Author: Seth Roberts

Unhelpful Answers (Ancestral Health Symposium 2013)

Seth Roberts15 Comments

At the Ancestral Health Symposium, I went to a talk about food and the brain, a great interest of mine. The speaker said that flaxseed oil was ineffective because only a small fraction (5%) gets converted into DHA — a common claim.

During the question period, I objected.

Seth I found that after I ate some flaxseed oil capsules, my balance improved. Apparently flaxseed oil improved my brain function. This disagrees with what you said.

Speaker Everyone’s different.

A man in the audience said what I observed might have been a placebo effect. I said that couldn’t be true because the effect was a surprise. He disagreed. (The next day, in the lunch line, he spoke to a friend about getting in a kerfuffle with “an emeritus professor who wasn’t used to being disagreed with.”) I spoke to the speaker again:

Seth Is it possible that flaxseed oil is converted to DHA at a higher rate than you said?

Speaker Anything’s possible.

This reminded me of a public lecture by Danny Kahneman at UC Berkeley. During the question period, a man, who appeared to have some kind of impairment, asked a question that was hard to understand. Kahneman gave a very brief answer, something like “No.”

Afterwards, a woman came over to me. Maybe flaxseed oil reduced inflammation, she said. Given that the brain is very high in omega-3, and so is flaxseed oil, this struck me as unlikely. I said I didn’t like how my question had been answered. I’ve been there, she said. Other members of her family were doctors, she said. She would object to what they said and they would respond in a dismissive way.

The speaker is/was a doctor. Her talk consisted of repeating what she had read, apparently. The possibility that something she read was wrong . . . well, anything’s possible.

 

 

 

Correlation of Body and Soul (Ancestral Health Symposium 2013)

Seth Roberts5 Comments

Geoffrey Miller, speaking at the Ancestral Health Symposium, said that every mental disorder impairs your sense of humor, so sense of humor is a good marker for overall brain function. It’s a fascinating point: what is the evolutionary reason that humor exists? Miller says it helps in mate choice. We select people in many ways (spouse, lover, business partner, friend, student, teacher, etc.). Maybe sense of humor is a general signal of health.

At the first Ancestral Health Symposium, Tucker Max noted that the attendees looked much better — healthier — than usual. It was a good point. Almost no one was fat, for example. And a large fraction of them became interested in paleo because of their own poor health, which paleo helped with. At this year’s symposium, I’ve noticed that the attendees strike me as in unusually good mental health, in the sense that I find everyone easy to talk to. For example, I had an interesting talk with a woman about “unschooling”. (I realized from what she said that non-traditional schooling is close to common sense when it is done with kids who are doing badly in school Why repeat what isn’t working? My experience suggests it also helps kids who have done well in school. Where it is non-intuitive. If something is working, why change it?) Likewise, all of the questions after talks are polite, none are too long, none are grandstanding.

 

“Hunger is a Necessary Nutrient” (Ancestral Health Symposium 2013)

Seth Roberts9 Comments

Nassim Taleb said this or something close to it on the first day of the Ancestral Health Symposium in Atlanta, which was yesterday. Danielle Fong told me something similar last week: We should use all of our metabolic pathways. Of course it is hard to know what metabolic pathways you are using. In contrast, Taleb’s point — not original with him, but a new way (at least to me) of summarizing research — is easily applied.

What I know overwhelmingly supports Taleb’s point. 1. When I did the Shangri-La Diet the first time, I was stunned how little hunger I felt. This wasn’t bad — presumably my set point had been too high, lack of hunger reflected the dropping set point, it was good to know how to lower the set point — but it was dreary, not feeling hunger. It was as if life had gone from color to black and white. Something was missing. 2. Data supporting the health benefits of intermittent fasting, which produces more hunger than the control condition. 3. The experience of my friend who had great benefits from alternate-day fasting. He told me he had never felt hunger before, at least of that magnitude. A great increase in hunger, in other words, happened at exactly the same time as a great improvement in health.

