IN DEFENSE OF LOW FAT: A CALL FOR

SOME EVOLUTION OF THOUGHT

(PART 1)
Not a typo.

Not April Fool’s Day.

Not a spontaneous and mystical possession by the spirit of George McGovern.

Not even a social experiment to see how many people I can get to unsubscribe from this
blog in the span of a day (PLEASE STAY, I LOVE YOU).

Maybe a little bit of this, though:

Oh, Homer!

Over a year ago, I gave a presentation at the Ancestral Health Symposium called “Lessons
From the Vegans: What the Paleo Movement Can Learn From the Success of Plant-Based
Diets.” In retrospect, I probably should’ve called it “Lessons from the Low-Fatters: What the
Paleo Movement Can Learn from the Success of People Who Eat Ridiculous Amounts of Carbs
and Don’t Keel Over,” but that was too long for the conference brochure. And for my
verbally dyslexic mouth. And also, I didn’t know it was really going to be about fat until I fell
down an extended PubMed rabbit hole and, upon regaining consciousness two days later,
realized I had found the Nerd Project to end all Nerd Projects.

In truth, though, this post started brewing long before my talk. Having witnessed some
pretty impressive healing when I noshed among the low-fat raw vegans (and, after a decade
of self-experimenting, concluding I do best on a lower fat diet myself), I just can’t get on
board with the categorical “Fat rules, carbs drool!” trend infiltrating both mainstream and
alternative nutrition. There are too many exceptions to the rule, too many gaps in the
theory, and too many skinny fruitarians frolicking in the sun-dappled fig orchards.

But even beyond that, this post is born of a belief I hold dearly—one that guides my
approach to research and underlies the very mission of this blog:

We can’t ignore evidence in order to preserve an ideology.

At least not under the guise of “science.”

When confronted with something that challenges our belief system, the worst possible
thing we can do is clamp our hands over our eyes and say, “You do not fit into my
understanding of reality; therefore, you do not exist. BE GONE, NON-EXISTING ANOMALY.”
Yet that’s what so many of us do—often without even realizing it—when faced with
outcomes our chosen philosophy can’t explain. On the flip side of cherry picking, we
cherry-throw-out: selectively deleting data that threatens our version of the truth, nipping
any cognitive dissonance in the bud before it has a chance to rattle our worldview. It’s easy
to be “right” when we’ve shoved all competing evidence into the wood chipper!

For a long time in the nutrition world, our thrown-out cherries were the ones challenging
the low fat ideology. We discarded the high fat Inuit cherries and the milky, bloody Masai
cherries; the coconut-filled cherries of the Tokelau; the cherries of the traditional reindeer-
herding Sami; even the smothered-in-butter French cherries—just to name a few.* It didn’t
make sense that these populations could exist and be healthy with their fat-gorging ways,
so we slapped them with a “paradox” sticker and deemed them weird exceptions to the
Dietary Laws that govern the rest of us.
* For the record, all these examples come with some major caveats, and I don’t think they
should be used as evidence to support the kind of high-fat diets many people are eating
today (though they don’t necessarily stand as counter-evidence either). More on that in an
upcoming post!

Only in more recent years have those cherries been rescued from the compost bin and
plopped back into the world’s collective fruit bowl (please wash before
consumption). Bestselling books like “Good Calories, Bad Calories” and “The Big Fat
Surprise” carved new histories in which fat was an innocent bystander, dragged into the mud
by bad science and even badder scientists. The phrase “healthy fat” moved from oxymoron
status to popular catchphrase. People whir 80 grams of butter into their coffee and call it
breakfast. Apparently Bob Dylan had it right in all but plurality: Time,  it is a-changin’!

As awesome as the pro-fat movement has been for challenging outdated beliefs and
reviving some truly nutritious foods, there’s been a dark side to the process as well. All of a
sudden, the same rhetoric once leveled against high-fat diets is being slung against low-fat
ones. Not only is low fat (and by consequence, high carb) not the dietary angel we once
thought, the new story goes, but it’s actually the source of all edible evil: the driving force
behind our obesity epidemic, a major contributor to heart disease, the puppet master
pulling those blood-sugary strings of insulin resistance and diabetes. If only the USDA had
recommended 6 to 11 servings of bacon instead of 6 to 11 servings of grains, we wouldn’t
be in this mess!

See the problem here?

In the process of redeeming fat, we traded one form of oversimplified blame for another.
And it’s led to a brand new wave of cherry genocide. We now dismiss (or paradox-sticker)
high-carb populations in the same way we justified ignoring the high-fat ones. We snub
decades of clinical success involving fat reduction (to the point where you might think such
evidence doesn’t even exist—in which case, you’re in for a surprise with this post!). We deny
the potential for low-fat diets to be anything other than a metabolic train wreck, ending in a
smoking heap of shrapnel and insulin injections. “Surely those low-fatters are starving all
the time,” we proclaim. “Surely they’re making themselves diabetic! They might feel okay
right now, but won’t those carby diets go all Cujo on them as the years progress, eating
their souls and whatnot?”

Let me be frank here.

If we’re really after the truth, we can’t keep throwing away perfectly good cherries.
Seriously. It’s gotta stop. When we censor data we don’t like instead of revising our theories
accordingly, we perpetuate the same problems we’ve been battling for decades: partial
truths treated as gospel; public policies that do more harm than good; baffled consumers
who can’t figure out if it’s the omelet that’s killing them or the OJ they wash it down with.

Do we really want to keep heading down that road? It probably goes somewhere awful! Like
Stockton. (Sorry, Stockton.)

Hence why we’re gathered here today, around this massive compilation of pixels, delving
into a decidedly hot topic. This post is my attempt to rescue some discarded cherries and
return them to the Fruit Bowl of Our Lives. Which, if nothing else, will one day make a
fantastic soap opera.

I do want to make one thing abundantly clear before we continue, though. The title “In
Defense of Low Fat” doesn’t imply its inverse, “In Attack of High Fat.” Quite the opposite! My
goal here is to create a space where two very different dietary approaches can sit down for
tea, respectfully coexist, and interact without any subsequent homicide investigations. In
fact, I’ll be arguing for a more panoramic view of nutrition where the success of both high-
fat and low-fat diets are compatible, and maybe even make sense. It just requires zooming
out farther than we’re used to looking, and acknowledging that our ever-rivaling
communities could actually learn a lot from each other.

For the sake of reading ease, this sucker is divvied up into two parts: this one, which
discusses the crazy-huge body of research behind truly low-fat diets (especially the really
obscure stuff!), and the upcoming Part 2, which ties everything together with science, and
whatnot. And because this post is long even by my standards, I’ve created a clickable Table
of Contents to help you navigate the labyrinth. Good luck! (You’ll need it…)

TABLE OF CONTENTS

1. Carbosis: The Magic of Truly Low-Fat Diets

2. The Low-Fat History You Probably Haven’t Heard

 Walter Kempner: Rice and sugar and diabetes reversal, oh my

 Roy Swank: Kickin’ some Multiple Sclerosis butt… by nixing saturated fat
 Lester Morrison: ???
 Nathan Pritikin: Heart-unbreaker extraordinaire
 Ancel Who?

4. Modern Diet Doctor Squad: An update and apology for jumping the gun

5. Up Next…

Note:  a lot of the papers discussed in this post are trapped behind paywalls. I have copies of
the full text for all of the ones I discuss in depth, though, so shoot me an email if you’d like
to read any!

1. Carbosis: The Magic of Truly Low Fat Diets

Let’s cut to the chase. My thesis, if all this can be boiled down into one, is that two unique
metabolic states exist on either extreme of the fat-intake spectrum. One ends around 10%
fat and the other begins around 65%. Both zones have their own benefits, and can elicit
surprisingly similar effects.

This is a PowerPoint slide I made representing what seems to be going on.

Image rejected from the  Lancet  due to insufficient sparkles.

In sum:

1. Something special happens at very high levels of fat intake (and very low levels of
carbohydrate intake). That thing’s called ketosis. It’s where your body creates
ketones to use when glucose is scarce, and where fat metabolism is optimized.
2. Something equally special happens at very low levels of fat intake (and very high
levels of carbohydrate intake). I’m not aware of a formal name for this, so I’m
dubbing it carbosis until further notice. It’s a state where insulin sensitivity
dramatically improves, and where carbohydrate metabolism is optimized .
3. Between those two extremes, especially towards the very middle, is what I’m calling
the Macronutrient Swampland. It’s not necessarily a bad place to be if you’re eating a
high quality, non-energy-surplus diet and are at a healthy weight (or getting there!),
but it’s hard to see the therapeutic effects of reducing fat intake while you’re in this
zone. And it tends to be the most potent area for food reward, making it easy for
people to overeat here. Any health improvements seen in the Swampland will
typically be from losing weight, eating more protein (which has its own special
metabolic effects), or boosting food quality (i.e., switching to less processed, “low
reward,” nutrient-denser fare), rather than from moving laterally across the
macronutrient spectrum.

Here’s the kicker: the Macronutrient Swampland is where our standard definition of “low fat”
squarely lands—30% of calories. When we conduct those “low fat” studies with sucky results,
they’re almost always using a fat intake of 30% of calories. When the USDA tells us to eat
low fat, they mean 30% of calories. When the American Heart Association tells us to eat low
fat, they mean 30% of calories. This number has been parroted far and wide across the
Western world, drilled into our noggins, and slapped with a skull and crossbones in the
“LOW FAT SCREWED UP AMERICA” narrative.

The only problem? It’s not actually low fat.

It’s not low fat relative to the many populations that eat (or ate) their traditional starchy
diets: the Okinawans (12% of calories as fat), the Tarahumara Indians (12% of calories as fat),
the pre-industrialized Thai (8.9% of calories as fat), the traditional Hawaiian (10% of calories
as fat), the traditional Taiwanese (16% of calories as fat), the African Bantu (14 – 17% of
calories fat), the traditional Pima (8 – 12% of calories as fat), and the highlanders of Papua
New Guinea (3% of calories as fat), just to name a few. It’s not low fat relative to the carby
diets that really do  have clinical track records for treating modern diseases (which, as we’ll
see in this post, hover almost universally at that 10% mark). And perhaps most importantly,
it’s not low fat relative to what Americans already eat—which is about 34% of our calories
these days, per the most recent available data.

That last point is what utterly handicaps our modern “low fat” research. Nudging 34% fat
down to 30% in studies and then claiming nope didn’t work is absolutely face-palm worthy.
It’d be like dismissing low-carbohydrate diets because switching from 50% carbohydrate to
46% doesn’t have a profound clinical affect. We’d unleash the hounds on a logical blunder
like that, right?

This is a problem that tends to get the plant-based diet community a bit hot under the
collar, and I have to agree with them. One of our biggest scientific bloopers was choosing a
Swamplandy 30% of total calories as the benchmark for “low fat.” It’s resulted in a slew of
unimpressive studies that make us think low-fatting is categorically worthless. I’ll probably
never live this down, but I mostly agree with an article T. Colin Campbell wrote about the
“low fat mythology” addressing this very topic . (Though in case you’re wondering, I stand by
my criticisms of the China Study and Campbell’s rat studies. Nothing in this post supports
the idea that animal protein is uniquely harmful, and acknowledging when some parts of the
plant-based movement are legit doesn’t give a free pass to the ones that aren’t!)

And that’s just the tip of the iceberg lettuce. On top of our wonky definition of where “low
fat” starts and ends, we’ve erroneously conflated “low fat” with the corn-syrup-injected,
processed-up-the-wazoo, won’t-rot-for-200-years-because-woah-preservatives menu
that emerged when the food industry found a new market to tap. As soon as the USDA
released the Food Guide Pyramid in 1992, food manufacturers were all “Let’s low-fat ALL OF
THE THINGS,” and accomplished that very feat. So now we hear “low fat” and remember the
era of Fig Newtons and rice cakes and sadness, so much sadness. And also Susan Powter .

Once upon a time, though, low fat meant something different. Something hopeful.
Something positive. Something that didn’t taste like regurgitated cardboard turd pellets.
And the research that emerged from this era was a thing of great beauty! There were low-fat
diet studies that actually studied low fat diets (imagine that!), and the notion that 30% fat
was equivalent to 10% fat was just a twinkle in a future USDA employee’s eye. Even though
our understanding of nutrition’s nitty gritty was less sophisticated back then, research
designs were often better,  testing “high fat” with things like fresh cream instead of the
confounder-riddled carrot cake and milkshakes used in more recent trials.

