Rhonda: You actually showed something very interesting about the effects of sulforaphane on a certain type of microbe species, H. pylori.

Jed: So H. pylori, it's full name is Helicobacter pylori. Helicobacter pylori is a very interesting organism in that it grows primarily or exclusively in the stomach. And it occupies that niche in a very unique fashion. It apparently has an enzyme that is called urease, but an enzyme that allows it to neutralize the pH in a little micro-environment around the bacterial cells in the stomach. We shouldn't use the term "gut" because we also use the term "gut" to refer to the intestines.

So the stomach is very acid, extremely acid, that's part of the way it does its job. And Helicobacter tunnels into the mucus layer inside the stomach and, with enzymes, creates this little zone of neutral pH which allows it to thrive, otherwise it would be killed as are any other, or almost any other bacteria that enter the stomach. And it's a very interesting critter, if I can use the term. Can I call it "critter"?

Rhonda: Yeah.

Jed: It's a very interesting critter because some people, some very well-respected and well-known microbiologists, for example, Martin Blaser at NYU, maintains and I happen to drink this Kool-Aid, I happen to believe this, that Helicobacter has been around all during the evolution of humankind. Certainly, for tens of thousands of years, people have had Helicobacter in their systems. And something like 55% of the world's population at the moment has Helicobacter in their systems. In some areas, recently in Japan and certainly some areas in Africa and Asia, almost all people have Helicobacter, and some areas of South America. And it's a colonizer. It's a commensal symbiotic organism, it would appear. It may actually confer benefit on its host, in other words, you, the person.

If levels of Helicobacter get too high, if the number of bacterial cells per square millimeter or per square inch or per square mile or however you want to quantify them gets too great, then they start to have clearly pathological effects. They can cause ulcers. They do cause ulcers and that can eventually lead to stomach cancer. I believe the last estimate I saw was that the World Health Organization considers Helicobacter to confer, I think, a three or four to six fold increased risk of stomach cancer if you are colonized. But the question is if you are colonized with Helicobacter, can you reduce the levels of colonization, keep it down to a low roar, as it were. In other words, let a few of them hang around in your stomach as long as they don't overrun the system?

And so the prescription for someone who has Helicobacter in this country and I believe in Europe, I'm not a gastroenterologist, but, is to wipe it out. So to treat it with so-called triple therapy, three separate antibiotics and kill it so you can't find it anymore. And I should say about 15% of people who are given that treatment either can't take it or it doesn't work. So an alternative that many people find appealing is a dietary approach to controlling Helicobacter. In other words, and we don't have answers to these questions, but if so many people around the world are colonized and it's been with us for so long and humankind is still humankind, are there perhaps benefits to having it? So, for example, it's been shown, I believe this was Martin Blaser who showed this a number of years ago, that there is an inverse correlation between Helicobacter infection and childhood asthma. So it may protect, due to stimulation of the immune system, other mechanisms. It may protect against certain diseases, but we just don't know enough.

So maybe reducing the levels of Helicobacter in the stomach, again, keeping it to a low roar where it can't cause or where it doesn't cause major inflammation, doesn't give you ulcers may be enough to reduce the risk of its causing stomach cancer at some point in the future. If it doesn't cause inflammation and there are only a few cells here and there that are sort of hanging on, maybe that's okay. So that can be done by a dietary approach. And with that in mind, we actually looked at the ability of sulforaphane to kill Helicobacter. Of course, if it had wiped out all the Helicobacter in people who are infected, I would have been happy with that also. That would have certainly been an interesting finding.

What we ultimately found, and this was done with collaborators in Japan in a 50-person trial, we found that Helicobacter can reduce the levels...sorry, the sulforaphane or broccoli sprouts, actually, fresh broccoli sprouts were able to reduce levels of colonization in infected people or colonized people and were able to reduce markers of inflammation in those same people. That work grew from an observation that I made with a different colleague, a French colleague who was visiting the U.S. on sabbatical, Alain Lozniewski. So he and I discovered and published in about 2002 that in vitro, in a test tube, sulforaphane was very capable of killing Helicobacter. Not only did it kill natural strains, but it killed strains that he had re-cultured from some of his patients. He's a gastroenterologist, and it killed singly and doubly antibiotic-resistant strains. So, as you know, antibiotic resistance in bacteria of all sorts in all settings is a huge problem and Helicobacter is no different. Once Helicobacter in people starts seeing a bunch of antibiotics, some of them develop resistance including resistance to two of the commonly used antibiotics that are used to treat it. So the fact that sulforaphane was equally effective in killing them was, we thought, quite significant. And interestingly, sulforaphane is not as potently antibiotic against a whole variety of other bacteria.

