks, cancer, prostatic hypertrophy...

Andrew: Diabetes.

Mark: Diabetes. We prop up white men, and as she said, beyond their use-by date, we fail to pay attention to the things we could do for prevention for women, for childbirth, for developmental disorders in children. And so, I think it's kind of God's revenge, if you like. If you hang around long enough you're going to have some... 

Andrew: Coming from somebody who is not religious, but anyway… But I do have to raise this question. You talk about white men, there are actually racial issues here.

Mark: Yes, there are.

Andrew: You know, African-American men have a far worse prognosis of prostate cancer.

Mark: It's not the reason, prostate cancer research went ahead though. So, the point is not that. There may be differences. But when something is effectively nearly 100% of the population, you can say, this was just one of the discardable genes. You've done your procreating by the time prostates become an issue. There may be something about prostates that work hyper efficiently or hyper productive, that makes fertility even higher. But you cannot sustain a gland like that with hormonal controls over a 70-year period, without there being consequences. 

And so you can make a strong case that benign prostatic hypertrophy is the physiological state progressively as you go from around about, say age 55 up to around about whenever we tend to die. So, I think that we've got to be careful about... what do we call it? It's kind of disease mongering. It's this idea that we've got to do something about everything. There are differences between having a prostate growing and it causing problems. We doctors deal with the problems that are caused. So, when a person turns up and says, "Doc, I can hardly start peeing and when I do it's just a dribble, but...

Andrew: But then it catches me later on, yeah.

Mark: That usually means that something has been going on for some years. And males being who they are, don't tend to get to the doctors' all that quickly. And so that progression has occurred to the point that it becomes a problem. And they can become, you know, incontinent, urine incontinence, a lot of them are wearing pads. We do a lot of things to cover up for this. 

What I suppose, the important question is, what could we be doing better lifestyle-wise that would mean this was less of a clinical problem even if the prostate is to grow. 

Andrew: Okay, so talking about lifestyle issues, I have to take you back to a word you said, and we've discussed this just before; the difference between hypertrophy and hyperplasia. 

Now my way of knowing BPH is benign prostatic hyperplasia, you learned hypertrophy, but I looked up...

Mark: I'm not that much older…

Andrew: Hyperplasia and hyper, hypertrophy is the increase in size of an existing cell. 

Mark: Yes. 

Andrew: So, if you think about four cells in a row, increasing in size, and they increase their volume, but they take up a certain space. 

Mark: Yes. 

Andrew: Rather than that you've got hyperplasia, so you've got an increase in the number of cells, smaller cells, but they can still take up that same amount of space. 

So, we're talking about BPH, and my level learning it was hyperplasia. Now you speak about lifestyle factors and I'm wondering here about, you know, as we age, the testosterone declines, the oestrogens increase, particularly because white males become more obese in an affluent society. 

Mark: Yep.

Andrew: But there are also those, you know, African-American men that are quite obese, and there is that potential for diabesity in certain races.

Mark: Yes. 

Andrew: What's happening here? Are we talking about just being fat, and that oestrogenic drive?

Mark: We're talking about a whole range of things. In my defence, I came from a time…

Andrew: Your defence.

Mark: I came from a time where hypertrophy was a clinical discussion. The term hypertrophy was not particular, it was just it's bigger. 

Andrew: Yep. 

Mark: And we didn't have a cellular diagnosis really much to run on then. Technically hyperplasia is increased number of cell, hypertrophy is bigger cells. They probably both occur when it comes to prostate cancer. And well they certainly both occur when it comes to prostate cancer. But hypertrophy is a bit of both as well. 

So, the benign side of it is the cell growth... every time you get cell growth in any organ and you have a stimulus in the prostates turn, say, testosterone, you will have abnormal cells appear. The more growth of cells, the higher the prostate cancer risk.

And so there is a link between benign prostatic hypertrophy, the same as there is between oestrogen use as we now understand with the pill. You know, the recent studies now say that it's not just progesterone, but if you stimulate cells to grow... this comes back to Bruce Ames' idea of all cancers are mutagen plus mitogen. 

Mutagenesis takes place for a whole lot of reasons which we can discuss, even down this list once again, is smoking. But mitogenesis, the stimulation of cellular growth and production of new cells or bigger cells in the prostate, is a separate process. You tend to get cancer when the mutagenic cells, the ones that have been damaged suddenly get a proliferative push, by some kind of thing, such as the hormones that males have. 

Now the beautiful discussion we can have is, just at the time when the prostate is getting bigger, males tend to have their testosterone dropping away. And this has always been a problem for us as doctors. We have this idea of youthful testosterone. And the question for doctors has always been if we give older males testosterone, are we proliferating potential tumour cells in the prostate? Are we giving testosterone with the risk of more prostate cancer? 

Still hard to tell what the answer to that is, but you would generally say that anything that stimulates cell growth, is a bad idea when there is such a high rate of conversion to prostate cancer in the normal community. 

Andrew: So, going back to lifestyle. You know, we talk about our affluence being the root of all of our chronic diseases, or many of them. Do you think this is something that can be adequately controlled by changes in lifestyle?

Mark: There is good evidence that you can help control it. However, you need to remember that a couple of the things we cannot control. So, risk factor one, is age. We have this concept of anti-aging, but it's not really anti-aging. 

Andrew: Optimal aging. 