Obviously Taleb is talking about hunger caused by lack of food, rather than hunger caused by learned association (if you eat at noon every day you will become hungry at noon, if you eat every time you enter Store X, you will be come hungry when you enter Store X, the existence of this effect is why they are called appetizers). The Shangri-La Diet reduces your set point but only if your set point controls when/how much you eat is this going to make a difference. So to lose weight you need to do two things: 1. Lower your set point. 2. Lower your weight to your set point. While SLD certainly does #1, it does not do #2. You can make sure your weight is near your set point if you feel strong hunger if you don’t eat for a while.

Taleb’s comment suggests focussing on the outcome of fasting, rather than on its duration or frequency. Instead of fasting every other day (or whatever), fast until you feel strong hunger. How often you need to do this, how strong the hunger should be, are questions to answer via trial and error.

 

 

Smoking and Cancer

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In his interview with me about The Truth in Small Doses (Part 1, Part 2), Clifton Leaf praised Racing to the Beginning of the Road (1996) by Robert Weinberg. “A masterful job . . . the single best book on cancer,” wrote Leaf. In an email, he continued:

In Chapter 3 of “Racing to the Beginning of the Road,” Weinberg goes through much of the early epidemiological work linking tobacco to smoking (John Hill, Percivall Pott, Katsusaburo Yamagiwa, Richard Doll), but then focuses on the story of Ernst Wynder, who just happens to be one of Weinberg’s cousins. [As a medical student, Wynder found a strong correlation between smoking and lung cancer.] Building on his own prior epidemiological work, and that of many others, Wynder actually built an experimental “smoking machine” at the Sloan-Kettering Institute in New York in the early 1950s. The machine collected the tar from cigarette smoke (and later, the condensate from the smoke) and Wynder used those to produce skin cancers in mice and rabbits. But the amazing part of the story is what happened later…with Wynder’s bosses at Sloan-Kettering and with one of the legendary figures in cancer research, Clarence Cook Little. I don’t want to give the story away. (If you have the time, you really would love reading the book.) But it’s one of the most damning stories of scientific interference I’ve read.

Wynder met a lot of opposition. His superiors at Sloan-Kettering required that his papers be okayed by his boss, who disagreed with his conclusions. Clarence Cook Little, according to Weinberg, made the following arguments:

The greater rates of lung cancer in smokers only gave evidence of a correlation, but hardly proved a causal connection. One’s credulity had to be strained to accept the ability of a single agent [he means smoking] to cause lung cancer along with so many other diseases including bronchitis, emphysema, coronary artery disease, and a variety of cancers of the mouth, pharynx, esophagus, bladder and kidney. After all, many of these diseases existed long before people started smoking.

A little masterpiece of foolishness . . . and more reason to never ever say correlation does not equal causation. Little was at one point President of the University of Michigan. Later he worked for the tobacco industry. It wasn’t just Little. Weinberg says that Wynder’s colleagues complained about his “statistical analyses and experimental protocols, which they found to be less than rigorous.”

Weinberg says little about epidemiology in the rest of the book — which, to be fair, is about the laboratory study of cancer. At the very end of the book, he writes:

We learned much about how cancer begins; it is no longer a mystery. We will surely learn more . . . but the major answers already rest firmly in our hands. . . . No, we have still not found the cure. But after so long, we know where to look.

The claim that “we know where to look” is not supported by examples. And Weinberg says nothing about prevention.

Weinberg’s book reminded me of a new-music concert I attended at the Brooklyn Academy of Music. Hard to listen to (non-melodic, etc.) like lots of new non-popular music. I didn’t enjoy it, but surely the composer did — this was fascinating. How did it happen? I wondered. Weinberg describes a great deal of research that has so far produced little practical benefit. Weinberg, it seems, has managed to avoid being bothered by this — if he even notices it. How did this happen?

I don’t think it’s “bad” or wrong or undesirable to do science with no practical benefit, just as I don’t complain about “unlistenable” music. Plenty of “useless” science has ultimately proved useful, but the transition from useless to useful can take hundreds of years, which is why there must be “scaffolding,” sources of support other than practicality. This is why scientists use the word elegant so much. Their enjoyment of “elegance” is scaffolding. Long before “useless” science, there was “useless” decoration (and nowadays there is “unlistenable” music). Thorstein Veblen showed no sign of understanding that the “waste” he mocked made possible exploration of the unknown, which is necessary for progress. (By supporting artisans, such as the artisans who make decorations, we support their research.) What is undesirable is when someone (like Wynder) manages to do something useful, to foolishly criticize it, as Little and Wynder’s colleagues did.

