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The mystery of hippopotamus fat

A friend recently drew my attention to an historical essay about a plan to bring hippos to the U.S. primarily for eating.
Unfortunately, that plan never came to fruition.
Hippos are one of the fatter animals left,
endangered because their meat is so prized,
and I wonder why we don’t just farm them.
In any case, I was curious about eating hippopotamus, and found an interesting section on hippopotamus fat in The Paleoanthropology and Archaeology of Big-Game Hunting: Protein, Fat, or Politics?.

As is evident from some of the previous quotes, the hippo, like the eland, was clearly highly prized for its fat (e.g. Andersson 1857:414; St. Gibbons 1898:9). While hippos may have been too difficult and too dangerous for Paleolithic hunters to kill, it is perhaps not surprising that (presumably) scavenged hippo remains, with clearly cutmarked bones, often show up in some of our earliest archeological sites in East Africa, such as the famous HAS (“Hippo and Artefact”) Site immortalised in a stamp issued jointly in 1975 by Kenya, Tanzania, and Uganda (see Fug. 4.4; Isaac and Harris 1997; for additional early cases, see also Bunn 1994; Clark 1987; Fiore et al. 2004; Harmand et al. 2009; Johanson and Wong 2009:255; Leakey 1996:70-71; Plummer et al. 1999;Pobiner et al. 2008).
William Burchell in 1822 provides a concise but useful description of hippo fat, noting its quantity and its somewhat unusually low melting point:

The ribs [of the hippo] are covered with a thick layer of fat, celebrated as the greatest delicacy; and known to the colonists as a rarity by the name of `Zeekoe-spek’ (Seacow-pork). This can only be preserved by salting; as, on attempting to dry it in the sun in the same manner as other parts of the animal, it melts away. The rest of the flesh consists entirely of lean; and was, as usual with all other game, cut into large slices, and dried on the bushes; reserving only enough for present use.
Burchell(1822:411)

Schweinfurth’s (1978) interesting narrative provides additional insights into the amount of fat that one can obtain from a single hippo carcass; he also comments on the low melting point of the fat, noting additionally that the fat does not go rancid easily:

We were hard at work on the following day in turning the huge carcass of the hippopotamus to account for our domestic use. My people boiled down great flasks of the fat which they took from the layers between the ribs, but what the entire produce of grease would have been I was unable to determine, as hundreds of natives had already cut off and appropriated pieces of the flesh. When it is boiled, hippopotamus fat is very similar to pork-lard, though in the warm climate of Central Africa it never attains a consistency firmer than that of oil. Of all animal fats it appears to be the purest, and at any rate never becomes rancid, and will keep for many years without requiring any special process of clarifying….
Schweinfurth (1878:192)

I then became curious about the composition of hippopotamus fat.
What could make it both have a low melting point and be resistant to rancidity?
Generally, the more saturated a fat is, the more solid it is (that is, the higher a melting point),
but at the same time, the more stable it is — the less it is susceptible to rancidity, because it can’t be easily oxidised.
So how could hippopotamus fat be both very liquid, and very stable?
I eventually found a paper which gives the composition of the fat of a variety of even-toed (cloven-hoofed) animals.
I was perplexed,
because hippo fat appears to be almost the same as beef,
and although it has a little more oleic acid and a little less stearic [*],
which should make it slightly less solid than beef tallow,
it should still be firmer than
lard,
which has even more oleic and less stearic.
Hope temporarily returned when I realised what the point of the paper was, and I learned something new to me.
Fat is usually in the form of a triglyceride.
It’s called that because it consists of three fatty acids held together by a glycerol “backbone”.
The thing I hadn’t read about or thought about before,
is that the properties of triglycerides depend not just on which fatty acids are in them,
but what position they are in the triglyceride.
There appears to be a whole industry built around that.
For example, now that consumers avoid hydrogenated oils,
but still think they should avoid saturated fat,
and still want something spreadable,
engineers have discovered they can make vegetable oils more solid by manipulating the position of fatty acids within triglycerides [†].
Nonetheless, looking at the table in the paper [‡], not only is the proportion fatty acids in hippo fat similar to beef, so is the distribution of those fats into the middle position of the triglyceride.
So, the mystery isn’t solved that way.
I don’t know what to think.
Another friend pointed out that there are feral hippos in Columbia that no one knows what to do with.
I have an idea…