Hence, much of this post will be a blast to the pre-low-fat-craze past—a romp through the
research that artfully dodged the Macronutrient Swampland, and an introduction to the
thought-leaders that have all but vanished from scientific memory. After that, in the next
post, we’ll explore the mechanisms that tie it all together.

LET US BEGIN.

The Low-Fat History You Probably Never Heard

The popular version of events goes something like this:

America was happily eating its buttery, meaty, cholesteroley fare until Ancel Keys came
along with the idea that fat causes heart disease. He cherry-picked data to make it seem like
his theory was true, narrowed the culprit down to saturated fat, manipulated the Powers
That Be into believing him, and then bull-horned the message far and wide until we all
bought his myth. Low fat started with him!

Unfortunately, that’s a big, pre-chewed wad of baloney.

Here’s the deal. People were already whipping out low-fat diets to treat diabetes, multiple
sclerosis, high blood pressure, kidney failure, heart disease, and obesity when Keys was a
mere young’un shoveling bat poop in Arizona. Heck, the ancient Egyptians prescribed a
near-fat-free diet of wheat, grapes, honey, and berries for what was almost certainly
diabetes (“too great emptying of urine”). And contrary to popular belief, the early-1900s
evidence supporting low fat didn’t come exclusively from rabbits and test tube experiments
and correlative scatterplots: it came from actual human people eating actual food with their
actual mouths.

If anything, our pal Keys was a latecomer to the idea that fat could play a role in chronic
disease. The notion that he single-handedly criminalized fat is complete and utter
fiction. He might’ve been the loudest and most unflappably confident voice in the choir, but
he certainly wasn’t singing solo.

Here’s a more realistic timeline of the past century, albeit still very incomplete. (Click to
make ‘er big!)
Without further ado, let me introduce you to some of these disembodied heads.

Walter Kempner: Rice and sugar and diabetes reversal, oh my

Here’s one for the Paradox Files.

In the 1930s, a man by the name of Walter Kempner fled an increasingly Jew-hostile

Germany and landed square in the halls of Duke University… where he proceeded to totally
blow the medical community’s mind.  His mission: treat kidney disease. His solution: put
renal-failing folks on a special diet low in sodium, protein, and fat—a menu devised from in
vitro experiments he’d done on kidney tissue.
At the time, very few researchers believed that food could have any effect on kidney disease.
Or high blood pressure. Or diabetes. Or heart disease. Or most other chronically wrong-
going things in the body. As with Ancel Keys, who was pretty much laughed out of the WHO
conference where he presented his “fat causes heart disease” idea, Kempner spent the first
chunk of his career swimming upstream in a river of skepticism.

But his colleagues’ dubiousness didn’t last long. After placing patient after so-called-
hopeless patient on his unique regimen, it became clear that Kempner’s diet worked. Really
ridiculously well. And it became equally clear that the kidney wasn’t the only body part
made happy by the new cuisine. Obesity, diabetes, high blood pressure, heart failure,
coronary artery disease, psoriasis, and arthritis often saw major improvement or total
reversal as a result of the diet. During the course of his career, Kempner treated
over 18,000 patients with the above conditions—all by changing what went on the stabby
end of their forks.

So what was in this mystical diet of his? Brace yourself!

 White rice
 Fruit
 Fruit juice
 Refined table sugar
 In some cases, vitamin supplements (A, D, thiamine, riboflavin, and niacin)

…And not a darned thing else. Kempner summed up the details himself in a 1974
article, readable here:

A patient takes an average of 250 to 350 gm. of rice (dry weight) daily; any kind of rice may
be used provided no sodium, chloride, milk, etc. has been added during its processing. …
All fruit juices and fruits are allowed, with the exception of nuts, dates, avocados and any
dried or canned fruit or fruit derivatives to which substances other than white sugar have
been added. Not more than one banana a day should be taken. White sugar and dextrose
may be used  ad libitum; on an average a patient takes about 100 grams daily, but, if
necessary, as much as 500 grams daily should be used. Tomato and vegetable juices are
not allowed.

In other words, it was the CARBPOCALYPSE. Along with feasting on impressive amounts of
white rice, people were averaging 100 grams of pure sugar a day, and some ate over
a pound of it. That’s up to 2,000 calories from refined sugar alone—the same amount
deliciously packed into 25 Cadbury Creme Eggs.

(Wisely, Kempner knew his diet was at no risk of being crowned Dietary Homecoming
Queen. He apparently described it as a “monotonous and tasteless diet which would never
become popular,” and whose only saving grace was the fact that it worked. And as I
mentioned in my AHS presentation, he apparently whipped some of his patients in order to
help them comply, as—in his words—”the risk to their life was so great that it warranted
harshness.” Ouch!)
Here’s a breakdown of how the diet panned out, macronutrient-wise. Image from Duke
University files; red graffiti my own doing, to indicate percent of total calories:

What’s really  noteworthy is that the diet wasn’t automatically calorie restricted. In fact, some
patients had to increase their energy intake to help them gain weight, or to stabilize their
weight if they were losing too much. That’s important, because it means we can’t write this
off as a diet that improved biomarkers solely by inducing weight loss (Twinkie Diet, I bow in
your general direction). It also means that many people spontaneously ate less than they
needed when stuffing their faces with unlimited amounts of starch and sugar… as long as
fat intake was super low.

If this seems totally baffling and Twilight-Zoney, that’s because it is. According to my
calculations, there is an 84% chance that you are now Googling “rice diet Snopes” or
contacting my mother to inquire about my recent psychotic break (joke’s on you; she thinks
I’m great!). I urge you to keep reading, though, because we’re about to get to the ooey,
gooey data at the center of this carb-filled Tootsie Pop.

Let’s start with something weighty: an obesity paper published in 1975 in the Archives of
Internal Medicine, which should be of particular interest to anyone convinced refined carbs
are inherently fattening:

 Treatment of massive obesity with rice/reduction diet program. An analysis of 106

patients with at least a 45-kg weight loss.

Here, Kempner compiled data from 106 slimmed-down patients—a mere slice of the
thousands he treated over the years—who all dropped at least 100 pounds on his program
and achieved a normal weight. (The average loss amongst them was 140 pounds, and one
man melted away over 300). These particular losers ranged from 16 to 65 years old, and
featured a mix of women and men.
When it came to blasting obesity, Kempner employed what he called a “rice-reduction
diet”—the same protocol he’d designed for renal failure and hypertension, but with lower
calories:

In the unmodified initial diet, 90% to 95% of the caloric intake is carbohydrate, taken as rice
and fruit. As in the original rice diet, salt intake is exceedingly low (less than 60 mg of
sodium per day) and fluid intake is thus markedly reduced to prevent water intoxication.
Thus, the initial diet is low-calorie, low-salt, low-protein, low-fat, and essentially free of
cholesterol.

After getting into that sugary, starchy groove for a month, the dieters could start eating
veggies again (which were initially nixed due to their sodium content—kept low, in part, to
help tame high blood pressure and “reduce the stimulatory effect of salt on food intake”). A
bit later on, lean meats could also make a triumphant gustatory return.

Thanks to Kempner’s hawkish monitoring and dietary tweaking, obedient dieters were
greeted with a steady (and often plateau-free) slide towards a healthy weight, like so:
And since we’re all such visual creatures, here are some photos demonstrating the rice diet
in action, first published in Kempner’s aforementioned obesity paper. This young woman
lost 123 pounds in just shy of a year:
And here we have 278 pounds obliterated in a bit over a year, doing the same. His fasting
triglycerides dropped from 187 mg/dL to 85 mg/dL:
And this lovely lady lost 115 pounds in 33 weeks. Her fasting blood sugar dropped from
315 mg/dL to 100 mg/dL, and her triglycerides plummeted from 516 mg/dL to a peachy
keen 79 mg/dL—after eating a diet literally made of refined sugar and starch.

Looking at these sugar-fueled Incredible Shrinking People brings an important point to

mind. If we assume weight loss is just a matter of calories in versus calories out, the rice
diet isn’t any more remarkable than other low-calorie bootcamps: folks ate less and lost
weight. Dur. But if you’ve hung around the internet for very long, you might’ve seen the
theory—popular within some corners of the low-carb world—that successful weight-loss
diets are invariably low carbohydrate diets (or at least low refined sugar and starch  diets),
regardless of what other rationale those diets masquerade under (low fat, high fiber, low
calorie, food combining, eating only on Tuesdays in the presence of an ovulating jackalope,
etc.).

How? Because folks inevitably slash their carb intake when they eat less food overall, the
theory goes. This rests on the premise that insulin is the wizard behind the curtain of
obesity, and that quelling its wrathful swings—triggered by carbohydrates
and refined carbohydrates in particular—is necessary for losing weight. Gary Taubes
explained this concept in detail in a 2010 blog post:

Simply put, anyone who tries to diet by any of the more accepted methods (i.e., Weight
Watchers), and anyone who decides to “eat healthy” as its currently defined, will remove the
carbohydrates from the diet that may be — if the carbohydrate/insulin hypothesis is correct
— the most fattening. And if they’re trying to cut calories, they’ll be removing some number
of total carbohydrates as well. And if these people lose fat on these diets, this is a very
likely reason why.

The rice diet might be the most compelling hole-poker we have for that theory. While most
carby programs—say, Pritikin or McDougall or Ornish—eschew refined grains and sugar (and
thus could fit snugly into the insulin-centric concept above), Kempner’s program sure
didn’t. He fed folks almost nothing but the “most fattening” carbohydrates and still
managed to slim them down. Does your brain hurt yet?

Of course, losing weight is a far different beast than maintaining a 100-pounds-lighter

frame after the losing’s been done—leading us to the question: what happened to these
folks in the long run? Did they maintain their weight loss? Gain it all back? Develop a
crippling phobia of small, white, oblong granules, requiring years of psychotherapy and Riki
Lake guest appearances to overcome?

Alas, Kempner noted that long-term results were “not yet available for the patients analyzed
in this report,” and I’ve yet to find any follow-up papers revealing their fate. The only clue
I’ve seen comes from the first page of the “Rice Diet Renewal” book, which states that 43%
of rice dieters had maintained their weight loss (or lost even more) six years after their stint
in the program. (For comparison’s sake, an Annual Review of Nutrition paper estimates that
on average, about 20% of folks who’ve lost significant weight are able to maintain that loss
for at least a year.)

All that said, the rice diet was about far more than impressively svelte before-and-after
shots. As alluded to earlier, it also had the uncanny side effect of improving diabetes and
insulin resistance—even when weight loss wasn’t part of the equation. I warned you this was
gonna get weird! Kempner published a whole paper on the topic in 1958, which you
wouldn’t know by looking at its hauntingly empty PubMed entry:

 Effect of rice diet on diabetes mellitus associated with vascular disease.

(Email me if you want the full text!)

For starters, Kempner was just as perplexed as us modern-day health enthusiasts might be
when it comes to the effect his diet had on diabetics. As he penned in the paper you cannot
see:

We have for the past 15 years treated numerous diabetic patients with the rice diet. Since
more than 90 percent of the calories in this diet are derived from carbohydrates, it was
anticipated that increased amounts of insulin would be necessary to keep the blood sugar at
its previous level. However, the opposite proved to be true. … Not only is the rice diet well
tolerated but  in many instances the blood sugar and the insulin requirements decrease.

In this report, Kempner analyzed 100 diabetics who’d entered the rice diet program between
1944 and 1955. All of them strictly followed the diet for at least three months (often much
longer), and they were observed an average of nearly two years—with some folks monitored
for up to eleven years after they’d first embarked on the carby cuisine.

The findings? Ladies and gents, place your bets…

More than half of those 100 diabetic ricers—63%—actually   saw their fasting blood sugar
drop by at least 20 mg/dL during the diet. Only 15% had their blood sugar go up
significantly. The remaining 22 saw little to no change.

To get a visual sense of those numbers, here’s an aptly named pie graph (don’t worry; it’s
fat and carb free!). “Increased” or “decreased” is defined as a change of at least 20 mg/dL:

Let’s repeat that: eating almost nothing but starch and sugar and fruit, the majority of
diabetic patients lowered their blood sugar levels. In fact, when everyone’s results were
pooled together, the average blood sugar change was a drop of 47 points.