The Truth in Small Doses: Interview with Clifton Leaf (Part 2 of 2)

Seth Roberts1 Comment

Part 1 of this interview about Leaf’s book The Truth in Small Doses: Why We’re Losing the War on Cancer — and How to Win It was posted yesterday.

SR You say we should “let scientists learn as they go”. For example, reduce the need for grant proposals to require tests of hypotheses. I agree. I think most scientists know very little about how to generate plausible ideas. If they were allowed to try to do this, as you propose, they would learn how to do it. However, I failed to find evidence in your book that a “let scientists learn as they go” strategy works better (leaving aside Burkitt). Did I miss something?

CL Honestly, I don’t think we know yet that such a strategy would work. What we have in the way of evidence is a historical control (to some extent, we did try this approach in pediatric cancers in the 1940s through the 1960s) and a comparator arm (the current system) that so far has been shown to be ineffective.

As I tried to show in the book, the process now isn’t working. And much of what doesn’t work is what we’ve added in the way of bad management. Start with a lengthy, arduous, grants applications process that squelches innovative ideas, that funds barely 10 percent of a highly trained corps of academic scientists and demoralizes the rest, and that rewards the same applicants (and types of proposals) over and over despite little success or accountability. This isn’t the natural state of science. We BUILT that. We created it through bad management and lousy systems.
Same for where we are in drug development. We’ve set up clinical trials rules that force developers to spend years ramping up expensive human studies to test for statistical significance, even when the vast majority of the time, the question being asked is of little clinical significance. The human cost of this is enormous, as so many have acknowledged.

With regard to basic research, one has only to talk to young researchers (and examine the funding data) to see how badly skewed the grants process has become. As difficult (and sometimes inhospitable) as science has always been, it has never been THIS hard for a young scientist to follow up on questions that he or she thinks are important. In 1980, more than 40 percent of major research grants went to investigators under 40; today it’s less than 10 percent. For anyone asking provocative, novel questions (those that the study section doesn’t “already know the answer to,” as the saying goes), the odds of funding are even worse.

So, while I can’t say for sure that an alternative system would be better, I believe that given the current state of affairs, taking a leap into the unknown might be worth it.

SR I came across nothing about how it was discovered that smoking causes lung cancer. Why not? I would have thought we can learn a lot from how this discovery was made.

CL I wish I had spent more time on smoking. I mention it a few times in the book. In discussing Hoffman (pg. 34, and footnote, pg. 317), I say:

He also found more evidence to support the connection of “chronic irritation” from smoking with the rise in cancers of the mouth and throat. “The relation of smoking to cancer of the buccal [oral] cavity,” he wrote, “is apparently so well established as not to admit of even a question of doubt.” (By 1931, he would draw an unequivocal link between smoking and lung cancer—a connection it would take the surgeon general an additional three decades to accept.)

And I make a few other brief allusions to smoking throughout the book. But you’re right, I gave this preventable scourge short shrift. Part of why I didn’t spend more time on smoking was that I felt its role in cancer was well known, and by now, well accepted. Another reason (though I won’t claim it’s an excusable one) is that Robert Weinberg did such a masterful job of talking about this discovery in “Racing to the Beginning of the Road,” which I consider to be the single best book on cancer.

I do talk about Weinberg’s book in my own, but I should have singled out his chapter on the discovery of this link (titled “Smoke and Mirrors”), which is as much a story of science as it is a story of scientific culture.

SR Overall you say little about epidemiology. You write about Burkitt but the value of his epidemiology is unclear. Epidemiology has found many times that there are big differences in cancer rates between different places (with different lifestyles). This suggests that something about lifestyle has a big effect on cancer rates. This seems to me a very useful clue about how to prevent cancer. Why do you say nothing about this line of research (lifestyle epidemiology)?