[*] ‘Stearic’ comes from one of the many different Greek words for fat (as important as snow to the Inuit): στεαρ (stear): ‘hard fat’,
whereas ‘oleic’ probably comes from ελαιον (elaion): ‘oil’. See The lore of lipids, by Lewis Gidez, in the Journal of Lipid Research 1984 Dec 15;25(13):1430-6
[†] Here is a fascinating review of the effects of these ‘interesterification’ manipulations:

Effects of stereospecific positioning of fatty acids in triacylglycerol structures in native and randomized fats: a review of their nutritional implications
Tilakavati Karupaiah1 and Kalyana Sundramcorresponding author
Nutr Metab (Lond). 2007; 4: 16.
[‡] The fatty acid numbers represent chain length and number of double bonds (places where hydrogen could attach), i.e. 0 means saturated, 1 means monounsaturated, and >1 means polyunsaturated. The corresponding names are fatty acid names are:

14:0 16:0 18:0 16:1 18:1 18:2 18:3
mystiric palmitic stearic palmitoleic oleic linoleic α-linolenic

“The fatty acid distribution in the triglycerides of these various fats is shown in Table 1. For each fat, the first line gives the composition of the whole triglyceride, the second line gives the composition of the fatty acids in the 2-position of the triglyceride, and the third line (Proportion) reports the percentage of each fatty acid that is in the 2-position. If a fatty acid is randomly distributed among all three positions in the triglyceride molecule, the proportion value will be 33%. The occasional proportion value that is in excess of 100% is attributable to the large relative error where a fatty acid is present in very small amounts.”

https://lh3.googleusercontent.com/-jaxhTDj3p-Q/VLv2pn150wI/AAAAAAAAJrw/sH2aOt9UK0k/w308-h565-no/sn2fat.png

For more tables of the composition of fats and their second-position fatty acids in a variety plants and animals, see: TRIACYLGLYCEROLS PART 1. STRUCTURE AND COMPOSITION

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Dear Lyle McDonald,

I read your Open Apology to the Internet yesterday.
You are courageous to talk about it,
and my heart goes out to you.
Although I don’t know exactly what trouble you’ve gotten yourself into, I know the pain of Bipolar II, because I have it.
Or I had it.
Words get a bit tricky, and I have written an entire essay on whether someone has a disease or not when they show no symptoms .
I have no symptoms of bipolar and have been completely off of medication since I started my current diet.
How I stumbled upon what has been my cure was sort of an accident, but having a strong background in ketogenic diets played a role,
and much of my expertise, at least in the beginning, was given to me by you, Lyle.
You probably don’t know of me, but of course I know of you.
I read your work in the late 90’s while playing around with the CKD.
Later, in 2002, The Ketogenic Diet was out of print and very hard to get, but Zooko somehow procured me a copy, presenting it to me on the occasion of our second wedding anniversary.
I studied it carefully.
Lowering carbs always helped my mood,
and there are many plausible reasons to believe that a ketogenic diet might treat bipolar (see below),
but a ketogenic diet by itself didn’t cure my disease, and didn’t prevent it from progressing.

Progressing

As you say, bipolar progresses.
And one thing that may catalyse the progression is antidepressants.
From PsychEducation.org, an excellent resource on Bipolar II:

That antidepressants can cause “switching”, bringing on a manic or hypomanic phase, is generally accepted, although how often this occurs is still hotly debated (somewhere between 4% and 40% of the time?).
However, antidepressants may pose bigger risks in the long term. Substantial evidence suggests that antidepressants can induce “rapid cycling”.
Indeed, it is a standard recommendation for the treatment of rapid cycling to gradually withdraw any antidepressant.
In addition, more subtle “destabilizing” effects are possible.
Antidepressants may make it more difficult to get a good outcome from an otherwise effective mood stabilizer treatment.
There is even a concern that antidepressants may permanently alter the course of a person’s bipolar illness, through a phenomenon called “kindling”.