‘Twas a similar story in Insulin Land. Of the study’s participants, 68 entered the scene
already dependent on insulin. As the carbs raged on, 21 of those insulin-injecters didn’t
have to change their dosage; nine needed an increase (including four people who initially
weren’t on any insulin at all); and—again comes the cruel, cruel defiance of prediction—
42 slashed their usage significantly. In fact, 18 folks were able to discontinue their insulin
entirely. Feasting on white rice. And sugar. And fruit juice.

Here’s another delicious graph of pie, calculated for the 72 patients who needed insulin at

some point during the study:

Once again: eating virtually nothing but this…

…the majority of diabetics ended up with better glucose control and insulin sensitivity, and
in some cases freed themselves from diabetes entirely.

Let that sink in for a minute.

Or two, if you need to grab a glass of water and ward off the vapours.

Just to be clear, the point here isn’t that the rice diet is the Best Thing Ever for diabetics and
everyone should trade their insulin pumps for a metric ton of Skittles (nobody needs to
taste that  many rainbows). After all, 15% of the rice-dieting diabetics actually got worse,
many of the improvers still had above-normal blood sugar (despite huge drops from
baseline), and we could probably hack Kempner’s protocol to make it more nutritionally
sound without ruining its therapeutic effects. Clearly, it ain’t perfect. All I’m saying is that
these results totally fly in the face of what most of us consider possible.  Sugar and white
rice improving diabetes? Blasphemy!

All that said, an important critical-thinky question remains: was this all just a byproduct of
weight loss? We know that restricting calories and dropping pounds can definitely boost
insulin sensitivity and glucose control, regardless of whether the diet used is particularly
healthy. It’s one thing to not be diabetic because you’re eating kale and grass-fed buffalo
whose ancestors were blessed by Sacagawea, and another to not be diabetic because you’re
living on napkins and crack. Can we at least say that the successful diabetics were the ones
who lost weight throughout the program, spontaneously eating less, unamused by a diet
that had exactly one-and-a-half flavors?

NOPE. As Kempner pointed out, any obese patients were indeed encouraged to lose weight
—but the improvements in blood sugar levels and insulin requirements occurred “both in
patients who lost weight  and in those who did not have a significant weight change”  (his
words). Kempner’s data, both in this paper and in the massive collection of his work filed
away at Duke University, showed that the diet could benefit diabetics even when their weight
and energy intake didn’t budge. Even supplements such as Kratom (you can always buy
kratom from here) showed no increased benefits in diabetics.

And it didn’t end there. The rice diet also proved helpful for heart failure. It rapidly healed
psoriasis. It excelled at its original goal of treating high blood pressure. The “good for” list
stretched on nearly as far as those endless bowls of rice! As early as 1949, Kempner had
observed that the rice diet was healing more than 70% of his seriously ill, not-responding-
to-other-treatments patients from a wide spectrum of disease backgrounds. That figure
stayed pretty stable as the decades rolled on.

Psoriasis obliteration on the rice diet.

Just last year, the Journal of Electrocardiology published something of a Rice Diet
Resurrection, dredging up Kempner’s key findings and blasting open his oft-forgotten
legacy: “An archaeologic dig: A rice-fruit diet reverses ECG changes in hypertension.” In it,
the authors pointed out something pretty important regarding the ultimate success of the
diet. A band-aid treatment it was not; the rice diet actually seemed to permanently
reverse the conditions it set out to treat, at least for many adherents:

A poorly known but important observation was that patients who were able to follow the
regime, and who were slowly guided through a gradual modification of the diet over many
months, were able to transition into a very tolerable low fat, largely vegetarian diet, while
leading a normal, active life, without medications, indicating that the disease state had been
permanently modified.

“Permanently modified” probably needs a qualifier, since those folks couldn’t make
a total return to their former gustatory ways. But over time, they could start eating a more
diverse diet with (lean) animal foods, all manner of vegetables, a moderate level of salt, and
the magnificent return of tastiness. Not too shabby, considering many of those folks were
initially riding a bullet train towards death. (In another very recent article, “Who and what
drove Walter Kempner?“, the authors noted that in Kempner’s day, life expectancy for
anyone with malignant hypertension—one of Kempner’s main patient demographics—was
only six months. The fact that he gave most of them decades of recouped earth time was
pretty fantastic.)

So whatever became of the rice diet? Like most things in life, it lost out to stuff that was
newer, prettier, shinier, and easier to squeeze inside an FDA-approved pill. Kempner
relinquished the Rice Diet throne in 1992 (and in case you’re wondering, died of a heart
attack five years later, at the age of 94—though it’s unclear what his own diet and lifestyle
actually were). After his departure, the rice diet predictably loosened up: the program later
allowed “a wider selection of largely vegetarian food choices,” though still with low sodium
and protein intake (and ostensibly less whipping).

In his 1983 article “Kempner Revisited,” Eugene Stead—who’d worked at Duke alongside the
Rice Man himself—summed up Kempner’s unorthodox legacy in a way that captures my own
thoughts:

Who in his right mind would have ever thought that rice and fruit could modify vascular
disease appreciably? Who would have fed a protein-deficient patient, losing large quantities
of protein in his urine, a protein-poor diet? Who would have dared to give a more than 90%
carbohydrate diet to a diabetic? Every expert knew that cholesterol levels were not
influenced by diet. Nevertheless, all these leads have paid off richly.
Kempner walkin’ the talk. From Duke University files.

Ultimately, I find Kempner’s work both important and wildly uncomfortable.

Important, because it exposes some cracks in our current view of carbohydrates and sugar—
areas where our thinking has room to grow and our assumptions have room to crumble.

Uncomfortable, because it demolishes my long-held rationale for why low fat, veganish
diets can be successful: that they work because they involve switching to whole foods
(Kempner’s sure didn’t!); that they work because they reduce refined sugar and starch intake
(the very lifeblood of the rice diet!); that they work because they increase disease-fighting
plant compounds (nary a vegetable to be seen under Kempner’s strictest watch). Let me go
on record here:  I TOTALLY stand corrected!

Perhaps the only areas of overlap with an ancestral framework are that all that rice would’ve
provided a decent source of resistant starch, gluten was nowhere to be seen, and the uber-
lean diet would’ve smashed polyunsaturated fat (PUFA) intake to smithereens. (If you haven’t
caught wind of the PUFA-hatin’ yet, these fats are garnering quite a bad rap due to their
unstable, oxidation-prone structure—especially omega-6 PUFAs, the pro-inflammatory Evil
Cousins of omega-3s. But even PUFAs as a whole have taken a clobbering in some spheres
(hello Ray Peat!), and higher-than-trivial intakes have been indicted as a cause of many
terrible things.)

Indeed, after my AHS talk, a few people contacted me suggesting it may be the PUFA
reduction that improved sugar metabolism and other aspects of health, thus allowing rice
dieters to thrive on an otherwise nonsensical diet. And more broadly, that rock-bottom
PUFA intake might be the biggest reason low fat, plant-based diets have any positive effect
on chronic diseases to begin with. That would leave saturated and monounsaturated fat in
the clear, needlessly nixed in the quest for better health.
I might be inclined to guess the same thing, if not for one human-sized monkey wrench by
the name of Roy Swank.

Roy Swank: Kickin’ some multiple sclerosis butt… by nixing saturated fat

You might be familiar with our current diet-wielding, multiple-sclerosis-blasting

warrior Terry Wahls, but less known is the fellow who preceded her by over half a century:
Roy Swank. And what a story he had!

Swank exited the womb practically destined for greatness. Along with growing up near my
beloved home city of Portland, young Swank was musically gifted, athletically inclined, and
devastatingly suave. He spent his formative years wooing his future wife, Eulalia, in his dad’s
mortuary hearse (chicks dig that stuff),  and started driving a local doctor around town to
see patients when he was just 13. It was then that his interest in medicine roared to life! By
the time he was 26, Swank had racked up a Bachelor of Science, a PhD, a medical degree,
and a fitting destiny for his surname.

But our relevant saga began in 1948, when Swank got invited to Montreal to
research multiple sclerosis (MS)—a devastating autoimmune disease affecting the brain and
spinal chord. He soon discovered a peculiar trend: across the globe, MS was rare in areas
where saturated fat intake was low, but much more common where meat and dairy were a
mainstay. And as he scoured disease patterns from the previous two decades, Swank
noticed that World War II heralded a drop in MS rates wherever meat and dairy were
rationed. The clincher came with a Norwegian survey he helped conduct, which showed MS
was clustering around the country’s rural, mountainous, dairy-noshing farming regions,
while coastal fishing communities—whose fat intake was lower and mostly polyunsaturated
—were pretty much spared.

And you might get a kick out of this: when plotting MS prevalence against national intake of
animal fat, Swank arrived at a perfect upward curve that was nearly indistinguishable from
the one we vilified Ancel Keys for. Here’s Keys’ six-country graph overlaid with Swank’s MS
data. Eerie, no?

From page 13 of “The Multiple Sclerosis Diet Book” by Roy Swank.

We can (and should!) fly our “correlation isn’t causation” flag here, but keep in mind that MS
research was in its infancy back then. Population trends were the only thing researchers had
to work with. So, armed with the scant clues of his time, Swank put his thinking cap on and
devised the first-ever dietary experiment for multiple sclerosis. And it went a little
somethin’ like this:

 Low total fat

 Very low saturated fat (10 – 15 grams per day, maximum)
 Small amounts of polyunsaturated vegetable oils and fish oil (10 – 40 grams per day)
 Grains
 Vegetables
 Fruit
 Skim milk
 Fish and other seafood
 Extremely lean land-animal products (skinless chicken and turkey; egg whites;
trimmed meats)
 60 to 90 grams of protein daily, mostly from fat-free animal foods

To put his hopeful menu to the test, Swank rounded up 150 MS patients—70 men and 80
women—to guinea-pig his diet in real life. And we’re not just talking a breezy month or two
of experimenting; starting in 1948, he meticulously followed these folks for 50 years and
beyond, keeping track of what each person ate and how much their disease progressed after
they entered the study. One of his most detailed papers, “Multiple sclerosis: fat-oil
relationship,” documented the 34-year results of that massive undertaking.

As Swank explained in his paper, the patients had to keep detailed food logs of their daily
gustatory adventures. They also trekked to a Montreal clinic once every two weeks to get
their MS assessed and endure a pop quiz about their eating habits. (Due to humans being
sucky remember-ers (and notorious “historical revisionists” of our own mistakes), dietary
recalls are often unreliable—but Swank collected so many of them, over such a vast span of
years, that he could paint a pretty accurate picture for each patient.) Once their new, Swank-
approved eating habits had stabilized, those patients were weaned onto less frequent clinic
checkups and did much of their reporting by snail mail.

To gauge how each person’s disease changed throughout the study, Swank used a
neurological grading system ranging from 0 to 6, abridged here for reading ease:

0. Remission, more or less

1. Some neurological symptoms, with fatigue and periodic exhaustion

2. Mild physical impairments

3. Severe physical impairments

4. Wheelchair-bound, with memory impairment

5. Confined to bed and chair

6. Dead

From the get-go, the goal was to slash participants’ animal fat intake down from an average
of 125 grams per day (pre-Swankification) to a maximum of 10 to 15 grams per day (post-
Swankification). Starting in 1951, they could also add 5 grams of cod liver oil and eat
between 10 and 40 grams of “fluid vegetable oils” daily, though saturated fat was supposed
to stay as low as possible.

Of course, we humans are wont to err, and not all of the patients colored within the low-fat
lines. Swank noted that some people “doubled or even tripled the amount of [saturated] fat*
recommended,” and that in lieu of a control group, those variations made it possible to see
how different fat intakes correlated with MS progression over the decades. Yay math!

* A Swanky disclaimer: although I’m employing more familiar terminology for the sake of
this blog post, note that Swank uses the words “fat” and “oil” a bit differently in his papers.
“Fat” in his work refers only to  saturated  fat, while “oil” refers only to  unsaturated  fats. So if
you take a gander at any of his publications (which I recommend you do!), just keep in mind
that his “fat” translates to our definition of “saturated fat” rather than “total fat.”