Mark: Yeah, optimal aging is minimising the damage done along the process of time. Time takes its toll, we all pay the price for it to a greater or lesser extent. And the concept of the one horseshoe, you get to the end of life, everything's working until the very last step, and it all falls to bits and goes to buggery, you know, straightaway. 

Andrew: Yep, yep. 

Mark: A perfect life will be one where you don't have a day of illness, and at about age 92, you suddenly drop dead for no particularly good reason. Except all...

Andrew: Go to sleep, yeah. 

Mark: All the wheels fall off at the same time. 

Andrew: Unfortunately.

Mark: Yes, it doesn't work that way. 

Andrew: It doesn't happen that way.

Mark: Given that we can't change the number of years we've been here, we can change certain risk factors for both benign prostatic hypertrophy and secondarily for prostate cancer risk. 

I keep saying hypertrophy, it is habit. I'm not insulting you in any possible way. It is in fact, hyperplasia, slash hypertrophy. But I'll keep going back to my own. 

But the two that we can't change, probably are, you know, our race. Caucasians, dark skin from Africa, dark skin from Asia, all have very different risk factors. And so...

Andrew: I don't know much about the Asian risk.

Mark: It's much less than it is for the Caucasians. So Caucasians are around the middle, if you like. That the lifetime risk is X for Caucasians. It's about two and a half times higher for African Americans, but not for Africans still in Africa. So there's something about moving to America...

Andrew: That smacks of lifestyle.

Mark: It does. And a part of it is also that an African person has a higher lifetime risk. In Asia, about a third of the risk for prostate cancer compared to Caucasians. 

So that's given any other changes, we have about a 2.5 increase on one side, and a third on the other. That's nearly a six-fold variation just by race, just by the where you are brought up. 

Andrew: Forgive my weird mind going on about this. But when you're talking about that increased risk from moving from Africa to America, is there part of that being the life duration of those people that live in Africa, compared to those people that live in America?

Mark: Can be. I mean, when we look at these, they're corrected for age. Probably the bigger thing moving from Africa to America is dark skin in a very high sunlight exposure does not leave you vitamin D deficient. Black skin in America, in an environment where you're in the temperate zones leaves you vitamin D deficient. So we do understand that move of nationality, unrelated to race, the move of nationality from Africa to America is where the majority of that risk comes.

And so we'll come down the line to that, but vitamin D or latitude where, you know, we have these kind of concepts of the higher the latitude the further from the equator the less the vitamin D, is particularly applicable to people with dark skin. 

Now, the paradox is, that people with different types of dark skin from Southeast Asia, don't have that risk factor in any way similar to African Americans, when they move to countries like Australia. It does increase risk for about one third the risk of BPH and prostate cancer to around about half, but it still remains less. 

And so, we have a concept of, if cells are proliferating full stop around the body, the prostate in an aging male is an ideal place to see that take place. It's not that the prostate gets a lot of sunlight, it actually doesn't, unless you have very strange sun tanning processes going on. So, I'm not suggesting that sunlight is the way to do it. 

But what we can say is genetics... nearly all of prostate… 75% of prostate risk can be found by saying, what did your granddad, your dad, your uncles, what did they have? Did they have benign prostates, did they have no prostate problems? And there's about a three-fold risk increase depending on your family history. You don't have to be a rocket scientist to ask about family history. I know my own grandfather had prostate cancer and died of prostate cancer. None of his male children... he had five of them, none of his male children had prostate issues whatsoever. So there is a kind of generational gap, and none of the grandchildren of that family have, so far, had it. So if there is a genetic risk it seems to have died somewhere along the line ending with my grandfather.

Go back the other side, it was always prostates. So there are factors of food, diet, lifestyle there's a lot of factors involved in that. He was a racehorse trainer, everyone was in pubs. There were other risk factors about diet and lifestyle, that would have played out but didn't in my own family. 

Andrew: So, he was a racehorse trainer. 

Mark: Yes.

Andrew: So I'm just thinking about lifestyle things here. One is of that era, smoking was much more prevalent. The other thing is, he was a racehorse trainer, he rode horses, what about local agitation? 

Mark: I did not say he rode horses, he was a racehorse trainer. But he used to take...

Andrew: Ahh, but come on.

Mark: He had jockeys to take hit for him.

Andrew: Really, he never got on a horse?

Mark: He was never fond of riding the horses, but others did. 

But look, what I can say is, I remember being in his house in the, shall we say the early 1960s. They had DDT sprays that they used for everything. The pesticides that were use to keep everything under control. Every fly spray was a DDT spray, sprayed into the air in massive amounts. The world has changed in the last 50 or 60 years, and some of those changes are probably going to be for the better. 

The highly lipid-soluble toxic pesticides that we used, probably had a good part to play in mutagenesis. When we talk about that, what stimulates growth, what damages DNA? They are known mutagens and they stay in the lipid tissues, and the prostate is one of those, for long periods of time. 

It's not so much the focus on that family, it is that genetics and your family history are a huge reason to pay attention to do I have prostatic hypertrophy, or do I have cancer? What we're now trying to do in medicine, is get out of the diagnostic quandary we got ourselves into. Can we find a test so sensitive, that every possible prostatic hypertrophy and cancer will be identified, and we will do something to them? And then after 40 years of doing it, backing off and say, good God...