I feel strongly that my hypomanias were related to my extensive use of antidepressants.

A hijacked brain

You described bipolar as having a hijacked brain.
This is exactly my experience.
Last summer I gave a lightning talk at HOPE X on exactly this.
(Unfortunately, it was not recorded.)
I compared bipolar disorder to having your brain hacked.
I argued that mood states in bipolar act like drugs in state dependent learning.
For example, when I had periodic bouts of anger (which increased in frequency as time went on),
it was very easy to remember all the things I had been thinking about last time I was angry.
It gave the illusion of continuity; that my entire life was one constant stream of things making me angry.
But I had multiple moods, and my beliefs about life in different states were beginning to diverge from each other, based on this contrast in the strength of memory of evidence.
I knew this was happening, but it created a dilemma:
Do I act on what I think I might believe later, or what I believe now?
To whom am I loyal — myself now, or the self I know I will be later?
Specifically, what should I do when in that state in which I know that life is not worth living, because my whole life, it seems then, has been one long stream of futility?
I chose to be loyal to a future self, in that case.
But there is no doubt that betraying yourself in the now because you lack trust in your own brain is a shitty place to be.

The future

You have a life to recreate, and consequences to bear, but I have faith in you.
It is not easy to be creative and highly intelligent in that bipolar way,
because you will discover truths that other people can’t see,
and thus have to deal with the constant criticism of wrong people, sometimes very intelligent wrong people.
You have been through this and are obviously strong, even if we couldn’t see all that was going on.
Turn your natural abilities and your strength to curing yourself as best you can.
What worked for me might work for you!
I hope you try it and it does.
But if you don’t or if it doesn’t then I think you will find a way.
Study the drugs (many modern bipolar drugs are anti-convulsants, suggesting that what helps epilepsy might help bipolar).
Study the physiology.
You already know way more than I do.
Look at plausible fringe theories (some interesting things to be found on the site I mentioned above).
You will find something, and your life will get better.

My own apology

I hope you take this letter as I intend it:
as an expression of care, sympathy, and of hope that perhaps what I have learned could help you in some way.
Please forgive my boldness to speak to you personally when I don’t know you, or all of what you are going through.
Most of all, I just want to say that I admire you for your openness, your willingness to admit to mistakes, and your commitment to change.
With love and encouragement,
Amber

Resources

Jim Phelps’ Bipolar II site
Some papers that might be of use:

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Experiences of a five-year carnivore: Part II

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Part II: Eating, then and now

When I first was thinking about trying an all-meat diet (Part I),
I worried about things like boredom, and missing favourite plants.
In practice this hasn’t been a problem, because…

…my concept of what constitutes food has changed.

You may have have experienced this if you don’t normally eat “processed” foods [1],
and then are offered some blue, grocery-store-birthday-cake monstrosity,
or “fruit” punch.
It’s about as appealing as plastic.
When I started out, I avoided all spices, and ate plain meat.
It was a little bland the first few days, but
my tastes quickly adapted to animal foods.
Even though I have always loved vegetables,
I don’t miss them.
I can see that they are pretty, and I can imagine their sweetness or texture if pressed,
but it’s really no big deal.



Amber eats chicken bones

Perhaps unsurprisingly, I started appreciating meat more.

I’ve always liked meat, but
I eat meat differently from when I started.
The first thing that happened was that I started liking it cooked more rare.
Brought up vegetarian,
I’d learned pride in my palate for the exotic,
but I was not a connoisseur of flesh.
I preferred my steak well-done.
When meat was the only thing I ate, I began to notice that I liked it more rare,
sometimes even raw, though admittedly, I don’t eat raw often.
I also eat all the fat and gristle, and as much of the bone as I can chew, and marrow as I can access, but this has always been the case.
A trick I have learned on that front, is that boiling bones results not only in delicious broth, but often in bones that are soft enough to simply eat.