By the 34-year mark, a bit over half of the original group—81 people—had passed away.
That’s actually pretty promising: Swank noted that when he first started studying MS, most
patients were expected to end up bedridden or wheelchair-bound within a decade or two,
and the assumption was that “all would be dead within 35 years.”

But where it gets really  interesting is when the Swankers were divided up based on their
average saturated fat intake. Of those who didn’t exceed 20 grams per day (70 people), only
31% died over the course of the study (20% specifically from MS). But of those who
ate more than 20 grams of saturated fat per day (74 people), a whoppin’ 80% perished in
that same time frame (62% specifically from MS). Voila:

And when we break it down a bit further,

something even more interesting emerges: the saturated fat/mortality trend wasn’t
linear.  Like, at all. Folks eating between 20.1 and 30 grams per day had ridiculously similar
mortality rates to those eating 30.1 to 50 grams and beyond. Basically, once people crossed
the 20-grams-per-day threshold, it didn’t seem to matter how much saturated fat they
were eating: mortality rates rapidly maxed out and then stayed relatively constant. It’s like a
saturated-fatty version of the Macronutrient Swampland, where everything outside the
“magic” zone is super samey!
FYI: average saturated fat intake for the lowest bracket was 17 grams per day; for the
middle bracket, 25 grams per day; and for the highest bracket, 42 grams per day.

(In case you’re wondering, it didn’t seem to be a matter of having a longer but more
miserable, enfeebled life for the low-fat adherents. As Swank noted, “Patients on our low-fat
diet have been remarkably free of bacterial and viral infections, ‘colds and flu’ occur rarely,
and recovering from urinary and other bacterial infections has been rapid when
appropriately treated.” Indeed, quite a few measures of their health improved.)

The Swankers’ disease progression—as tracked by that neurological scale mentioned earlier
—followed a similar trend. For the folks eating 20 or fewer grams of saturated fat per day,
the disease remained relatively stable, with just over half a grade of progression (worsening)
on average. But for the subset of folks eating between 20.1 and 30 grams per day, the
disease progressed an average of 2.6 grades. And for those chowing down on more than 30
grams per day, the disease worsened by an average of 3.0 grades. (To help conceptualize
that, a three-grade change is the equivalent of going from “mild physical impairments” to
“confined to bed and chair.”)

Here are more Smurf-colored bars for the visually inclined:

And because I love me some graphs, here’s another one straight from Swank’s paper,
showing the dramatic drop in exacerbation (flare-up) rates before and after folks got all
Swanky:

Pretty impressive, no?

In addition to all this fun stuff, Swank commented (again, in his 1991 paper “Multiple
sclerosis: fat-oil relationship“), that some patients needed an even steeper slash in their
saturated fat intake—down to 10 grams per day, maximum—in order to “gain an
improvement in energy and freedom from severe fluctuations of disease.” Swank wrote:

In recent years, this experience induced us to eliminate all meats and other sources of fat
from the diet of many patients when first seen. We estimate that saturated animal fat was
reduced to ~5 g/day plus the fractional or trace amounts of fat contained in many foods. It
is our impression that these patients improved faster than others in whom this was not
done.

In the vein of Devil’s Advocation, though, we should give our critical-thinking wheels a whirl
and see if there are any alternative explanations for these findings. Could there be some
suspicious lifestyle confounders like we see in studies today? Were saturated fats lumped in
with hydrogenated ones and mutually given the boot, while only the latter was a true
health-harmer? Was the supplementation of cod liver oil, chock full of omega-3 and
vitamin-A-rich goodness, enough to explain the mortality patterns? Was the culprit
saturated fat itself, or was it just guilty by association—maybe serving as a proxy for
generalized I-Don’t-Give-A-Hoot-About-My-Health-itis, as the rebels who ignored Swank’s
“eat less saturated fat!” message were more likely to ignore the “sugar is bad” or “vegetables
are good” or “don’t run with scissors while chewing arsenic candy” messages as well?

As much as I love wailing my confounder alarms, I don’t think the usual suspects apply in
this case. Here’s why!

 Hydrogenated fats were indeed banned from the menu, but not until 1951—two or
three years after folks started the diet, at which point they’d already seen profound
improvements.
 Likewise, cod liver oil (and other omega-3-rich fluid oils) weren’t allowed during the
first couple years of the diet, and again, folks saw an 80% decrease in their MS flare-
up rates during that time.
 As for potential bad-guy carbs skewing the results? Remember, Swank developed his
diet in the late 1940s—decades  before refined grains and sugar joined the Dietary
Villain ranks and were widely considered harmful. In fact, his diet didn’t restrict
refined grains or sugar to begin with, so it wouldn’t make sense that a “screw it all”
mentality would result in folks rebelliously downing processed carbs. (Heck, in
Swank’s Multiple Sclerosis Diet book, there are plenty of recipes calling for white
flour and sugar, and no indication that his patients—at least during the first few
decades—were told to stick to whole-food sources of carbohydrate.)

And lest we wonder if the folks eating more saturated fat were also eating more of those
gnarly, high-PUFA vegetable oils we so love to hate (thus obscuring the real relationship
between saturated fat and MS progression): no dice! Swank’s data showed pretty clearly that
the more saturated fat people ate, the less  vegetable oil they were eating—an inverse
correlation of -0.62 by the study’s 22nd year. Likewise, as Swank explained in the paper
we’ve been discussing, higher unsaturated oil intake went hand-in-hand
with better outcomes in terms of disability and mortality. The inclusion of vegetable oils
“seemed to make patients feel better, increased their energy, and improved the condition of
hair and skin,” even though Swank maintained they weren’t necessary for treating MS itself
(since his patients took a fantastic turn for the better before those oils were added back to
the diet).

Hence why I called Swank a “monkey wrench” a bit earlier on. In contrast to the theory that
rock-bottom PUFA levels are the real reason very low fat diets work (while saturated fat
would be an innocent, needlessly reduced bystander), Swank found the opposite  to be true
—that saturated fat had the strongest relationship with MS progression and mortality, while
polyunsaturated fat levels could be scaled up or down without negatively impacting health.
At least within that 10 to 40 gram range. And at least for multiple sclerosis (although
mortality from other chronic diseases dropped during Swank’s diet as well).

That said, there is another possibility that could maybe, maybe, MAYBE  be obscuring the
saturated fat trend: Neu5Gc. This is a little sialic acid molecule that humans, rather
uniquely, can’t synthesize. We produce a similar molecule called Neu5Ac, but lost the ability
to make Neu5Gc after splitting from our last common ancestor with the great apes. Because
gene mutations ‘n stuff. Other primates (and almost all mammals) can still synthesize
Neu5Gc just fine!

Here’s why it matters: even though we can’t make Neu5Gc on our own, we can  incorporate
it into our tissues when we ingest it from food. And the prime sources of Neu5Gc happen to
be red meat and dairy, the same food-vehicles that deliver most of our saturated fat.
Because Neu5Gc looks like a foreign substance to our paranoid human innards, we’re
capable of producing antibodies against it (although levels of those antibodies vary widely
from person to person), which, in turn, can stir up all sorts of trouble. So far, we’ve got
theories about a potential role for anti-Neu5Gc’s antibodies in systemic inflammation,
cancer, heart disease, hypothyroidism, and also… WAIT FOR IT… multiple sclerosis. (See:
“Why does multiple sclerosis only affect human primates?” and “Missing links in multiple
sclerosis etiology. A working connecting hypothesis.“)
From “Quantitative analysis of sialic acids in Chinese conventional foods by HPLC-FLD,”
2014.

I waffled over whether to even include this speculation here, since Neu5Gc research is just a
wobbly-kneed babe in the woods right now, and we’d need a lot more data before we could
definitively link it to any disease. But, considering that 1) humans are the only primate that
develops multiple sclerosis, 2) humans are the only mammal that can’t make Neu5Gc (and
that produce antibodies against it), 3) multiple sclerosis tends to cluster around areas with a
higher intake of Neu5Gc-containing foods (land meat and dairy), and 4) there’s a plausible
mechanism linking Neu5Gc with the development of multiple sclerosis (through the effects
of antibodies on the blood-brain barrier and axon-myelin unit)… well, all I’m sayin’ is it
seems quite intriguing!

That said, Swank actually had some compelling, research-backed ideas about why saturated
fat per se could trigger MS, which we’ll discuss in Part 2 of this post. It’s worth noting that
he didn’t believe saturated fat  causes  multiple sclerosis, just that it “precipitates or
accelerates it in susceptible individuals,” as he wrote in 1954. It’s not outside the realm of
possibility that Neu5Gc somehow plays the role in the development of MS, while saturated
fat, under specific conditions, aggravates it. So, even if this Neu5Gc stuff pans out, it
doesn’t necessarily pardon saturated fat!

At any rate, we’re not quite at the end of Swank’s research rope. In 2003, he published
the 50-year results of his never-ending study: “Review of MS patient survival on a Swank
low saturated fat diet.” By that time, after 16 years of letting them do their own thang, he’d
managed to track down 15 of his surviving participants and pull them in for interviews and
in-person visits. They were all between 72 and 84 years old. (Swank himself was 94, and in
case you’re wondering, was still goin’ strong until he passed away in 2008 at the age of 99).
Amazingly, only two survivors needed help walking and had any sign of their disease; as for
the others, Swank described it thusly:

The remaining 13 patients were remarkably well. They were very active, could care for
themselves, could walk as necessary, and were normal mentally. … [They] stood and were
active and unusually youthful looking, with very smooth facial skin devoid of wrinkles due
to good subcutaneous circulation. They were all in friendly, good spirits, had joyful
laughter, and generally quite youthful behavior. This study also indicated that patients with
MS, if they rigorously follow the extremely low-fat diet proposed by Swank, which contains
no more than 10 to 15 g/d of saturated fat, can expect to survive and be ambulant and
otherwise normal to an advanced age.

Take note of that “good subcutaneous circulation” comment, because it’s at the crux of
Swank’s theory about why saturated fat is harmful for MS patients (hint: it has to do with
blood cell aggregation and oxygenation). More on that in the next blog-post installment!
We’ll be coming back to some of Swank’s research and ideas when we discuss the science
behind why low-fatting works, because he’s just that  awesome.

In the meantime, we’re hardly done with our historical saga. Next up is another obscure
figure from the dusty, carb-encrusted pages of science’s past: Lester Morrison.

Lester Morrison: ???

Lester Morrison is a man of mystery. A mystery, in part, because he was using low-fat diets
to treat heart disease years before Ancel Keys supposedly introduced the idea to the world.
A mystery also because for a guy who did some neat stuff, he’s totally not Google-
stalkable. Nary a pixel of his face could be found in my sleuthing efforts, and the only bio-
esque document seems to be his obituary.

Here’s what we do  know. A rather precocious and multitalented individual (along with being
a physician, he was an accomplished violinist, historian, symphony concertmaster, novelist,
and maybe also Spiderman, and won his first research award when he was a sweet 16),
Morrison plunged into the research field with an initial focus on gastroenterology. His first
taste of Fat Suspiciousness came in the 1940s, after noticing heart disease and stroke
mortality dropped hand-in-hand with wartime food rationing—which curbed, among other
things, dietary fat. As he explained in his 1955 article, “A nutritional program for
prolongation of life in coronary atherosclerosis,” World War I saw the first parallel dance
between food rationing and heart disease, with the British blockade of Germany; World War
II was fat-jà-vu all over again:

During World War II … the various Scandinavian governments supplied the information that,
when fat in the diets of the population had to be reduced to a minimum because of the
scarcity of dietary fats, the death and sickness rate from atherosclerosis was likewise
reduced to a minimum. As soon as the war ended and dietary fat once again became
plentiful, the mortality rate and morbidity rates from coronary and cerebrovascular disease
promptly soared to prewar levels and even began to surpass them.

If you’ve read my critique of Forks Over Knives—a documentary that cited the same wartime
stats as evidence for low-fat-plant-based superiority—then you already know I have some
bones to pick with those correlations. As I explained in my critique, the rationing-induced
changges involved far more than tanking total dietary fat: during World War II, seafood
consumption doubled; sugar intake halved; vitamin K2 intake rose; trans-fat-containing-
margarines all but exited the table. Not to mention, any situation of food restriction tends to
boost vascular health, at least initially.