CL Seth, again, I agree. I don’t spend enough time discussing the role that good epidemiology can play in cancer prevention. In truth, I had an additional chapter on the subject, which began by discussing decades of epidemiological work linking the herbicide 2-4-D with various cancers, particularly with prostate cancer in the wheat-growing states of the American west (Montana, the Dakotas and Minnesota). I ended up cutting the chapter in an effort to make the book a bit shorter (and perhaps faster). But maybe that was a mistake.

For what’s it worth, I do believe that epidemiology is an extremely valuable tool for cancer prevention.

[End of Part 2 of 2]

The Truth in Small Doses: Interview with Clifton Leaf (Part 1 of 2)

Seth Roberts3 Comments

I found a lot to like and agree with in The Truth in Small Doses: Why We’re Losing the War on Cancer — and How to Win It by Clifton Leaf, published recently. It grew out of a 2004 article in Fortune in which Leaf described poor results from cancer research and said that cancer researchers work under a system that “rewards academic achievement and publication over all else” — in particular, over “genuine breakthroughs.” I did not agree, however, with his recommendations for improvement, which seemed to reflect the same thinking that got us here. It reminded me of President Obama putting in charge of fixing the economy the people who messed it up. However, Leaf had spent a lot of time on the book, and obviously cared deeply, and had freedom of speech (he doesn’t have to worry about offending anyone, as far as I can tell) so I wondered how he would defend his point of view.

Here is Part 1 of an interview in which Leaf answered written questions.

SR Let me begin by saying I think the part of the book that describes the problem – little progress in reducing cancer – is excellent. You do a good job of contrasting the amount of time and money spent with progress actually made and pointing out that the system seems designed to produce papers rather than progress. What I found puzzling is the part about how to do better. That’s what I want to ask you about.

In the Acknowledgements, you say Andy Grove said “a few perfect words” that helped shape your thesis. What were those words?

CL “It’s like a Greek tragedy. Everybody plays his individual part to perfection, everybody does what’s right by his own life, and the total just doesn’t work.” Andy had come to a meeting at Fortune, mostly just to chat. I can’t remember what the main topic of conversation was, but when I asked him a question about progress in the war on cancer, he said the above. (I quote this in the 2004 piece I wrote for Fortune.)

SR You praise Michael Sporn. His great contribution, you say, is an emphasis on prevention. I have a hard time seeing this as much of a contribution. The notion that “an ounce of prevention is worth a pound of cure” is ancient. What progress has Sporn made in the prevention of anything?

CL Would it be alright, Seth, if before I answer the question, I bring us back to what I said in the book? Because I think the point I was trying to make — successfully or not (and I’m guessing you would conclude “not” here) — is more nuanced than “an ounce of prevention is worth a pound of cure.”

Here’s what I see as the key passage regarding Dr. Sporn (pgs. 133-135):

For all his contributions to biology, biochemistry, and pharmacology, though, Sporn is still better known for something else. Rather than any one molecular discovery, it is an idea. The notion is so straightforward—so damned obvious, really—that it is easy to forget how revolutionary it was when he first proposed it in the mid-1970s: cancer, Sporn contended, could (and should) be chemically stopped, slowed, or reversed in its earliest preinvasive stages.

That was it. That was the whole radical idea.

Sporn was not the first to propose such an idea. Lee Wattenberg at the University of Minnesota had suggested the strategy in 1966 to little response. But Sporn refined it, pushed it, and branded it: To distinguish such intervention from the standard form of cancer treatment, chemotherapy—a therapy that sadly comes too late for roughly a third of patients to be therapeutic—he coined the term chemoprevention in 1976.

The name stuck.

On first reading, the concept might seem no more than a truism. But to grasp the importance of chemoprevention, one has first to dislodge the mind-set that has long reigned over the field of oncology: that cancer is a disease state. “One has cancer or one doesn’t.” Such a view, indeed, is central to the current practice of cancer medicine: oncologists today discover the event of cancer in a patient and respond—typically, quite urgently. This thinking is shared by patients, the FDA, drug developers, and health insurers (who decide what to pay for). This is the default view of cancer.