Changes in fat intake

When I started out, I ate fatty cuts, and I sometimes added fat in the form of butter, and later (though not now) coconut oil [2].
When I measured, the fat-to-protein ratio was usually at about 65:35 — 70:30.
But back then I had a lot of excess body fat, which I was losing at a good pace.
So the true ratio, from a metabolic perspective, was actually higher.

If you hear the argument that a carnivorous diet is too relatively high in protein to be ketogenic, remember that if you are losing fat, that fat counts toward your consumption.

After my weight stabilised, I started wanting even more fat.

This was a gradual process.
At first, I started drinking more in my coffee.
I had been ordering occasional lattés made with heavy cream, and butter melted in, since the early days, when a fellow carnivore suggested it.
This was before the days of
Bulletproof Coffee (BPC).
When BPC started trending, I butchered it made it my own by blending butter and coconut oil along with heavy cream into my coffee at home.At the beginning of this year,
I reported that
I had all but stopped eating cream, butter, and coconut oil, in favour of lard.
As I mentioned in that post,
I’ve also been drinking cups of blended, fatty, homemade broth [3], liberally salted.
It emulsifies to a thick cream, just like BPC, but it’s just animal fat, and the minerals extracted from the bones, along with small amounts of collagen, and related proteins.
It feels more nourishing to me.

Before and after blending broth.

https://lh3.googleusercontent.com/-1hYTPmBK6ZM/VGK8dZJNxtI/AAAAAAAAHXI/K7gfTZgZe7U/w879-h580-no/broth-before-after.jpg

Over the summer, another carnivorous friend taught me how to make beautifully clear, pure bacon drippings by cooking bacon in the oven in a glass pan.
It comes out so mild and creamy that I have been eating it not merely as a spread, but by itself on a spoon.

Oven bacon and drippings.

https://lh4.googleusercontent.com/-uXYQkxzPmUU/VGK8c4i9KRI/AAAAAAAAHW8/zMqbYlYQQKs/w916-h316-no/glassbacon-and-drippings.jpg

https://lh4.googleusercontent.com/-_gvpv_5lnvo/VGK8c0ypXJI/AAAAAAAAHXA/SX3rrMv9-Ng/w498-h580-no/tallow-spoon-cropped.jpgI am the candle. See me glow.
He also introduced me to tallow as a food.
I had no idea that tallow was so delicious.
(It’s best at room temperature.)
I also find that the satiety I get from eating tallow is superior to any of butter, coconut oil, or even bacon drippings.

An acquaintance seeing me eat tallow, said that people make candles out of tallow. I am the candle. See me glow.

These days, my total fat intake is more than it has been in previous years (once I stopped getting much from my own stores).
The superior satiety effect I am getting also seems to be resulting in eating less protein generally, an effect I didn’t personally experience with the BPC approach [4].

A typical day

Last time I described my eating was two years ago.
At that time I mentioned having occasional pickles, baker’s chocolate, or sashimi garnish.
I rarely do that these days.
It simply appeals less.
My appetite is stimulated by the presence of (what I consider) food even if I’m not hungry.
That is, if I walk into a kitchen where bacon or steak is frying, I’m likely to want to eat it, and often will.
However, if left to my own devices,
this is the pattern I have been falling into lately.

  • Throughout the morning, I alternate cups of black coffee with cups of blended broth.
    The broth is usually made from bones from roasts, though I also buy beef bones.
    If it is not sufficiently fatty, I may add bacon drippings or butter.
  • Sometime in the afternoon, I often (but not always) start feeling hungry, and I will usually respond to this by eating some tallow, possibly followed by some cold leftovers from the previous meal.
  • Supper is usually one or two of these:
    • roast beef, leg of lamb, pork shoulder, or chicken thighs
    • broiled or fried fish, pork or lamb shoulder chops, or steaks.
    • hamburgers, or fried pieces of fat trimmings, if I can get them from the meat counter.

    I usually eat more tallow or lard with the leaner bites of these.