Nonetheless, the link between war rationing and mortality seemed to catch a lot of eyes, and
Morrison’s were two of ’em. Cardiovascular disease had slayed a hefty portion of family
(including his mom and dad), so the issue was quite near to his heart (literally!). Thus, he
was inspired to investigate the matter in a more controlled setting.

In 1946—years,  again, before Keys was hot on fat’s trail—Morrison launched a dietary

study involving 100 people who’d recently survived a heart attack. For 50 patients, he left
their menu as-is: fairly high in fat (80 – 160 grams per day) and high in cholesterol (200 –
1800 mg per day). For the other 50, he prescribed a war-rationing-inspired diet limited to
20 – 25 grams of fat per day—with continual supervision for both the patients and their
families to ensure they stuck with it (and the boot given to anyone who couldn’t promise
total compliance). He then followed everyone for eight years to see how many folks perished
from each group.
In his papers “Arteriosclerosis: Recent advances in the dietary and medicinal treatment”
(1951) and “A nutritional program for prolongation of life in coronary atherosclerosis”
(1955), Morrison gave a detailed outline of his experimental diet, which was designed
specifically to lower folks’ cholesterol. (Worth noting: the diet didn’t limit sugar or other
sweeteners, and didn’t reduce animal protein intake, as a variety of lean meats and dairy
were allowed. In fact, it prescribed 60 – 100 grams of mostly animal-based protein per day,
and folks ended up eating closer to 120 grams on average—well above the 5% threshold
deemed toxic by T. Colin Campbell. Just sayin’!)

The encouraged edibles:

 And the no-nos:

(Patients were also encouraged

to take a multivitamin containing vitamin A.)

The results? You can probably guess where this is headed! As intended, the diet tanked
people’s total cholesterol—by an average of almost 100 mg/dL, in fact. But that’s just the
beginning. At the three year mark, 15 people from the control group had died of heart
disease, compared to only seven from the low-fat group. (That’s a difference of 70% versus
84% survival.) By the eight year mark, the survival rates had whittled down to 24% of the
control group versus 56% of the low-fat group (again, most deaths being from heart
disease). And by the study’s 12th year? A whoppin’ nobody was alive from the control
group, whereas 34% of the low-fat group was still roaming this lovely green earth.

12-year data taken from Morrison’s “Diet in Coronary Atherosclerosis,” JAMA, June 25,
1960.

(Along with the whole “dying less” thing, Morrison noted that his fat-restricted patients
frequently reported “a sense of optimism, well-being, and good spirits” after adopting the
diet—a sentiment Swank echoed as well, though without either of their studies
being blinded, it’s hard to say how much was just a placebo effect.)

As with the other old research we’re resurrecting in this post, the beauty of Morrison’s study
is that it gracefully dodged some confounders that muck up science today. Back when he
conducted his fat-slashing experiment, nobody was telling the public that sugar and refined
carbs were bad along with fat. No one had an inbox full of Meat’s gonna kill ya news
headlines. No one had nutrition labels on their food, or a reason to fear egg yolks, or retinas
permanently emblazoned with the image of the Food Pyramid. Heck, even smoking wasn’t
widely considered a health hazard yet (the Surgeon General didn’t officially declare a causal
link between smoking and lung cancer until 1957). Americans’ minds were clean slates, and
prescribing a shiny new dietary change (like reducing fat) didn’t invoke the same confounder
cascade we see today. How grand!

All that said, in Morrison’s case, there were  two potential caveats we should take note of.
One, the low-fat group saw some initial weight loss—an average of 21 pounds for men and
17 for women during the first three years, but with no additional changes during the rest of
the study—whereas the control group remained weight-stable the whole time. And two, the
low-fatters appeared to spontaneously increase their protein intake, making it hard to know
what macronutrient change—the uppage of protein or downage of fat—was really driving
the results. Could these be the true wizards behind the better-survival curtain?

It’s certainly possible, though I’m hesitant to say they could fully account for 12 years of
dramatically lower death rates. Protein doesn’t seem uniquely beneficial for heart disease
patients, and there’s a dearth of research looking at intentional weight loss on post-heart-
attack survival—so we really have no way of knowing how big a factor that was for
Morrison’s patients. (Oddly enough, population studies show that being overweight rather
than normal-weight actually predicts better long-term survival for people who have heart
disease—and what’s more, losing weight after having a heart attack is counter-
intuitively associated with higher mortality rates. Researchers call this the “obesity paradox“:
carrying extra weight tends to increase people’s risk of getting heart disease, but for folks
who already have the disease, it seems to prolong life. Of course, there could be quite a few
alternative explanations for that trend, which are thoroughly discussed here. Interesting,
nonetheless!)

At any rate, Morrison was excited (but wisely cautious) about his study’s results, and ended
up penning a book called “The Low-Fat Way to Health and Longer Life,” which he published
in 1958—the same year Ancel Keys launched the Seven Countries Study. But, refreshingly
non-gun-jumping scientist that he was, he also called for “similar surveys utilizing larger
numbers of cases for statistical evaluation” in order to deepen and replicate his findings.

And as luck would have it, those surveys eventually came from one of his very own patients:
Nathan Pritikin!

Nathan Pritikin: heart un-breaker extraordinaire

(NOTE: unless otherwise referenced, the background

info in this section comes from the memoir, “Pritikin: The Man Who Healed America’s
Heart,” which is actually one of the most interesting biographies I’ve ever read!)
Small world gettin’ smaller, eh?

Nathan Pritikin is probably best known for two things: 1) promoting an uber-low-fat diet
(and running a longevity center dedicated to such); and 2) being downright chummy with
George McGovern—the senator in charge of the 1977 Dietary Goals for the United
States.  (As I detailed in “Death by Food Pyramid,” McGovern ate a quasi-Pritikin diet for
many years, delivered Pritikin’s eulogy, and drew a fair bit of inspiration from the man while
crafting America’s new low-fat food recs.)

Pritikin’s dietary saga started with the same World War II trends that inspired so many of his
fat-slashing contemporaries. Thanks to some work he’d done on bombsights for the Air
Force (he was a prolific inventor and engineer by trade), Pritikin had free-for-all access to
classified military documents—including the mortality data being churned out for civilians
and prisoners. His puzzle-loving mind was intrigued that heart disease rates
were dropping  in areas plagued by intense stress and low food availability, when most
health authorities expected the opposite to occur.

In 1955, an increasingly health-interested Pritikin made a trek to visit Mystery Man

Morrison. The two nerded out about heart disease theories, and at the good doctor’s urging,
Pritikin had his cholesterol tested for the first time—revealing a borderline-high level of 280
mg/dL. Although he started making some minor dietary tweaks after that, it wasn’t until an
official heart disease diagnosis in 1958 that Pritikin kicked his nightly-pint-of-ice-cream
habit and got serious about healing himself.

And we’re talking serious  serious. For the next ten years, Pritikin guinea-pigged his body
with every dietary permutation imaginable. He’d go for weeks eating almost nothing but
lentils, or brown rice, or brown rice plus beef; he’d make slight or dramatic adjustments to
his vegetable-grain-meat ratios; he’d experiment with eating ten dates after dinner (fruit,
not women; this was before Tinder). And in true scientist fashion, he got his blood tested
after each new food stint—meticulously documenting changes in his cholesterol levels,
triglycerides, fasting and non-fasting glucose, red blood cell count, white blood cell count,
hemoglobin, platelets, carbon dioxide, electrolytes, free thyroxine, and pretty much
everything else he could cajole his docs into measuring. Be still, my nerd heart!

Although he managed to whittle his cholesterol down to 155 mg/dL with a lowish-fat menu
(including a daily helping of nuts, tiny amounts of oil, and some fish and meat), his next
EKG didn’t show a lick of improvement. But the man was not deterred! Pritikin low-fatted
harder. He nixed the nuts and oil and meat. He pounded his total cholesterol down to 120
mg/dL. And at his next EKG six months later, the report was music to his ears (and a shock
to his diet-skeptical doctors): “Definite improvement since the [last] tracing … Normal
electrocardiogram.”

Ensuing stress tests over the next few years confirmed that his once-diseased ticker was,
for all intents and purposes, healed.
By the 1970s, Pritikin had not only dialed in his own diet to his strict standards of
perfection; he’d also amassed hundreds of low-fat devotees—family, friends, friends of
friends, and eventually word-of-mouthers—whom he counseled over the phone for free.
And in 1976, the real fun began: Pritikin opened the doors of his first Longevity Center in
California. Riiiiight here:

The Casa Del Mar building, later transformed into Pritikin’s healing grounds. From Santa
Monica Library Archive.

It was in this magical palace, wringing patients through a 26-day diet overhaul and
hawkishly watching their food intake, that Pritikin could document the effects of his
program on a large-scale basis.

And document he did! Although his reputation was that of a heart-healer, Pritikin’s diet did
far more than assuage troubled arteries. Just as Kempner saw, the uber-fatlessness had the
fortunate side effect of rapidly—and often permanently—healing diabetes. The earliest
PubMed-able record of Pritikin’s success with diabetics came in 1976, with this little gem:

 Beneficial effects of a high carbohydrate, high fiber diet on hyperglycemic diabetic

men

(FYI: Pritikin’s name isn’t on this paper, but it darn well should be. Scandalous tidbit alert! In
1974, Pritikin divulged the details of his diet to a Dr. James W. Anderson—an internationally
acclaimed diabetes researcher at the time—and proposed an official study to test the uber-
low-fatness on diabetics. Pritikin designed every detail of the study, drummed up $10,000
to fund it, created meal plans, and then received a grand total of zero credit for any of his
contributions once the study was completed and published. In fact, Anderson proceeded to
repackage Pritikin’s diet under a different name (the “HFC Diet,” standing for the “High
Fiber, High Carbohydrate Diet”) and claimed it as his own invention—conducting a number
of additional studies so successful that, in 1979, the American Diabetes Association was
inspired to downsize its recommended fat intake. Despite years of haranguing Pritikin for
more funding money (and thanking him profusely in their private correspondences),
Anderson never publicly mentioned his collaboration with Pritikin or credited him for
originating the diet. Buuuurn.)
So what was this study all about? For one week, 13 diabetic men—all who needed either
insulin or oral drugs to control their blood sugar—ate the standard American Diabetes
Association diet of the time: 34% fat and 43% carbohydrate, the rest made up of protein and
wishful thinking. After that, they spent at least two weeks in Carbsville, eating a diet of only
9% fat and 75% carbohydrate. (The two diets were isocaloric,  meaning they had the same
number of calories, and were designed to help folks maintain their weight rather than lose
or gain any.)

Surely that carb palooza sent their blood sugar into a frenzy! …Except it didn’t. After
switching from the ADA diet to Pritikin-hijacked-by-Anderson one, nine patients had their
insulin and oral drugs completely discontinued—at which point their fasting blood sugar
was actually lower than it had been when they were still on medication. (The cutoff for drug
discontinuation was a fasting blood sugar of 120 mg/dL.) It only took nine days of low-
fatting to make that happen! Another patient’s insulin needs dropped from 28 to 15 units
per day. As a further head-scratcher, fasting triglycerides, contrary to what we might
expect, dropped significantly for ten men. The only folks who didn’t see any benefit from
the 9% fat diet were the three who had the most advanced diabetes at the study’s onset—
needing 40 to 55 units of insulin per day.

A tabular and graph-ular representation of changes in fasting blood sugar, in case you’re
curious:
Even more intriguing, those results weren’t just a result of weight loss. Only five patients
dropped more than three pounds, and there was no difference in fasting blood sugar and
triglyceride levels between them and the weight-stable folk. And most importantly, the
results seemed to stick: after the study, the nine most successful patients were weaned onto
more flexible diets—60 to 65% carbohydrate instead of 75%. And after at least four months
of followup, the researchers noted their blood markers hadn’t changed and the “control of
the diabetes has been satisfactory without any drug therapy.” Pretty neat, huh?

Okay, okay: this study was tiny and used only men and we could find plenty of things to
complain about (more womenfolk! Longer time frame! More Instagram pictures of the
researchers’ feet overlooking exotic and envy-inducing locales!). Those are fair criticisms, to
be sure. But this study does offer something we hardly ever see: a direct comparison
between a Swampland menu (34% fat) and a Carbosis menu (9%), with the subsequent
revelation that Oh hey, they actually have totally different results!