Andrew: We’re we doing the right thing, yeah. 

Mark: We have overtreated massively, we've done a lot of damage. And what we’ve found is a number of cancers that never ever match the death rate from cancer. So I think you expressed it well. There's a massive difference between dying of cancer, and dying with cancer. 

If you die over 80, there's an 80% chance that if we look at your prostate, there will be a cancer there. Did it do anything in about 90% of the people who have it? No, not at all. Yes, it's still the most common cancer, and it's the most common cause of males dying of a particular type of cancer, now that smoking has disappeared and lung-cancer rates have come down for males. 

Andrew: The most common cause?

Mark: The most common cancer for a male.

Andrew: The most cancer, not the most common death?

Mark: Yeah, no. 

Andrew: Right, got you.

Mark: So the most common cancer for a male. There were other common cancers, as we've got smoking out of the way for males, weirdly not for females, females taking it up at a higher rate again now. 

But as we've got the prostate cancer rate matches a downward trend with the lung cancer rates. So there is a contribution of smoking, but smoking doesn't have the hormonal effects on the prostate, it has direct effects on the lung. Nonspecific mutagenesis when it comes to males. So being off smoking is maybe a 10% to 20% risk reduction, but still important. 

The big changeable ones are diet and exercise. So when I've said three-quarters of it it's genetics, I don't want people to think you just give up if your genetics are bad. What you do is say, 'My genetics give me a reason to check myself and to take actions elsewhere that are going to make a risk reduction.' You can get up to 30% to 50% reduction in prostate cancer risk by eating vegetables primarily, instead of having high fats and red meat in the diet. And it seems not so much that red meat is the damager, but the vegetables are the protector. That we fill ourselves up with those lycopenes and with the good antioxidants, and with the tissue-protective effects.

Andrew: But also reducing circulating hormones.

Mark: Yes. 

Andrew: By binding them. 

Mark: Yes. And having... there are lots of good things about vegetables, there are lots of good things about vegetables, and there's lots of bad things about excessive meat. But in terms of lifestyle, it doesn't seem that the amount of meat that you eat is the problem. It's the amount of fresh fruits and vegetables that you consume, that is protective. 

Andrew: Yep, yep. 

Mark: And I think we've misinterpreted that, what happens often...

Andrew: As we often do. 

Mark: Yeah, people misinterpret okay, those on higher meat who are eating these vegetables are at risk, so we blame meat. Rather than say if you get the balance right with your vegetables you can probably get out of prostate-cancer risk with that diet.

Andrew: But I know we're getting on to the microbiota again, but one of the things that I seem to be...

Mark: God forbid we should ever touch on that subject.

Andrew: But one of the things that I seem to be picking up now is we're blaming the red meat it may not be that per se, but when the red meat interacts with the certain microbiota of a high red meat, low vegetable diet, well then you've got an issue. But that's not because of the red meat per se. It's because you're not eating enough vegetables to be able to have the right microbiota...

Mark: And the utter lack of stewed apple. 

Andrew: Oh no. You had to.

Mark: I just cannot let that go. I had to.

Andrew: Okay the Hadza tribe. So, forgive me listeners...

Mark: We just mention these to get these off our chest every time.

Andrew: I did just want to tie off one thing with regards to vitamin D. And, you know, there does seem to be this association with low vitamin D levels and prostate cancer risk and even survival. 

Mark: Yes. 

Andrew: But whether that is going to be corrected or improved on the prognosis by giving vitamin D is moot. 

Mark: Yeah. 

Andrew: It may well be this very long term. However, I think it is always reasonable to correct a deficiency. For whatever the benefits may be, be they bone or muscle.

Mark: Look, you've been on about this for a while, about don't measure everyone. But when a person with dark skin in a temperate environment comes along, when you suspect there could be a problem...

Andrew: They're a risk factor. They're at high risk. 

Mark: It's very important to know that one measure and then what to do about it. And dark skin...

Andrew: That's appropriate.

Mark: That is a very difficult thing to raise sunlight exposure sufficiently to bring vitamin D levels up. And I think that we have to accept that evolutionary biology is such that people didn't travel vast distances as we do today. You can be born in one country, live in another country, your entire life. And part of the risk you take is how you adapted to the... how your ancestors and you adapted to the original environment versus what you are now exposed to as your new environment. 

And we know for say, heart disease, obesity, diabetes, but the risks transfer very much environmentally. That we can push people from low breast cancer risk, for example, in an area in Asia, and when they come to America or Australia, the breast cancer risk tends to rise significantly. 

Same with prostate cancer, when you move nations you're moving from a home environment where you are the successful evolutionary outcome, and you're moving to one where you may or may not be. So I'm not trying to induce paranoia, but when it comes to dark skin in low sunlight environments...

Andrew: That's a high risk

Mark: Vitamin Ds get down to very, very low levels. We see vitamin D down in the 10s and 20s. And we ideally want them at the 80 to 120 range when it comes to protection. So that's a protectable thing..

Andrew: Yeah. 

Mark: And it's hard to get that much vitamin D from a diet, it really, really is. 

Andrew: No way.

Mark: You've got to get it from sun.

Andrew: Sun, definitely sun. And I should point out to our listeners, certainly in Australia, probably around the rest of the world they're looking at restricting vitamin D testing. In Australia, there was a saving of I think it was 14 million in the first year that they restricted the...