And, to Sporn, it is dead wrong. Cancer is not an event or a “state” of any kind. The disease does not suddenly come into being with a discovered lump on the mammogram. It does not begin with the microscopic lesion found on the chest X-ray. Nor when the physician lowers his or her voice and tells the patient, “I’m sorry. The pathology report came back positive. . . . You have cancer.”

Nor does the disease begin, says Sporn, when the medical textbooks say it does: when the first neoplastic cell breaks through the “basement membrane,” the meshwork layers of collagen and other proteins that separate compartments of bodily tissue. In such traditional thinking, it matters little whether a cell, or population of cells, has become immortalized through mutation. Or how irregular or jumbled the group might look under the microscope. Or how otherwise disturbed their genomes are. As long as none of the clones have breached the basement membrane, the pathology is not (yet) considered “cancer.”

For more than a century, this barrier has been the semantic line that separates the fearsome “invader” from the merely “abnormal.” It is the Rubicon of cancer diagnosis. From the standpoint of disease mechanics, the rationale is easy to understand, because just beyond this fibrous gateway are fast-moving channels (the blood and lymphatic vessels) that can conceivably transport a predatory cell, or cells, to any terrain in the body. Busting through the basement is therefore a seeming leap past the point of no return, a signal that a local disturbance is potentially emerging into a disseminating mob.*

But while invasion may define so-called clinical cancer for legions of first-year medical students, it is by no means the start of the pathology. Cancer is not any one act; it is a process. It begins with the first hints of subversion in the normal differentiation of a cell—with the first disruption of communication between that cell and its immediate environment. There is, perhaps, no precise moment of conception in this regard, no universally accepted beginning—which makes delineating the process that much harder. But most, if not all, types of “cancer” have their own somewhat recognizable stages of evolution along the route to clinically apparent disease.

“Saying it’s not cancer until the cells are through the basement membrane,” says Sporn, “is like saying the barn isn’t on fire until there are bright red flames coming out of the roof. It’s absolute nonsense!”

(Sorry for that long excerpt.) I think that Dr. Sporn’s greatest contribution was to reframe cancer as a continually evolving, dynamic process — carcinogenesis — rather than an event or state of being. And it was one that, conceivably at least, we could interrupt — and interrupt earlier than at the point at which it was clinically manifested. This was distinct from early detection, which, while effective to some extent and in some cancers, was both detecting cancers too late and “catching” many lesions that weren’t likely to develop any further (or didn’t really exist to begin with), adding to the already-great cancer burden.

There was a potential, said Sporn, to intervene in a way that might stop developing cancers in their tracks, and yet would not necessarily have to add to the burden of cancer overtreatment.

As I spend most of Chapter 7 discussing, there are enormous barriers to pulling this of—and I did my best to lay out the challenges. But I do believe that this is the way to go in the end.

SR You praise Kathy Giusti for her effect on multiple myeloma research. I couldn’t find the part where that research (“a worthy model for cancer research that can serve as a guidepost for the future . . . that teaches everything there is to teach about the power of collaborative science”, p. 260) came up with something useful.

CL Seth, sorry this again may be me not being very clear in my writing. I apologize for that. But the lines you cite actually are intended to set up the Burkitt story in the following chapter. It was Burkitt’s effort against the mysterious African lymphoma, that remains, in my view, “a worthy model for cancer research…”

SR You praise Burkitt’s epidemiology. How did that epidemiology help find out that Burkitt’s lymphoma responds to certain drugs? I couldn’t see a connection.

CL Good question. I think Burkitt’s very old-fashioned epidemiological investigation identified a widespread, terrible cancer that had been seen many times, but not noticed for what it was. It helped narrow down who was getting this cancer and—at least in a broad, geographical sense—why. But it wasn’t epidemiology that helped discover that this lymphoma was responsive to certain drugs—that was trial and error. As with the case of Farber and ALL [acute lymphocytic leukemia], many today would blanch at the primitive experimental protocols that tested these toxic drugs in children. But with an extraordinarily aggressive tumor that was killing these kids in weeks, Burkitt felt he had to try something. Again, that’s not epidemiology, but it is an understanding of the urgency of this disease that we can, perhaps, learn from.

[End of Part 1 of 2]

Alternate Day Fasting: Not For Everyone?