Again, as I’m trying to hammer home in this post, most of our “low fat” studies are actually
only comparing different shades of Swamplandness—without ever hitting that fantastical
10% that brings a dramatic metabolic shift. And that makes us think that low fat is just a
sham that does nothing except make our food taste like rabbit chow. So finding a study-
gem like this, where fat intake actually does  dip into the magic zone, and where the
impressive results challenge our “low fat is bunk” narrative, is a rare and valuable find—even
if it could be better designed.

That said, we’re in luck because Pritikin actually published some of his own studies on
diabetics, and they were bigger and longer. Two of those papers came out in 1982 and
1983, respectively:

1. Response of non-insulin-dependent diabetic patients to an intensive program of diet

and exercise.
2. Long-term use of a high-complex-carbohydrate, high-fiber, low-fat diet and
exercise in the treatment of NIDDM patients.

The first paper looks at how 60 diabetics fared during the 26-day program; the second
paper looks at how they did once released back into the scary, high-fat-food-filled ‘real
world.’ In the latter, Pritikin described the in-house program as such:

During the 26-day session, the patients were served and taught to prepare the Pritikin
high-complex-carbohydrate, high-fiber, low-fat diet. The diet consisted of unprocessed
natural food with no supplements, e.g. guar. Less than 10% of the total calories were
obtained from fat, … 13% from protein, and the remainder from carbohydrate (90% complex
—whole wheat grain, rice and bread, beans, peas and other vegetables, and fresh fruit). …
Protein was derived primarily from vegetable sources, except for nonfat milk, which was
served daily, and small amounts of fish or fowl, of which 85 g/wk were provided.

Right off the bat, we can see the study wasn’t free from animal protein, as folks were
allowed to drink a fair amount of skim milk,  chock full of that awful casein vilified in The
China Study. It also contained very small (but not irrelevant) amounts of poultry and fish—
about this much per week:

Image from HealthFinders Collaborative.

On top of that, the Pritikinites who started out overweight had their calories restricted, but
everyone else could eat as much as they wanted (ad libitum).  And all the participants were
encouraged to go on short walks each day.

So what happened? At the end of their 26-day bootcamp, their pancreases exploded! Just
kidding. They did super well. Of the 23 patients who’d entered the program needing to take
oral hypoglycemic drugs, all but two had ditched them by the end of the program:

And of the 17 folks who’d been taking insulin

(with dosages ranging from 14 to 75 units per day), all but four were released from its
needly shackles:
 (After crunching the numbers, it turned out
people’s reduction in fasting blood sugar was not correlated with weight loss, or with the
amount of walking they did, or other changes that we might suspect played a role. Dietary
adherence reigned supreme!)

Okay, I know what you’re thinking. Those results are nice and all, but 26 days is nothing in
the span of a person’s disease history. Heck, I’ve had hold-sessions with Comcast last
longer than that! What happened afterwards? Did Carbjo cometh?

Luckily, Pritikin wanted to know the answer to those questions too. Between two and three
years after their romp at the Longevity Center, the patients got a phone call quizzing them
on how well they’d stuck with the diet, how much they were exercising, and whether their
medical status had changed. They also had to answer dietary recall surveys and food-
frequency questionnaires, and got a fasting blood-sample kit in the mail, which is kind of
weird but probably a lot more exciting than bills and MasterCard offers.

The results? Compared to when they were freshly released from their low-fat boot
camp, seven more people were taking oral hypoglycemic drugs, and four more people were
taking insulin. Does that mean the diet failed?! Can we sling a big, fat “I told you so!” to the
low-fat warlords and reassure ourselves that the diet is bogus? Actually:

… the main difference between those patients who went back on medication at follow-up
compared with those remaining off medication was the percent of calories derived from fat.

Basically, those who stuck with the diet kept reaping the initial rewards, but those who
gallivanted back into the Swampland paid dearly!

Of course, all that’s a mere smidgen of the data that got churned out from the Longevity
Center over the years. R. James Barnard, who’s served as Research Director at the Pritikin
Center (among quite a few other professional feats), published over 100 studies on the
Pritikin Program, looking at everything from cancer to diabetes to heart disease.
Hi, James!

And while part of me would love to sit here and write about EVERY SINGLE ONE of those
studies in attempt to explode the internet with Literally the Longest Blog Post Ever, another
part of me—the part that realizes even the most patient of my readers have sanity limits and
day jobs—has vetoed that plan in favor of a briefer sampling. Behold!

ESCAPE HATCH FOR THE FATIGUED OF BRAIN: what follows is a pretty long and sciency
scroll of scientific scienceness. I know this blog post is big. I know your brain is turning into
soup. CLICK HERE if you want to bypass the study summaries and get back to Pritikin’s life
narrative!

Note: the Pritikin Program involves both the Pritikin diet and an hour of daily walking.
Although we could definitely consider exercise a confounder (since it can independently
improve metabolic and hormonal markers), studies of walking alone haven’t demonstrated
anything nearly as dramatic as what’s been achieved with the Pritikin Program. At best, we
could wager that walking probably boosts the results of the program, but only contributes
to a fraction of its overall effects.

Another note! Unless otherwise mentioned, all the studies below allowed an  ad
libitum  (non-calorie-restricted) energy intake. The participants could eat as much as their
hearts desired out of any Pritikin-friendly item except for fish and poultry, which were
capped at three servings per week (combined).

Prostate Cancer Protection

 Long-term adherence to the Pritikin Program was a major boon for squashing out
insulin resistance and reducing prostate cancer risk. Folks who followed the diet
between 1 and 28 years reduced fasting insulin by 52%, fasting glucose by 20%,
HOMA IR (a measure of insulin resistance) by 62%, and fasting triglycerides by 45%.
And in a group of overweight men, even a quick jaunt on the program (two weeks)
reduced fasting insulin by 30%, fasting glucose by 14%, HOMA IR by 40%, and fasting
triglycerides by 33%. Not impressed yet? Blood from the Pritikin-fed fellows (both
 two-week and long-term) drastically slowed the growth of prostate epithelial cells,
suggesting benefit for the prevention of prostate cancer.

From “Effect of diet and exercise intervention on the growth of prostate epithelial cells.”
Barnard, 2008.

 In a similar study of both short-term (11 days) and long-term (average 14.2 years)
Pritikin followers, more evidence of prostate cancer protection emerged. The short-
termers saw a 20% drop in insulin-like growth factor 1 (IGF-1) levels and a 53% rise
(that’s a good thing!) in insulin-like growth factor binding protein 1 (IGFBP-1); the
long-termers saw a solid 55% drop in IGF-1 and 150% rise in IGFBP-1. (IGF-1 has
been strongly associated with cancer due to its role in regulating cell growth and
death, and and IGFBPs are proteins that bind insulin-like growth factors and
neutralize some of their unsavory activities.) Likewise, the short-term group saw a
25% drop in fasting insulin levels and the long-term group saw a 68% drop. As with
the previous study, both groups’ Pritikin-ified blood was particularly awesome at
fighting cancer: the serum from the short-termers caused a 30% decrease in the
 growth of LNCaP cells (a line of human prostate cancer cells) and serum from the
long-termers caused a 44% decrease, compared to baseline. Both groups’ blood also
increased the rate of death for those cancer cells.
 Yet another study of Pritikin dieters (27 obese men) showed the program may be an
excellent defense against the disease: the men saw a 28% increase of sex hormone-
binding globulin (which binds androgens and appears to help protect against
prostate cancer) and a 43% drop in fasting insulin; for three men who started out
with slightly elevated PSA (prostate-specific antigen) levels, the diet also reduced
that. According to the researchers, “The increase in SHBG would result in more
testosterone being bound and, therefore, less of the androgen available to act on the
prostate. The decrease in insulin might also decrease mitogenic activity in the
prostate.”
 One more on the prostate front! An analysis of post-Pritikin-Program blood shed
light on the mechanisms behind the aforementioned anti-cancer effects: apparently,
the Pritikin Program reduced tumor cell inflammation and resulted in
lower  NFκB  activation in LNCaP cells. (NFκB, or “nuclear factor kappa-light-chain-
enhancer of activated B cells” if you want to be fancy about it, is a protein complex
involved in DNA transcription, cell death, and cytokine production.) The program’s
results also seemed to hinge on reducing IGF-1 levels, because when the researchers
added back IGF-1 back to the participants’ squeaky clean, post-Pritikin-Program
serum, the results were completely reversed:

From “Analyzing serum-stimulated prostate cancer cell lines after low-fat, high-fiber diet
and exercise intervention.” Barnard, et al., 2011.
Reduced LDL Oxidation and Spiffed-Up HDL

 Three weeks on the Pritikin Program resulted in LDL particles that, even by paleo-
and low-carb-advocate standards, were much less likely to oxidize and promote
heart disease. In a group of 80 Pritikinning men and women, average LDL particle
size increased (with larger LDL considered less atherogenic), and 27% of the folks
who’d started out with LDL pattern B switched to LDL pattern A (again, considered
less atherogenic). In vitro,  the participants’ LDL also became more resistant to
copper-induced oxidation—with a 21% drop in initial oxidation, 13% increase in lag
time (the delay before oxidation happens, as the LDL’s antioxidants become
depleted), a 20% reduction in peak diene formation (a way to measure oxidation),
and a 17% reduction in maximal rate of diene formation. All of that jargon basically
means the LDL had become far more resistant to oxidation—at least based on this
particular assay (there’s always some uncertainty about how well in vitro  (outside the
body) studies translate to in vivo  (inside the body)).

From “Effects of diet and exercise on qualitative and quantitative measures of LDL and its
susceptibility to oxidation.” Barnard, 1996.

 Similarly, a study in postmenopausal women found that the Pritikin Program led to

more oxidation-resistant LDL particles.
  Even though the Pritikin Program often reduces HDL (the so-called “good
cholesterol” lipoprotein), it makes the existing HDL that much awesomer. A study of
obese men found that after three weeks in Pritikin Land, the HDL inflammatory index
(AKA the ability of HDL to prevent LDL from oxidizing) changed from “pro-
inflammatory” to “anti-inflammatory.” The activity of platelet activating factor
acetylhydrolase also increased, LDL decreased by 26%, and triglycerides decreased
by 29%. Basically, even though HDL was lower than at baseline, its function was
mucho improved—”suggesting increased turnover of proinflammatory HDL,”
according to the researchers.

From “Effect of a short-term diet and exercise intervention on inflammatory/anti-

inflammatory properties of HDL in overweight/obese men with cardiovascular risk factors.”
Barnard, et al., 2006.

Breast Cancer Protection

 In postmenopausal women, the Pritikin Program fantastically improved the major

metabolic and hormonal risk factors for breast cancer: on average, insulin dropped
29%, insulin-like growth factor 1 (IGF-1) dropped 19%, insulin-like growth factor
binding protein 1 (IGFBP-1) increased 32%, estradiol (among women who were on
hormone therapy) dropped 34%, and estradiol (among women who weren’t on
hormone therapy) dropped 37%. In vitro, serum from those Pritikinettes dramatically
slowed the growth (and induced apoptosis,  or programmed cell death) in three
 breast cancer cell lines (MCF-7, T-47D and ZR-75-1) compared to blood from the
same ladies before they’d started the diet.
 In a study of pre-menopausal women, two months of the Pritikin diet led to some
fun breast-cancer-protective hormonal changes: serum estrone and estradiol (types
of estrogens) fell during the women’s early folicular and late luteal phases (with
decreases ranging from 18% to 26%), with no negative impact on ovulation.
(Exposure to ovarian hormones, especially estrogen, appears to increase breast
cancer risk, so these changes could be expected to reduce it.)

From “Effects of a very low fat, high fiber diet on serum hormones and menstrual function.
Implications for breast cancer prevention.” Barnard, et al., 1995.

Colon Cancer Protection

 In women, a 26-day Pritikin diet improved some risk factors of colon cancer by

reducing fecal secondary bile acids (which are linked to the promotion of colon
cancer).