Mark: It sounds a big. The fact that it is point .01%. So it is a saving, but it's not a significant saving. The question has always been, did anything good come of the vitamin D testing? What happens with useless testing is that nothing happens, right? So if you invested 14 million or I think it was 140 million in vitamin D testing so I think it was a good deal higher. But if you invested...

Andrew: That was the total?

Mark: Yeah. If you invest that money and you save type two diabetes and you get prostate cancer risk down 20 years hence, it's very difficult to argue against it. 

If you just keep on doing the testing unnecessarily, testing doesn't help anyone. And so there has to be a strategy and what there never was with vitamin D was a reasonable strategy on the other side. Here we've identified those at risk. Dark skin, commuting, spending time indoors, all the things that change from our natural environment. What did we do about it? Almost nothing, some people went on 1,000 units of vitamin D a day and that was it, and never actually raised the vitamin D significantly whatsoever. 

Andrew: So the way I see it was part of the issue, certainly in some cases, not the majority, but certainly in some cases, there was an abuse of vitamin D testing. I think Kellie Bilinski, forgive me, it was something ludicrous, was it 79 times? Was it… It was something incredible. Absolutely waste of money, waste of the public purse. However, from the other side, talk about a waste of the reasonable use of testing to measure, is then to give an inappropriate or ineffective treatment level. And that was this 400 to 1,000 IU, particularly in patients who are more than likely going to be overweight, where you need three to five times the appropriate dose. So I think Michael Holick talks about 15,000 IU per day. 

Mark: I'm going to put a little gem here in on the side that is, what do we measure when we measure vitamin D? We measure the 25-hydroxyvitamin D. What do we produce from sunlight? The unhydroxylated vitamin D. Your steps to active vitamin D are a good liver, and I argued for years against the naturopaths and others who'd say, your liver is dodgy. But when it comes to giving vitamin D the failure of that 25-hydroxylation is that a perpetual problem that people get the vitamin D in, nothing comes of it and it effectively becomes wasted, unless it's firstly, hydroxylated in the liver then ultimately in the final tissue...

Andrew: Voila, 25…

Mark: Mainly kidneys, but the 1,25 is mainly kidneys, but the rest of it is in tissues all around the body. If you just give the blunt, 'Oh, let's give you this to fix your 25 hydroxy,’ you can put a person out in the sunlight and if all the vitamin D3 never becomes hydroxylated, it is never ever used. It's just another by product of cholesterol metabolism.

Andrew: So again, getting off the track of that, that is our want. So let's say somebody has...

Mark: We are parenthetical.

Andrew: Let's say somebody has diabesity, they are at higher risk of kidney disease, they probably have prostate cancer issues, or at least BPH. So do you think therefore we should not be giving vitamin D as in vitamin D3, but we should be giving rather Rocaltrol in 1,25 dihydroxy? 

Mark: Yes, it is interesting...

Andrew: In kidney disease.

Mark: Here's the problem we've got a good measure of 25-hydroxy because in nanomoles range. We can measure it and we can be reasonably confident about it. The 1,25, I think, is a mismeasure, because it varies massively over a day. Two samples taken in the one day could give you a 50% to 70% variance in a 24-hour period. And the majority of the 1,25 dihydroxycholecalciferol is in the cell. If it's in the bloodstream where we can measure it, that's wasted, that has nothing to do with anything. 

So we measure the store of it, we give vitamin D3 as a precursor, for a store to be held of the 25-hydroxy. What happens in the cell stays in the cell. And I have done this myself and I've seen the studies say, if you measure it at 8 a.m. and then measure at 3 p.m. one is clearly deficient and the other one is clearly excessive, what's the value of that? We're measuring in the bloodstream, where we want to know what's going on in the tissue. I don't think there be any call for measuring the 1,25-dihydroxy because it's too variable. 

Yes, it's what we wan to give, and if we're really severely deficient, and we're getting osteopenia, osteoporosis, or if we're getting any form of deficiency disease, the 1,25 dihydroxycholecalciferol is the thing to give. 

So that's a kind of technical parentheses is we like plenty of vitamin D, D3, from the cholesterol precursors, we measure the 25-hydroxy, which is the liver's done its job. And when I see people, especially with gastrointestinal inflammatory problems, the liver gives up that job. You can put 5,000, you can put 10,000 in, and you still raise the 25-hydroxy only trivially. Sometimes not at all. 

So, then the job is to get the liver uninflamed to do something about the gut and the liver and that's where we keep coming back to the microbiome. What's it doing for us when it comes to the vitamin D metabolism? And what load is upon the liver before we even start?

Andrew: So just trying to tie this in with lifestyle obesity, overweight, diabesity, all of that. Plus our, you know, preponderance for high fat, trans fat, sat fat, and worse than that, low vegetable, in the presence of high fat. And then tying this, with regards to what you're talking about vitamin D, and the issues of liver conversion. Then let's talk about the naturopathic axiom of treating the liver and the gut. 

So, tying this in with prostate, prostatic issues, do you always...

Mark: Yes, it does sound different doesn't it? That we're talking about the prostate now we're back to the gut and the liver.

Andrew: To the liver. Yeah. So do you always treat the gut and the liver when you're looking at somebody with a prostatic issue? 

Mark: The people that I see, yes. The reason is that I'm not a urological surgeon, I'm not a prostatologist, that's not my primary business. So I'm seeing people for different reasons. 