Rhonda: So do you know why the H. pylori is so sensitive to it?

Jed: You know, we don't. We thought we had some clues and, actually, Dr. Lozniewski's colleague in France had done some work on that which was never published. This colleague, for reasons that we need not get into here, is no longer in the business of science and so that paper never got published and we never really finished the proof. So we're not sure why it's so potently antibiotic. One thing I can tell you is that in the quest for that answer, quite recently, Kitty Stephenson who works here with us and I started looking at the ability of sulforaphane to inhibit urease, which is that enzyme that I told you that neutralizes the pH in the mucus of the stomach. And we found that, indeed, sulforaphane is quite an effective inhibitor of that enzyme.

But, so again, we thought we had a really eureka moment, but it turned out that wiping out that enzyme wasn't sufficient to kill Helicobacter because strains... How do I put this? Strains of Helicobacter that had been engineered by others to not contain urease were still killed by sulforaphane. So it wasn't...so the urease... So inhibiting urease might be important from a disease prevention standpoint, but it's not how the molecule killed the bacteria. Sorry to present such a complicated story, but that's the way things roll in this business.

Rhonda: That's science. Yeah, for sure. But the also very not surprising, to me, results of it lowering inflammation is one of my obsessions with sulforaphane, generally speaking. I'm very interested in anything in my diet, in my lifestyle that I can do that will lower the amount of systemic inflammation that I have in my body. And it's been shown, and you've shown this and others have shown that even broccoli sprout extract powder given to people can lower C-reactive protein levels by as much as 20%. Other inflammatory cytokines, IL-6, can be lowered by something similar. You know, so it's having a robust and measurable effect in people that's been repeatable in several different studies that I have seen.

But one of the reasons I'm so interested in this is because, well, inflammation really plays a role in a lot of diseases like cancer, but it really seems to be a driver of the aging process. And I don't know if you've...I think I mentioned this to you briefly, but I actually think that sulforaphane may be a anti-aging compound. It's one of the reasons I'm obsessed with sprouting and taking it. I think that actually not only is it preventing these diseases like cancer, but also may be actually delaying the aging process by activating Nrf2, which then activates all these anti-inflammatory genes, activates the antioxidant genes including all the glutathione-related enzymes. I don't know if you've seen the study, but I think I also mentioned to you that I would love to see some lifespan studies done in animals. I know those are not easy to do. They take a long time. But there was a study that was done in this red flower beetle. Have you seen this study?

Jed: No, no.

Rhonda: Okay. So let me tell you. So there's a red flower beetle. Yes, it's a bug, but they have an Nrf2 gene that's homologous to humans, also the FOXO gene, as well. So the scientists fed these red flower beetles different doses of broccoli sprout extract and the doses ranged from, it was low to high, I can't recall, but it was a dose response. And what they found is that at, I think it was at the highest dose, it extended the lifespan of these beetles by 15% and when they exposed these beetles to a high oxidative stress all the time by keeping them in a warmer environment constantly, it extended their lifespan by 30%. And it was totally dependent on Nrf2. So if they knocked down Nrf2, the lifespan extension went away. So I was, like, this is a great teaser, right? Because if it's happening and, I mean, obviously, it's a bug, but it's the same gene, they have a homologous gene and if it's extending this lifespan of this critter that has the same, similar gene that we have, then I feel like there is potential there.

Jed: That's fascinating. No, it wasn't for me...so I have ...

Rhonda: I will send you the paper.

Jed: Please. I have to ask you, is this a red beetle that likes flowers or a beetle that likes red flowers?

Rhonda: It eats red flowers.