Heart Disease, and Related Adventures

 Here’s a goodie called, “Effects of an intensive exercise and nutrition program on

patients with coronary heart disease: Five-year follow-up.” (There’s no link because
for some awfully frustrating reason, this paper is nonexistent online, and I was only
able to track it down via the library. Email me if you want a PDF copy!)  This study
followed the progress of 64 Pritikin adherents with coronary heart disease, five years
after they left the sheltered, intensive clutches of the residential program. Prior to
entering the program, 59% of the patients had experienced a heart attack and 80%
had angina (chest pain). During that five-year follow-up, four people died (one of
cancer, two of a heart attack, and one of heart failure during a mitral valve
 replacement), and two additional folks had non-fatal heart attacks. Reports of angina
dropped from the initial 80% to only 32%. Fascinatingly, despite the fact that this was
a highly diseased group with the odds stacked against them in terms of morbidity
and mortality, their annual death rates ended up being close to that of the “regular”
population after they Pritikinized their lives! (At the time the paper was written,
post-heart-attack mortality was around 10 to 15% for the first year following the
event, and as high as 50% by the third year.)

From “Effects of an intensive exercise and nutrition program on patients with coronary heart
disease: Five-year follow-up.” Barnard et al. J Cardiac Rehab 1983;3:183-190.

 In 31 obese men, the Pritikin Program brought awesome improvements in a huge

range of risk factors for heart disease—including blood lipids, oxidative stress,
inflammation, and cell adhesion. After just three weeks, there were significant drops
 in LDL (25% lower), triglycerides (28% lower), fasting glucose (12% lower), insulin
(30% lower), HOMA IR (33% lower), C-reactive protein (39% lower), soluble cell
adhesion molecules, inflammatory cytokines, and monocyte adhesion. And to
sweeten the deal, nine out of the 15 men who entered the program with an official
diagnosis of metabolic syndrome no longer met diagnostic criteria by the time their
three weeks of low-fatting was up.
 In 15 hyperlipidemic men, two weeks of the Pritikin bootcamp improved a number of
risk factors for heart disease: it lowered the men’s blood pressure, slashed
triglycerides, reduced the aggregation velocity and maximum aggregation of
platelets, and reduced the formation of thromboxane (which is made by platelets and
promotes blood clotting and constriction of blood vessels).
 Combined with daily aerobic exercise, the Pritikin diet facilitated major
improvements in myocardial blood flow. After six weeks, resting blood flow
decreased by 12%, and hyperemic blood flow increased by 9%—leading to an
improved myocardial flow. (It’s impossible to know how much diet versus exercise
played a role in these results, though!)
 In postmenopausal women on hormone replacement therapy, the Pritikin Program
heralded some promising changes on the heart-disease-protection front. After just
two weeks, 20 women saw significant drops in their BMI, glucose levels, insulin
levels, all serum lipids, and HOMA IR. The researchers conclude that these “rapid
improvements may reduce the risk of acute myocardial infarction (MI), and if
sustained, these changes may mitigate the risk for atherosclerosis progression and
its clinical consequences.” Not too shabby.
 In a small study of 11 men, the Pritikin Program appeared to be uber protective
against atherosclerosis progression. In the span of 21 days, the program dropped
LDL by 23%, triglycerides by 41%, fasting insulin by 46%, and fasting blood sugar by
7%. Serum 8-iso-PGF 2 alpha (a product of lipid perodixation) also sank, whereas
nitric oxide availability rose. In Barnard, et al.’s words: “The present study is the first
to show that unrestricted consumption of a low-fat, high-fiber diet and daily
exercise can mitigate oxidative stress, improve NO availability, and normalize BP in
obese men within 3 weeks.”
From “Effect of diet and exercise intervention on blood pressure, insulin, oxidative stress,
and nitric oxide availability.” Barnard, et al. 2002.
From “Effect of diet and exercise intervention on blood pressure, insulin, oxidative stress,
and nitric oxide availability.” Barnard, et al. 2002.

Diabetes Damage Control!

 For 70 diabetics, a 26-day jaunt in the world of Pritikin led to all sorts of disease-
blasting perks: fasting blood sugar fell by 24%, blood pressure dropped by 10%—and
even better, 71% of the folks who’d been taking oral hypoglycemic drugs pre-Pritikin
were able to ditch their prescription (ditto for 44% of the folks taking insulin and 61%
of the folks who’d been taking blood pressure medication)! Also, VO2max
(“functional maximum oxygen uptake) improved by 41%.
 In diabetic men, a three-week Pritikin Program reduced heart-disease risk factors
associated with diabetes: the program whipped down fasting glucose by 20%,
dropped fasting insulin by 30%, and totally clobbered markers of oxidative stress,
inflammation, and monocyte-endothelial interaction (a major part of the heart
disease process). Boom!
 Among 652 non-insulin-dependent diabetics, three weeks of the Pritikin
Program significantly improved their condition: fasting glucose dropped by 16%, and
71% of folks taking oral hypoglycemics (and 39% of the folks taking insulin) were
 able to discontinue those medications. Triglycerides and blood pressure also fell to
delightful new lows.
 In diabetics, the Pritikin Program reduced fasting insulin in diabetics by an average
of 33% in just three weeks, and restored normal fasting insulin levels in 59% of
insulin-resistant folks in the same time frame. (Triglycerides also dropped across the
board!)

In the Elderly

 Among 70 folks aged 70 and older (average age of the group being 78.7), 26 days of
the Pritikin Program totally spiffed up their health: they lost an average of five
pounds, total cholesterol and triglycerides fell significantly, their treadmill
performance increased by 49%, the type II diabetics of the group reduced their
fasting blood sugar by 27%, and half of the patients taking blood pressure
medication were able to discontinue it.

But What About the Children?!

 In overweight and normal-weight children, two weeks of the Pritikin Program yanked

down multiple cardiometabolic risk factors: insulin levels fell (by 28.1% in overweight
kiddos and 52.5% in normal-weight kiddos, respectively), HOMA-IR fell (28.4% and
53.1%, respectively), leptin levels fell (44.1% and 69.3%, respectively), and a variety of
proinflammatory cytokines were reduced (molecules that increase inflammation in
the body). LDL went down by 24.5% and 29.4%, while HDL hardly budged. Those
changes didn’t correlate with weight loss, either!

Effect of Pritikin Program on inflammatory cytokines. From “Effects of an intensive short-

term diet and exercise intervention: comparison between normal-weight and obese
children.” Barnard, 2013.
  Also in children, two weeks on the Pritikin Program (for 19 overweight
kiddos) massively improved factors associated with heart disease: the program
tanked LDL by 25.3% and triglycerides by 39.5% (HDL didn’t significantly change); 8-
isoprostaglandin F2 alpha (a marker of lipid peroxidation) fell by 81%, CRP fell by
41%, and MMP-9 (a measure of plaque stability and progression) fell by 49%. Markers
of endothelial cell activation (ICAM-1 and sE-selectin) also went kerplunk! As the
researchers summed it up:

“The primary findings of this study provide evidence that even a short-term
lifestyle modification program may (1) improve the lipid profile; (2) decrease
production of the reactive oxygen species superoxide and hydrogen peroxide
and increase NO production; (3) decrease endothelial cell activation and
adhesion; (4) decrease inflammation; (5) decrease monocyte chemoattraction;
and (6) decrease MMP-9, a marker of plaque destabilization, all of which may
contribute to a reduction in atherosclerosis progression.”

From “Effect of a short-term diet and exercise intervention in youth on atherosclerotic risk
factors.” Barnard, et al., 2007.
  WE’RE NOT DONE WITH YOU YET CHILDRUNS. Yet another study on overweight
youth found, again, a massive drop in insulin (33%), HOMA-IR (29%), triglycerides
(40%), systolic blood pressure (10%), diastolic blood pressure (10%), and LDL (27%),
with no change in HDL. All seven of the kiddos who were classified with metabolic
syndrome at the start of the study had reversed their diagnosis by the end of it!

And that’s just a freakin’ handful  of the research out there. Seriously. A handful.  If you want
to venture into the full-on Pritikin Research Safari, I recommend bringing snacks and water,
’cause you’ll be gone awhile!

Just to be clear, I’m not trying to say that the Pritikin Program is wildly successful for
everyone who jumps aboard, or that it’s unequivocally the best treatment for the diseases
it’s been used for. The point I want to make is more conceptual than anything. Contrary to
the belief that low-fat, high-carb diets raise insulin levels, muck up glucose control,
encourage obesity, and promote inflammation, the overwhelming majority of
studies published on the Pritikin diet have shown the polar opposite. That doesn’t mean
there isn’t a range of outcomes within each study; indeed, some participants do well, some
do really  well, and some don’t do well at all, even when the collective effect is positive. But
seriously, the Pritikin Program yields impressive results, and it’d take a whole lotta’
somersaults of logic to conclude otherwise.

I know your brain is probably maxed out on scienceness now, so let’s resume our narrative
of Mr. Pritikin’s life! First up, an interesting parallel between his way of thinking and that of
the modern Paleo community.
In the early ’70s, Pritikin wrote a three-volume opus compiling his theories—dotted with
hundreds of scientific references—about every major condition of the time: atherosclerosis,
angina, high blood pressure, gout, arthritis, gallstones, kidney stones, diabetes, lung
cancer, colon cancer, prostate cancer, breast cancer, as well as hearing and vision diseases.
He was convinced they were all, essentially, manifestations of a huge mistake called “What
Americans Typically Eat.” In fact, Pritikin had a fascinatingly ‘ancestral’ approach to nutrition
(back at a time when linking diet to chronic disease period was considered cuckoo for Cocoa
Puffs), which he discussed in the introduction to his three-volume work:

Such a postulation linking diet and the scourge of degenerative diseases may seem far-
fetched, until one reflects upon some basic biological facts. All animals, man included, have
a diet that emerged from the long-term experience of the species in nature over many
thousands of years. Now, man no longer eats foods his body was designed to eat, but has
created a synthetic diet—the penalty of which is to endure the adverse effects of short-term
experience. The more man’s diet departs from foods to which he is biologically suited, the
more the adverse effects.

Whereas the modern incarnation of Paleo has drawn heavily from higher-fat-eating societies
(the Inuit and Masaai are particularly cherished), Pritikin found dietary consistency among
the starch-based populations: the Tarahumara Indians, the Bantu, and the natives of New
Guinea, whose traditional low fat intake and virtual freedom from heart disease fed into his
overarching philosophy about food. Just keep that in mind if you find the idea of low-fat
eating to be ancestrally preposterous!

For what it’s worth, Pritikin certainly walked his talk. Before his mortal departure, he’d
requested an autopsy be performed so the world could have an honest look at his once-
diseased heart. The results were published in a New England Journal of Medicine article
called “Nathan Pritikin’s heart,” where the state of his ticker blew the pathologist away:

The epicardium was smooth, and no scars were visible. The endocardium and all valves
were normal. … The coronary arteries were soft and pliable … there were no raised plaques
and no compromise of the lumens. No clots were present. … No infarcts of any size, or
other finding referable to vascular disease, were present in any organ.

The report concluded, “In a man 69 years old, the near absence of atherosclerosis and the
complete absence of its effects are remarkable.”

Important note on Pritikin’s death: Critics of Pritikin (Priticritics?) often point to his

departure from the world—death by suicide, amidst a painful battle with leukemia—as
evidence that his low-fat diet either pulverized his mental health (suicide) or gave him
cancer (leukemia). Those are both pretty bold claims, so let’s take a moment to assess
them.

In the 1950s, Pritikin went through a series of high-dose radiation treatments for a skin
condition, pruritus ani,  that was stubbornly resisting all the pills and ointments he tried.
Over the course of two months, he got blasted with a total of 220 rads (“radiation absorbed
doses”) of unfiltered x-rays—the equivalent of getting 3700 chest x-rays or 22 million
dental x-rays. Not surprisingly, it wreaked havoc: he soon ended up with a blood condition
he’d battle for the rest of his life, later diagnosed as a rare form of leukemia. That all
happened before he embarked on a low-fat diet.

Pritikin actually managed to keep his disease in remission for almost three decades, but in
late 1984, saw an unfortunate resurgence of symptoms—including leg swelling so severe
that he had to stop going on his beloved daily runs. His docs ushered him onto some
experimental chemotherapy, telling him it was the only way he could ever resume jogging.
Not only did the chemo not  help, it also left Pritikin with crippling anemia, kidney failure,
diabetes, all-consuming pain, and 30 pounds stripped off his already slender body. In
February of 1985, he flew out to New York for a second opinion, was told his case was
hopeless and he would certainly die within the next six months, and proceeded to take his
own life in a hospital bed in Albany.