You forgot one important risk factor in there, a very modifiable risk factor so I... 

Andrew: Male?

Mark: No, no, no. 

Andrew: Not modifiable..

Mark: There's the diet, the exercise and the management of weight and the sunlight. So these are things that we can provide sensible advice on. High vegetable diet, a high variety of fruits and vegetable in season. The exercise. You get with reasonable exercise, moderate exercise, a 30% lifelong reduction in mortality from prostate cancer, just by being a moderate exerciser. Light exercise around about 10% improvement. So there might be a dose-response there as well. 

There's weight, definitely a dose-response. Meaning that the more the body-fat reduction, the higher the protection against prostate cancer, whether or not you have benign prostatic hypertrophy. 

And the one that I love, which I think we're going to have to make compulsory in Australia, is ejaculation rate. 

Andrew: Right. 

Mark: Sexual activity. 

Andrew: Of course.

Mark: There's a dose, an optimal dose for ejaculations.

Andrew: All men. Well, all women?

Mark: I'm not sure that we're talking the right way here. 

Andrew: No. I shouldn’t go here… 

Mark: I think that you’re going down a rat hole that you really don't want to explore. 

Andrew: I'm going to get lambasted for this.

Mark: What we do understand is that lifelong, three to five ejaculation per week seems to be the sweet spot if you like, the protective area. That if the prostate's doing its job and ejaculation is relatively frequent, that's not frequent for youngsters, I've got to say, but as time goes by, and interest may wane, one of the risk factors is, ejaculation rate may go down. 

And it seems to not matter how that ejaculation occurs, we're not going to get into the technicalities of this and there's no manual... I use that word advisedly. But we're going to be referring to at the end of this. But it is important. If you don't use something it will sit there, it will have the problems, and it will not have a method of functioning.

And the prostate seems to be like the heart in exercise. That you have to exercise your prostate a little bit. And that ejaculation and frequency of sexual activity is at least, as a minimum dose, of three ejaculations a week protective against lifelong prostate-cancer risk. 

Andrew: Is there a maximum? Just asking. 

Mark: Well, I've never heard of an overdose, but I imagine dehydration is going to be your primary problem at the kind of levels of overdose that we're talking about.

Andrew: For our listeners, I will be introducing a paper which Justin Sinclair introduced to me about a month ago with regards to the initiation of the endocannabinoid system by achieving orgasm.

Mark: All right and so... 

Andrew: It’s a cracker. 

Mark: Well cannabinoids I have never even researched this, but cannabidiols and the prostate? 

Andrew: But I digress.

Mark: Okay. But it is important, normal sexual function is an exerciser of that gland. Its production and elimination and ejaculation, these are normal processes. Then if you support those, if that is regular over the lifetime, there is definite evidence that that's a significant reducer of both benign prostatic hyperplasia/hypertrophy and cancer.

Andrew: Just me pondering but if...

Mark: I hate to think where this is about to go.

Andrew: If seminal fluid is high in zinc, and more ejaculations are better for the prostate. And there's been this weird association of zinc supplementation possibly having an adverse effect on prostatic cancer outcomes. Could it be that it's because when you're giving zinc to a prostate that's not doing anything, that you might be...

Mark: Loading it up?  

Andrew: Overloading something rather than turning it over.

Mark: If you allow stuff to accumulate in a particular gland and it's unused? Then the answer is yes. That somehow has to be managed and eliminated. And I do think we've got too much into the mindset of zinc good, copper bad, we keep on thinking of that. They're even some evidence...

Andrew: Without thinking about superoxide, but anyway…

Mark: Well, yes. There are balances there that are a little bit beyond us, but the hyper supplementation of zinc, I do find a problem. I see people, doctors especially, putting people on 50, 100, 150 milligrams of elemental zinc. At the very least the stomach is complaining. But the inability to drive the zinc up in the body, some point, you've got to step back and say, am I driving the wrong thing? If the body is working against me to keep zinc low, do I just keep on thinking of it as a good agent as opposed to a bad and evil agent? 

Zinc in excess is also corrosive. We think... we know it about iron, we know it about copper. And zinc itself has local corrosive activities on the gut and can disturb the microbial balance equally with any other hyper supplementation. 

So, we need to pay a little more attention to what our goals are, I do agree with that. In general, we always think of oysters as the kind of aphrodisiac, and you know, think of zinc as that part of the magic that happens. But oysters are not zinc supplements and I think oysters...

Andrew: Whoa, well, they are high in zinc. They are a zinc supplement…

Mark: But they are not zinc supplements...

Andrew: They can also be a heavy metal supplement depending on where you get them from. 

Mark: Okay, you take my point very well. I mean that the zinc... I do get people to have their dozen oysters a week. I think it's preferable, but we do need to know what's the environment that those oysters are in? Where are they from? What's the factories up stream? The problems with a lot of our foods is foods are great, except when you pollute them. And we did that to our fish and our oceans. And we're doing...

Andrew: Our meat, salmon.

Mark: That's right. And now what are we doing? We're paying enormous amounts of money to get back to a kind of organic, Paleolithic type of foods that could conceivably have been part of our evolutionary history. 

All I'm making the case for, is nothing in the supplementation range is entirely proven or disproven. And we run the risk always of thinking of single micro-nutrients as if they're cures, and most of the time they're not. 