  • Every few weeks I get a hankering for liver, and eat that for a day or two until it no longer appeals.
  • I also keep a supply of homemade jerky on hand, in case I feel like nibbling while I wait for something to cook.
https://lh6.googleusercontent.com/-ReNlEAbMCCk/VGKL9_wbsPI/AAAAAAAAHWI/8DJtM3LxYtM/w773-h580-no/IMG_20140925_075924.jpgA recent breakfast: espresso, chicken broth, bacon drippings, and a little bacon.

Footnotes:

[1] Let’s face it: almost all foods we eat are “processed”. It’s about as meaningless a phrase as “chemicals”, or “real” in “Just Eat Real Food”. What I mean here is a food product that is made by isolating specific components, usually from plants, in a way that typically couldn’t be done by hand, studying chemistry until you can figure out how to mix them back together so they stay solid, and calling it “food”. Think Twinkie.
https://lh3.googleusercontent.com/-5dZrrSqRENs/VGK8oASsOFI/AAAAAAAAHXc/K7nC66V_aoI/w251-h201-no/twinkie-ingredients.jpeg
[2] Coconut oil is a plant, it turns out. I used it because it has a favourable fat profile: lots of saturates and monounsaturates. It even has medium chain triglycerides, which are known to be ketogenic, even under glycolytic (sugar metabolism) conditions.
It also has a nice flavour, especially in coffee (my plant vice).
However, I had suspected it might be contributing to my rosacea, which has been in almost complete remission since I started carnivory. Coconut has salicylates, which may be incriminated in rosacea for me. This summer I went without it for a long time, and when I had it at last again, my face immediately flushed.
[3] [Added 2014-11-16] To make broth, I just take the leftover carcass from a roast, throw it in a crock pot with water, and let it simmer for about one and a half to two days. I don’t add anything else to it. Sometimes instead of leftovers, I buy beef bones, or shank. I have yet to try fish heads, but it’s on my list.
[4] I haven’t measured this.
As much of my food is broth or whole cuts of meat, it is hard to get high accuracy on fat and protein intake.
However, my ketosis readings would confirm this perception.
More on that in an upcoming post.
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The ketogenic diet as the default human diet: an energy perspective

The conditions under which the liver delivers optimal fuel on demand may be the conditions under which it evolved.

When you are on a ketogenic diet,
the mitochondria in your cells — the parts of the cells that produce energy — actually switch from primarily using sugar for fuel to primarily using fat for fuel.
They use fat mostly in a form called ketone bodies (or, commonly, ketones), thus a ketogenic diet.
(See Keto-adaptation: what it is and how to adjust for more on this process of switching fuels.)

Sugar-based living (from a diet with more than about 5% calories from carbohydrate)

When you are using the sugar-based system, all of the cells in your body constantly take sugar out of your bloodstream.
It’s hard for your body to keep up,
and you need to frequently refuel by eating carbohydrate-containing food.
Getting sugar out of the carbohydrates that you eat is a blunt tool.
Unless you eat in a trickling stream, you will consume more sugar than is safe to hold in the bloodstream at once.
That sugar has to be quickly removed,
because high blood sugar damages your cells.
So a flood of insulin comes in to initiate the process of sugar removal.
There is some limited storage space in the liver,
but when that is full, the rest basically gets stored as fat.
Soon however, the job is done.
Your blood sugar is back in a safe range.
Your body cells are still demanding sugar, though, and your blood sugar starts to drop too low.
Your liver can release some sugar back into the bloodstream, but not fast enough to keep up with demand,
so you get tired and hungry, and the process starts all over.

  • People on carbohydrate-based diets typically have to “snack” every couple of hours.
  • Endurance athletes have to stop and eat sugar just to get through their events.

On a sugar-based metabolism, you swing between too little blood sugar and too much, and you have to constantly adjust it “manually” by eating.