Seth Roberts9 Comments

I’ve been doing alternate day fasting for about two months. I find it very easy. In several ways it’s easier than eating every day:

  • save time
  • save money
  • less constrained on eating days
  • a little more hungry than usual on fasting days (up to a point hunger is pleasant — when the Shangri-La Diet wiped out all my hunger, I didn’t like it)
  • sense of accomplishment when I wake up after a fasting day (I did it)
  • food tastes better

Maybe my friends are unusually tolerant but I have yet to encounter a serious negative. Yesterday, a fasting day, I happily watched a friend eat dinner. I had two bites out of curiosity. I saw nothing to suggest it made her uncomfortable I wasn’t eating.

However, a different friend has told me that alternate day fasting made her sick. She did it for about three months, felt worse and worse, and finally stopped. She believes it works less well for women than for men. I suspect a heavy exercise routine (she ran a lot) made alternate day fasting more difficult. But there is also the best-selling book The FastDiet. It has two authors, a man (Michael Mosely, a doctor) and a woman (Mimi Spencer, a journalist). The book contains a remarkably short and remarkably unenthusiastic description of Spencer’s experience with intermittent fasting. Maybe it didn’t agree with her, either.

Cream Cheese Improves Brain Function

Seth Roberts3 Comments

Last night I had dinner with a friend in a restaurant. We chatted with a couple sitting next to us. They asked what I did research about. “Food and the brain,” I said. “What foods make the brain work best.” They asked for an example. “ Butter,” I said. The woman smiled. “That’s great news! Butter is delicious.” As they left, the woman said, “I feel like I’ve learned some really interesting things.”

I agree, great news — partly because butter is delicious. Yet it fits what we already know. It’s been known since the 1920′s that a high-fat (“ketogenic”) diet can ameliorate childhood epilepsy. I suppose it’s called “ketogenic diet” to avoid the term high-fat – or to sound more “scientific”. It’s an unfortunate name because why the diet helps is unclear. “Although many hypotheses have been put forward to explain how the ketogenic diet works, it remains a mystery,” says Wikipedia.

Another example of dairy fat improving brain function comes from a little girl with a rare genetic disease:

A 3-year-old girl, . . . thanks to a diet of cream cheese, gained the ability to speak despite a disease that [had] left her mute from birth.

Fields Taylor, from Melton Mowbray in Leicestershire, was born with the incurable genetic disease Glut 1 Deficiency that caused a lack of glucose to flow to her brain. Today, Taylor’s diet of four containers of the cream cheese per week gives her a voice. . . . ”The amount of Philadelphia [cream cheese] she goes through is mad but worth it. It really has been our saving grace. She loves the stuff and piles it on crackers,” The Mirror quoted her mother Stevie as saying. “The first time I heard Fields say ‘Mum’ it was just wonderful.” . . . Glut 1 affects just 26 people in the U.K.

Thanks to Tom George.

More Evidence Linking Fermentation and Complexity: Wild-Fermented Wine

Seth Roberts5 Comments

I came to believe that we need to eat fermented foods to be healthy partly because this idea solved an evolutionary question: why do we like food that is sour, umami-flavored, and complex? I realized that all three preferences could be explained the same way: All three push us to eat more fermented food. For example, fermented milk (yogurt) is sourer than fresh milk.

Fermentation also increases complexity. An example is miso. I noticed that miso by itself was sufficient flavoring for soup. I had to add quite a few spices to produce the same amount of complexity that miso alone produced — miso was a super-spice.

Wine is a fermented food, of course, but long ago all fermentation was “wild” — it proceeded from whatever fermenting agents were in the air, on people’s hands, and so on. Fermentation increased complexity not just because the microbes metabolized the food but because there were many kinds of microbes. Australian winemakers were recently given a lesson in the connection between wild fermentation and complexity:

We were tasting two glasses of pinot noir, blind, and the questions were: is there any difference between them? If so, how are they different?

Glass One was full purple-red in colour and smelled fresh and fruity, delightfully primary, with a bright raspberry aroma that was almost like bubble gum. It was pristinely clean, delicate, light on the palate and charming, but ultimately rather simple.