Closest I've ever seen to a single micro-nutrient cure is magnesium. That you give magnesium for a range of different conditions, and the heart rate settles, the muscular activity settles, you get improvements. But I have never heard of magnesium having anything to do with prostates. I'm now going to be proven wrong, we'll have 1,000 emails saying, 'Have you not read something or other?' So… 

Andrew: Getting back to prostate and the issue of screening, and diagnosis, and disease progression. You know, years ago the age-old thing was, once you reach 50, congratulations you now got a manual digital examination from your doctor. 

But then of course, we moved over to the supposedly better thing which was the prostate-specific antigen, which has caused all sorts of issues with regards to testing and now even over-treatment. Talk to us about this. 

Mark: I lived through this. You're right. What we thought was we don't have to glove-up anymore because there's a blood test that saves us from having to put the glove on. Now, we may not have to glove-up for an entirely different reason these days, but the hope and expectation was, a rising PSA was cancer until proven otherwise. And it's funny how that mindset takes you right into the wrong field. 

Doctors are pessimists, a rising PSA means more cells... in other words, you're hypertrophy in the prostate, it's an expanding prostate. It may be a marker also of inflammation, a specific antigen is one with an inflamed prostate, sending out more than a normal prostate. And the problem was, we just took the simple-minded interpretation, put a dividing line and said if it's above value X that equals cancer until proven otherwise. And then we did our best to prove that there was a cancer, and we will go hell for leather. 

And it got to the point which has just been dying down in the last few years. We got to the ridiculous point that we were doing transrectal biopsies, which are dirty and dangerous biopsies, with 27 needles, taking 27 samples searching for that elusive cancer so that...

Andrew: You were macerating the prostate.

Mark: You were. And the patients that had it done got sick, they got a mild septicaemia or at least a bacteraemia. They were unwell for periods of time, plus you penetrated the prostate multiply in a very aggressive attack. And if there were cells that were potentially metastatic, you've opened up a lot of barriers…

Andrew: Yeah. 

Mark: To them getting to the rest of the body.

Andrew: And a lot of pathways for them to actually metastasise. 

Mark: That's it. And so that's what I was meaning actually, I just said it the wrong way. 

But the potential for the cells to escape the boundaries that you'd carefully put around it over that 10 years of that slow, slow, slow cancer building up, you penetrate the walls of that and you open it up not just to the pathologist looking under the microscope, but those cells are elsewhere as well. 

And so that aggressive search was done on the basis that if there is a cancer, we will find you. We will hunt you down and we will tear you out. And then we've had to step back and say, okay, of all the ones we tore out, why were there so many when relatively so few people were actually dying of it. 

And so, this last decade of our time in medicine has been step back and say, hmm, lots of people die with prostate cancer and we're finding the ones that never would have done anything. The four out of five that we found, we were never going to help anyone, one out of five. That sounds a lot until you do absolute risks. Between age 55 and age 70, if you do this aggressive sampling you identify one extra case per 1,000 people that you would not have identified.

Andrew: Very much like a vitamin D test.

Mark: Yes. And that you go overboard then with the treatment, so that the four out of five that would never have had any problem, now have a problem. And that is the surgical and the medical intervention. 

We became so enthusiastic about treating something that four out of five chance nothing was going to happen with, that we became damagers, net damagers. And now we're just stepping back from that saying, is there a better way?

The PSA drove that. Bluntly, even the inventor of the PSA test has had to come out and say, "Do not use this as your diagnostic test for cancer." It is a test of a particular antigen released by the prostate under particular circumstances, don't mistake it for a failure to look any other way. And these days, we're looking more at MRIs, and non-invasive forms of saying. if we got a good microscopic picture of it, not only do we not puncture it, but we've got a sizing and a measuring system that can say has it increased? Is this one that's moving in the right direction? 

So I think everything now has changed from sampling or diagnosis, to trajectory. That in prostates, everybody has a trajectory. Some of these will be never cancerous, some will be cancerous but proceed so slowly that you know that by the time it grows to anything significant, the person is going to be 117 years of age. And some...

Andrew: Which of course is what we're aiming for, but anyway.

Mark: Some go very quickly and you want to find that one or two. And so the art of medicine now is, we're moving from the non-specific to what's your particular trajectory, the N of one trial rather than the randomised control trial. What's your direction? You start at point A, six months later, you're at point B, how does that look compared to others? 

There's a separate thing of the liquid biopsy. And I understand with Lise that there is some controversy about this. But liquid biopsy is the way medicine is going in cancer. Circulating tumour cells go up massively after you have done a biopsy. If you put something into a prostate, the circulating epithelial tumour cells are significantly raised, and they're raised for a long time. Does that mean anything? No, it means you've done a biopsy. But it has at least the potential for saying, well if those cells are migrating all the way through the bloodstream and the liquid biopsy can pick them up, don't be too surprised if what you've induced is metastatic outcomes instead of local outcomes.

Andrew: There was a couple of points I just wanted to make, just to tidy off a thought, if you like, from before. So firstly, PSA, it's a glycoprotein. It's produced by the prostate, only by the prostate. And its function is to liquefy semen right? Some leaks into the bloodstream and therefore has to be metabolised by the liver, and this is why that issue of the liver raises its head again. 