As George McGovern reflected, “He was always in charge of his life. It rather followed he’d
want to be in charge of his death.”

With all that in mind, can we implicate Pritikin’s diet in his sad demise? With enough mental
gymnastics and anti-low-fat bias, sure—but I don’t think it’s particularly logical or fair. Did
his diet shorten his life, or lengthen what was originally a grim prognosis? And if we make
an automatic diet-death jump, should we do the same for the recent passings we’ve seen in
the high-fat community (low-carb guru Barry Groves, saturated-fat-redeemer Mary Enig, or
“Carbohydrates Can Kill” author Robert Su)?

As drawn as our human brains are to stories and anecdotes, I think it’s wiser to look at
bigger, statistically stable data instead of case studies. Everyone has to die of something,
and food isn’t the only tool of the grim reaper.

Ancel Who?
 Oh hey! Remember this guy?

The one who allegedly pulled the low-fat theory out of thin air, manipulated the American
Heart Association into believing it, and took the world by storm with his Machiavellian wiles?

The one who cherry-picked his way into a groundless theory?

The one whose very countenance makes us tremble with rage, as we thrust our butter-
encrusted fists in the air in defiance?

Yeah… him.

Let’s get real here for a minute. When it comes to evidence supporting low-fat
recommendations, Keys was more like the ending caboose than the engineer driving the
train. He was far from the first person to think that fat could play a role in chronic
disease.  We didn’t need his suspiciously curvilinear six-countries graph, we didn’t need his
Seven Countries Study, and we didn’t need his can’t-prove-causation epidemiological
utterings to form our “low fat movement.” Those things certainly played a role in pushing
low-fat theory into the realm of public policy, but holy massive research pile Batman,  there
was plenty of evidence already there before he made his own contributions! Heck, Keys was
clearly aware of his low-fat predecessors by the time he hit the scene: he even referenced
the Rice Diet in his now-infamous 1953 paper “Atherosclerosis: A Problem in Newer Public
Health” (PDF), where his six-country graph made its grand debut.

Even if you exit this blog post still believing “low fat” is an awful sham, we can’t keep
spreading the myth that Keys was its originator. Every time we place the low-fat movement
squarely on his shoulders, a kitten gets ejected from a machine gun and blasts a hole
through the ozone. Do you really want to destroy the planet? Do you?  I didn’t think so! Let’s
just agree right now to put this whole myth to rest, and fill our alotted “hatin’ on Keys” time
with more important matters, such as how to invent prosthetic goosebumps for people who
cannot feel fear and/or coldness.
Modern Diet Doctor Squad: An update and apology for jumping the gun

Although this post isn’t diving into research by the modern “Plant-Based Diet Doctor Squad”
(Caldwell Esselstyn, John McDougall, Dean Ornish, Neal Barnard, and by some definitions
Joel Fuhrman), I do want to comment on the first gentleman in that lineup—the heart-
disease-bustin’ Esselstyn of the renowned Cleveland Clinic.

If you aren’t already familiar with him, Esselstyn is a super cool cat who I want to adopt as
my grandpa, and who’s been treating death-bed-borderline heart disease patients for
decades. In my Forks Over Knives critique, I criticized his fat-shunning program on account
of the high triglycerides and low HDL it produced in some of his patients, while also
pointing out the inconclusiveness of his published work due to its tiny sample size. Allow
me to awkwardly quote my self of four years ago:

Holy triglycerides, Batman! Although Esselstyn’s diet helped lower most of his patients’
triglycerides, a couple still have values in the major danger zone (362?). Some of those HDL
numbers are looking pretty sorry as well.

All in all, Esselstyn’s study shows that a whole-foods, plant-based diet is probably infinitely
better for cardiovascular health than the junky cuisine many folks eat. But it’s far from
conclusive evidence that this diet is the best we can do for reversing heart disease, or that it
would generally be effective in a population beyond his 11 self-selected subjects. A diet
that reduces triglycerides and increases HDL more than his did, for instance, might have an
even better outcome.

I’ve written a lot of things in my life. Some of those things have been wrong. This is one of
them.

While I still suspect Esselstyn’s diet could be unveganized without harming its therapeutic
effect (perhaps through the addition of gelatin, seafood, and whole-grain unicorn flour), I’m
no longer convinced that low HDL and high(ish) triglycerides are bad in the context of
unprocessed low-fat diets. I’ll explain why that’s the case in Part 2! But in a sneak-peek
nutshell, it has to do with the improved quality of HDL (which we saw with one of the Pritikin
Program papers) and the fact that higher trigs are typically a marker for insulin resistance,
and when that’s absent, a heftier number probably isn’t pathological (which you can read
more about in this paper yonder). We also have plenty examples of non-Western cultures
that remain virtually free from heart disease, despite having triglycerides we’d consider too
high and HDL we’d consider too low (hellooooo there Kitavans!)

As for the issue of Esselstyn’s statistically wobbly sample size (only 11 people who stuck
with the diet through its 10-year follow-up): it was a fair criticism at the time, and one
that’s been echoed by plenty of others. But it’s time to put that quibble to bed, preferably
with enough sleeping pills so that it never again rouses. Why? It just so happens that in July
of 2014, Esselstyn published a bigger, badder, bodacious-er study of 198 people  instead of
his original handful. The prescribed diet was the same oil-free, animal-food-free, whole
foods regimen he’d been using for decades—with no confounding elements from exercise,
meditation, psychosocial support, or yoga to be had. And the results were just as impressive
—if not more so—than the ones he achieved in his earlier work:

 Among the 177 folks who stuck with the diet (for an average length of 3.7 years),
there was only one cardiovascular event related to disease progression: a stroke.
That’s a recurrent event rate of 0.6%.
 Among the 21 folks who strayed from the program, 13 had cardiac events. That’s a
recurrent event rate of 62%.
 (The five other deaths in the adherent group included three cancers, one pulmonary
embolus, and one case of pneumonia.)

Image from “A way to reverse CAD?” Esselstyn, 2014.

Image from “A way to reverse CAD?” Esselstyn, 2014.

For sure, there’s still plenty of stuff we could nitpick about this study (and his previous
ones): there was no control group; the patients were abnormally motivated and self-selected
(rather than reflective of the general heart-disease population, who might not be so inclined
to give up steak forever); the study wasn’t randomized; and some level of self-fulfilling
prophecy could’ve been at play, since the patients were told initially how awesome the diet
was and how stupendously it was going to scrub out their arteries.

But even with those shortcomings, I’ll say it loud ‘n clear: I’m impressed.  The study
documents true heart disease arrest, and actual reversal for some. We don’t yet have any
published studies of that sort on ketogenic, low-carb, or paleolithic diets (as far as I’ve
seen!). And in my old age, I’ve come to appreciate the fact that real-world outcomes (i.e.,
whether or not someone keels over and dies) are more valuable than intermediate risk
markers (like specific blood lipid ratios). It doesn’t matter that your health looked good on
paper if you still end up in the ER!

And now, for an apology.

For the past few years (five? six? seven ate nine?), I’ve asserted that the success of plant-
based diets is due to their whole-foodsness (eliminating processed junk, refined sugar, and
refined flour), their low PUFA intake regardless of total fat (with the implication that higher
non-PUFA fat consumption would be hunky dory), and the increase in other health-
promoting behaviors that come with making a big change in the foods you eat (more
exercise, less drinking and smoking, less couch-potatoism, etc.). I still think those things
are relevant. But I now believe I dismissed the role of low total fat intake before I gave the
data a fair and thorough analysis. This is a breach of the standards I hold myself to as a
science blogger, which involve impartially examining all evidence before drawing
conclusions.

So, I’d like to take this opportunity to say, HEY GUYS: I’m sorry.

To the aforementioned doctors: I’m sorry for jumping the gun with your research and being
snarky when I reference you. I don’t always agree with the way you interpret your own work;
I’m often unsettled by your debate tactics; I worry that the co-mingling of animal rights
activism and nutritional research is toxic for remaining scientifically objective. But good
heavens, I sure dismissed y’alls results before digging as deep as I should have—and in the
process, missed out on some amazing opportunities to broaden my understanding of diet
(and communicate those findings to my readers). Thanks for being on this planet and
helping broken people heal.

To my readers: You guy are the best, seriously. Somehow you put up with these sporadic
and unreasonably long blog posts and say nice things to me and wish me a happy birthday,
sometimes with the inclusion of cat pictures, which is very wonderful. I don’t take your
readership, your trust, or my quasi-position in the public eye lightly. And while I can’t
guarantee that every word I write in this blog will be totally accurate, or that the ideas I
present now and in the future will stand the test of time, I   can  promise that I strive to
question my own biases just as rigorously as I question others’. That process of questioning
will result in errors coming to light, which I see as a very good thing indeed: science (and its
interpretation) should be self-correcting! Thanks for hanging in there with me. I’m honored
for your readership.

Up Next…

Hopefully by now, some things have become clear:

 We can’t categorically blame low-fat, high-carb diets for heart disease and diabetes
and obesity. We just can’t. NOT EVEN A LITTLE BIT. This needs to go away.
 We probably can’t even blame refined sugar for that stuff (at least not in isolation).
Oh, the pain of shattering assumptions!
 We can’t ascribe the effects of low-fat, plant-based diets to their lack of animal
products. Quite a few of the uber-low-fat studies here still allowed a fairly high
 animal protein intake, and still managed to whip people into diseaseless shape.
Sorry, vegans!
 Ancel Keys did not invent low-fat.
 Ancel Keys did not invent low-fat.
 Once more, with feeling! Ancel Keys did not invent low-fat.
 I need to employ the “delete” button a little more rigorously. (Can you imagine how
computer-crashy this blog post would be if I hadn’t split it into two parts?)

Admittedly, I’ve gone pretty easy on some studies in this post and—had I decided to devil’s-
advocate from the other side—could’ve critiqued certain ones far more aggressively. But
there’s a reason I didn’t go into BAD SCIENCE INCINERATOR MODE, and it’s not because I
got bought off by the garbanzo bean industry (they’re gonna have to try a lot harder than
43 cents). For one, the sheer volume and consistency of the research here points to
something very real, something totally non-under-the-rug-sweepable—and analyzing each
individual study in search of holes and inadequacies wouldn’t change that fact. And
secondly, there’s a whole universe of scientific mechanisms explaining why the diets
discussed here work: the ability of dietary fat to reduce insulin sensitivity, the effect of
different fats on tissue oxygenation and blood flow, the little-known ways that saturated fat
can make LDL more likely to get incorporated into plaque, and all sorts of other fun stuff.
That’s what the next post is about, so stay tuned!

In sum, there comes a point where it’s more of an intellectual stretch to rationalize
something away than to accept that it may have merit. My friends, we’ve reached this point
on the issue of low-fat diets. Let’s face it: they can actually do some good. And it’ll make a
whole lot more sense why after you read Part 2!

Guess what? You made it to the end! Please remove of your pixel-dizzy eyes from the
computer screen and get some fresh air. You freakin’ earned it!

here’s a whole tray of Internet Bonus Biscuits! Mwah!

I fear that a picture of actual biscuits may be offensive to some readers, so I’ve chosen a
picture of a cat “making biscuits,” which is the next best thing.
https://deniseminger.com/2015/10/06/in-defense-of-low-fat-a-call-for-some-evolution-of-thought-
part-1/#comments

Researchers call this the “obesity paradox“: carrying extra weight tends to increase people’s
risk of getting heart disease, but for folks who already have the disease, it seems to prolong
life. Of course, there could be quite a few alternative explanations for that trend, which
are thoroughly discussed here. Interesting, nonetheless!)

https://care.diabetesjournals.org/content/36/Supplement_2/S282.full

Defending the Con Side: Obesity Paradox Does Not Exist

The counterintuitive reverse epidemiology of body weight observed in some studies

in patients with existing CVD does not necessarily mean that an obesity paradox
exists. There seem to be a multitude of reasons why a lower or normal body weight in
those patients may be bad news rather than good news, signaling serious
comorbidities, cardiac cachexia, and anabolic deficiency induced by heart disease or
also underprivileged care. Selection or survival bias and treatment bias are other
important factors to be recognized and underline the need for evidence-based and
guideline-based medicine for all patients.