Glass Two had a darker colour and blacker fruit aromas, more complex and mysterious. Similarly, in the mouth it was fuller-bodied, richer and deeper, with greater textural interest, fleshier and denser, with more tannin. A beautiful wine, too, but much more profound and captivating than Glass One.

Winemaker David Bicknell then announced to the gathering [of winemakers] that the only difference between the wines was that Glass One had been fermented with a pure yeast strain and Glass Two had undergone a wild ferment. That means no yeast had been added: the juice had been fermented by whatever yeast strains happened to be in the air at the time.

“Both wines were picked from the same Upper Yarra Valley vineyard on the same day, and everything in the winemaking was the same except the yeast,” announced Bicknell, who is the winemaker at Oakridge. The class was asked to try to pick the wild ferment and say which wine they preferred. The great majority nominated the correct glass, and liked it more. There was nothing wrong with Glass One: it was simply that Glass Two was better – every way you looked at it.

The “class” was a wild-yeast workshop at the recent Australian Wine Industry Technical Conference in Sydney. The “students” consisted mainly of experienced winemakers. . . . The environment, especially the air, contains hundreds of thousands of strains of yeast, most of which occur naturally. The species present depend on what flowers, fruits, trees and grasses are in that locality. Recent New Zealand research has shown that yeasts are territorial, and the species present vary according to the place. . . .

Pairs of Hardys’ Eileen Hardy chardonnay and Mount Pleasant Hunter chardonnay, all 2013 vintage, one of each “wild” and the other seeded with cultured yeast, showed more permutations of character. With Mount Pleasant, the wild wine was cloudy in appearance, and quite stinky, but also showed density of flavour and richness, while the regular wine was good but not as interesting. The winemakers seemed to think the stinky one would clean up after a period of lees-stirring.

Of the Hardys wines, the regular ferment looked bright and clear in the glass, and was pristinely clean, intense and lively, with a spring water-like lightness of texture. The wild ferment was cloudy, smelled of cashews, bread, smoky oak, sulfides and spices, but the real difference was in the mouth. Its texture was far more rich and dense, fleshy and rounded, smooth and harmonious.

Eileen Hardy winemaker Tom Newton said he believed the sulfides were related to the wine’s greater textural density. Indeed, all winemakers I’ve quizzed who practise wild fermentation believe it gives their wines greater length of palate and improved texture as well as extra flavour complexity.

Even riesling responds to this ”rougher than usual handling”. Kerri Thompson’s wild-ferment Clare Valley riesling was a graphic illustration. Served beside a conventional Clare riesling, which was a perfectly good wine in its way, her KT Pazza Riesling 2013 was turbid (not clear) and smelled of apple, pear, yeast and a hint of nuttiness from time spent in old barrels. It was a more expressive, more textural and more layered wine than the conventional one. It’s on sale soon at $29.

And perhaps the most beautiful, exotic, fascinating wine of the day was Cullen’s Kevin John Chardonnay 2011. . . . Biodynamically grown and wild fermented, it’s a pioneer and benchmark of the genre. It’s so complex it’s difficult to describe, although honey and oak and what I call “balsamic” (like the smell of balsamic vinegar, without the vinegar or sweetness) aromas are all involved, welded to a razor-sharp, crisply tart, long and linear palate structure.

Will Australia become the new California? Decades ago, California winemakers figured out how to make wines that were the equal of French wines. No doubt French winemaking had stagnated. Australian winemakers have just been taught how to make much better wines for the same price. As far as I know, Californian and French winemakers have yet to learn this lesson.

Wine is a very old food. One remarkable thing about this demonstration is how long it took — how long it took to learn this lesson. Sure, we like hand-made this and artisanal that, but in so many ways we prize uniformity, no more so than in our educational system, to which we entrust the most precious thing we have: our children. Who are treated by that system in a factory-like way, in the sense that all children in a class get the same teaching materials and are given the same tests. I have yet to hear an education theorist say that the best education produces diversity not uniformity. When I let my students’ underlying diversity be expressed (for example, in what they chose to learn), teaching became much easier. Win-win. Essentially what the winemakers are figuring out: When you let the natural variation of yeasts be expressed, making great wine becomes much easier.