Mark: We are not just prostates. The idea... one well-known professor friend of mine said "An immunologist sees a human being as a T-cell support system, most of us see it as a penile support system.” That you know, that males, if given their choice would not preserve their T cells, they'd preserve their sexuality. 

Andrew: Yep. 

Mark: So it is something that our bodies do to handle and it can metabolise it at different rates, and you can get differences in PSA because of liver-function differences rather than prostate functions.

Andrew: And other... even riding bicycles, physical exercise can raise PSA. 

Mark: Yes. They change the saddles of the bikes.

Andrew: You know, ejaculation even if you did, in the olden days, a rectal examination, a digital rectal examination for the prostate, and then measured your PSA it could be raised, so this local agitation. But it's because the liver has to metabolise that and get rid of them, get rid of the PSA. So it, could be an issue of the liver?

Mark: Yes, it's important to say that PSA is not a pathological antigen, right, it's a glycoprotein which is normally produced. And it's a question of the level and the trajectory. So even PSA when I was talking about trajectory of change on an MRI, the trajectory of change of a PSA. A rapidly rising PSA gives you more concern, a low free PSA to bound PSA ratio gives you more concern. 

So what happened with PSA is we knew we were on the wrong path as a one-off, so we've tried to extend its usefulness. Now, the new guidelines say, if a person has never had a PSA, never, ever, ever have a PSA test. Because once you're on that roundabout, you're kind of obliged to follow it through.

Andrew: In the treatment. You know, the problem here seems to be that the problem, the big baddy of all of this, is that the treatment hasn't evolved. Over the decades since I was nursing, it's still a TURP.

Mark: It's brutal.

Andrew: Or a radical prostatectomy, which has got a massive issue of side effects. 

Mark: The treatment is brutal, and if treatment were perfect and simple, and there were no adverse effects... This is the mythological view of medicine. If we got so good at the prostate management that there was no downside, it would still be costly and unnecessary to do the things that we have done with prostates, pursue them relentlessly. 

The fact is, you damage the prostate to save a person's life, you'd better be sure you're saving their life, because the costs otherwise for that person and the risks of negative outcomes are extremely high.

And so the real reason for backing off again, going back to my daughter's thing is, white, privileged males of an old age don't want to have erectile dysfunction. And so we're putting a lot of effort into finding out what you do with a prostate that looks to be playing upwards, even cancerous. But where the treatment doesn't lead to any sexual dysfunction, doesn't lead to urological problems, and doesn't lead to any other negative outcomes in the pelvic area. 

Andrew: So, what about the facility then of managing BPH? Not saying that that's necessarily always going to progress to prostate cancer, that there may be other issues there. 

But, you know, you've got certain... dare I say the word hero herbs? Not without controversy, but things like Saw Palmetto was, you know, the ‘poster child’ like curcumin was for all other sorts of cancers. But BPH it was Saw Palmetto, and then it ran into some negative press. Then I seemed to look into it further, it might well be the quality of the supplements that they were using.

What's been your experience in using things like lycopene, astaxanthin, even green tea, Saw Palmetto, of course. Herbs like epilobium, soy, now, there's one. And this is the one area that I've actually used soy, very high levels of isoflavones from soy with beneficial effect.

Mark: You've got a good theoretical basis for it, haven't you?

Andrew: Yeah, but, you know, we don't like soy. This is the one area that I actually used to throw quite a lot of isoflavones at it. 

Mark: You can make cases for all of these. I think that the upside of backing off the aggressive treatment is that everyone's looking around for things which are effective. 

And still to this day, like every other form of cancer, diet and exercise, are being played up to a much greater extent. They are not as effective as surgical excision, but the downsides of them are negligible. And the other upsides of exercise, cardiovascular capabilities, inflammation control, those things are a positive benefit to an older person's life.

The cynic in me thinks, once a slightly older male, say of my generation, starts to get out and exercise, the loss of weight, the interest in sex again, a lot of things start to return. And we forget that normal life can be supplanted by a life where we just expect disease to occur.

Andrew: Right. 

Mark: That we so far just expect things are going to stuff up. People of my age keep on saying "Of course, I have to see doctors because now everything goes wrong." Everything goes wrong for a reason, it doesn't go wrong for no reason.

So, the finding of the risk factors coming back to a high vegetable high fruit... well not so high in the fruit, but high in vegetable, a wide variety of vegetables, getting the exercise happening, Mr. Digby, I'm sure is protecting my...

Andrew: Mr. Digby is Dr. Mark Donohoe's dog. 

Mark: Yes, he's my little poodle, but he takes me for my 8k to 10k every day. And I'm convinced that that 30 kilos of weight loss, and him doing that exercise is good for me generally. 

What happens then is interest in things like sex become a lot more apparent. When you are overworked, overweight, in the dark, in front of a machine, stressed to the eyeballs, it's very difficult to manage that dosage of three ejaculates a week, you just don't have the time, often. So each of those plays it's part...

Andrew: What's the joke though? Sorry. Men don't need the time, what is it? We just need the time, we don't need the place, what is it? Sorry.

Mark: Right. I cannot indulge you in these any longer. You know, all of these.

Andrew: You're far too serious for me.

Mark: You're a younger man, you haven't lived the extra years. 

But my point is you don't have to be a rocket scientist to do the 70% reduction in prostate cancer risk. The stuff that's in our hands in lifestyle medicine is already there. What naturopaths have done for years is already there. As you know and you torture me every time when we do this, I'm not a herbalist. It's something I aspire to, in my later years...

Andrew: Damn you.

Mark: And yes, the soy products. I do agree. I do agree that the soy products play a big part in this. My experience with Saw Palmetto is that it made a significant difference in benign prostatic hypertrophy. And I was a prescriber of it as many, many doctors were, irrespective of the finest of trials.

Andrew: Well, that's a herb. 

Mark: Yes I know. I know, but I feel embarrassed as an amateur herbalist when a doctor says, I'm going to give you Saw Palmetto, and I'm not well trained in it. I'd be irritated if a naturopath decided to do a radical prostatectomy. And so, we each have our areas of knowledge, I can keep people safe from unnecessary...

Andrew: Touché.

Mark: ...procedures, but I have a little difficulty moving into authoritative dosage and management of things where there are herbs. And it is a different world, it's complex multifactorial, and it's as much art form as it is medicine. And that's the reason I'm not going to dabble in it until I know what I'm doing. 

Andrew: What about...

Mark: I shall know my song well before I start singing. 

Andrew: What about the modified things then like, for instance, modified citrus pectin? 

Mark: Yes. 

Andrew: And you know, there is some research on a product called PectaSol-C. So, I will mention that product in this instance, rather than ingredient. But also things like BioResponse DIM. 

Mark: Again, I don't have experience. The DIM I am interested since our last symposium here, just haven't got into it enough. And so, I always have to take things up in my... what's on the horizon of the things I need to know. 

But the DIM is really interesting. There are lots of hormonal modifiers, there are lots of things where the interplay between the gut, the liver, and the general circulation for inflammogens are going to be explored. I'm keen on doing it, but I don't know enough yet. 

And I think all we can do first is, back off from unnecessary stuff, with the prostate, a normal growing prostate in our 21st-century environments, are almost a given because of the way that obesity, and diet, and smoking, which was a small contributed cancer risk, but still modifiable. That there are modifiable risks which if we do them right, take the next generation down by about 70%. 

Andrew: Just a note on safety. Given that we don't now want to do PSA, so, we don't have a baseline and treatment level. But we still want to be alert for progression of serious or sinister disease. Let's say a naturopath is treating urinary flow in an elderly male. 

Mark: Yes. 

Andrew: So, their treatment measure really is based on how is that urine flow improving, and how many times does the male get up during the night, and have leakage and things like that? So that's, you know, symptomatology. Where does that lead us on a point of safety, for let's say, prevention of missing a sinister issue, a prostatic cancer? What symptoms would you look for, to say, I need to investigate further?

Mark: Blood in the urine. Blood in the urine is it, primarily. Once you've got something getting across into the urinary tract and you have blood, you have to pay a whole level of different attention to that. And so that's a good hallmark. 

The Saw Palmetto did that job that you just described, of people who had slow initiation and slow flow improving that. At the clinical level people given just commercial products with Saw Palmetto in it did very, very well with that. The people who up their lycopenes I think, have an inflammation controlling effect. I would guess that that's part of the mechanism of that function. But they similarly did well at a clinical level.

You have to make clinical judgments. Our mistake with the prostate was to get too technical, and want to do a blood test and never feel the prostate with our fingers up the rear end. To get out of that to a very technical answer, only to find the technical answer over-estimated risk, overestimated what we should do, and a vast amount of unnecessary urological surgery did a lot of harm. 

And so, the break away from that is if we don't do the PSAs we go back to clinical medicine. Did it work? Exactly as well as doing the highly technical medicine. Did it do it well, at a low cost? Yes. Because people came in and complained of something as the reason for you checking them. And what we do as doctors and naturopaths? We take a family history and say, 'Wow, uncle, dad, and your grandfather, we got to check that prostate.'

Andrew: We will now be checking. 

Mark: Yeah. And so coming back to the basics, when we're talking about if you do all the technical stuff, you save, 1 life per 1,000 males per year at the cost of around 20 of them very badly damaged from something that never needed to be treated, that's a poor equation. 

Andrew: Yeah, yeah. 

Mark: If we come back and say, let's go back to clinical medicine, and if we need a technical answer, we've got this cute thing called the MRI. And the MRI is not useful, usually on the very first one, but the trajectory over time is just brilliant. And so hand over to the doctor at that point, get the pairing of the MRIs that gives you a bit of confidence...

Andrew: See if there's an issue.

Mark: … about change over time. And otherwise, manage the lifestyle, and manage the herbal and other ways in which we are able to help a person with a prostate.

Andrew: Salient words based in expertise. Dr. Mark Donohoe, thank you so much, once again, for taking us through that quagmire of the prostate. 

Mark: The quagmire of the prostate. No. 

Andrew: This is FX Medicine, I'm Andrew Whitfield-Cook.

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Dr Mark Donohoe

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Dr Mark Donohoe

Dr Mark Donohoe is one of Australia’s most experienced and best known medical practitioners in the fields of Nutritional and Environmental Medicine. He has a long history working in the emerging field of “integrative medicine”, and continues to bring orthodox and complementary medicine together in his medical practice. He is a regular guest on the FX Medicine Podcast and in 2019 became the host of FX Medicine's newest podcast series; FX Omics - blending genetics into the modern practice of personalised medicine.