Fat/ketone-based living

On the other hand,
when you are using the fat/ketone-based system,
there is relatively little demand on your blood sugar.
There are only a few kinds of cells that don’t have the ability to use ketones (or fat) for fuel, and have to use sugar.
That amount can easily be supplied by the liver,
which actually manufactures sugar out of protein on demand in response to changes in blood sugar.
The liver can do this at a rate that is more than adequate for normal energy requirements,
when the cells that can use fat/ketones are doing so, and thus not putting extra demand on blood sugar.
Your body makes significant ketones only when sugar levels are consistently low.

  • It is not uncommon for ketogenic adults to comfortably eat one meal a day.
    Even my children, when they are ketogenic, can go for several hours at a time without eating.
  • Endurance athletes on ketogenic diets don’t “hit the wall”. They have the ability to tap into fat stores for fuel; a supply that could last even a lean person for weeks.

On a fat/ketone-based metabolism, demand on sugar from the blood is gentle, and your liver refills it smoothly on demand as it is used, keeping it remarkably steady.

An argument for ketogenic metabolism as the default human state

Think about the role of the liver here.
When you are not consuming sugar in food (from carbohydrates),
your liver orchestrates fuel management precisely.
The liver makes ketones out of fat, thereby supplying almost all tissues with all the energy they need.
At the same time, it makes a moderate amount of sugar out of protein.
That sugar is stored right in the liver in the form of glycogen.
Not much is stored, but it is plenty for the purposes of keeping blood sugar steady,
because the blood sugar is depleted slowly: only a few tissues draw sugar from the blood.
The rest are using fat or ketones.
This system is efficient and effective.
By contrast, on a carbohydrate-based diet, the storage capacity of the liver overflows.
The excess sugar can be stored as fat, but that fat is not used efficiently as fuel.
For fat to be used efficiently as fuel, the liver would have to be turning it into ketones at a high rate [1].
But ketones aren’t produced much in a high sugar condition.
It takes several days of low sugar intake to start producing significant ketones.

Considering how well the liver manages energy when you don’t eat carbohydrates,
and the disruption caused to this system by eating them,
I would suggest:
The conditions under which the liver delivers optimal fuel on demand may be the conditions under which it evolved.

Footnotes

[1] As pointed out by Valerie and Ash in the comments, and by Carol Loffelmann on Twitter, fat remains an important fuel in its own right, increasingly so after keto-adaptation.
I oversimplified here, but the point about efficient fat/ketone-based metabolism under low sugar conditions still stands.
[2] Consider a popular alternative explanation:
Noticing that excess sugar can be stored as fat,
and yet knowing that excess fat storage is not healthy in humans,
some people have argued that excess fat storage in humans represents an adaptation gone awry:
The thrifty gene hypothesis supposes that we used to go through periods of feast and famine, getting fat, and then using it up.
People who were well adapted got fat easily, and thus survived the famines better.
Here and now, where famines are rare, those people would simply get fatter and fatter.
There are at least two problems with this idea.
First, the evidence doesn’t seem to bear it:
famines may not have been particularly common in Paleolithic times, they don’t appear to have occured at all in some populations that we know later developed obesity on modern diets, and modern hunter-gathers don’t get fat in times of plenty.
Second, even if this were essentially correct, that would mean that humans were adapted to go through regular periods of using up the fat.
In other words, it would mean humans were adapted to regular periods of ketogenic metabolism!
So, at best, this theory supports ketogenic metabolism being a regular part of life in some kind of alternation with carbohydrate-based metabolism.
There are animals that use this kind of strategy.
Those animals hibernate.
Humans can’t hibernate.
Even very fat humans need some level of protein to survive, to make into sugar for the few tissues that need it.
If they don’t get it, they will start tearing down essential muscle tissues such as heart, and they will die.
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Experiences of a Five-Year Carnivore, Part I

Part I: How I became a carnivore

It took me about three weeks to get up the nerve to try an all-meat diet.
I had been reading about it since before the New Year.
It seemed extreme, but I was just so desperate about my weight.
An all-meat diet is, in some ways, just a radical version of a low carb diet.
I had been an advocate of low carb diets for a long time:
it was 1997 that I first read Drs. Eades’ Protein Power, gave up my vegetarian diet, and finally (easily!) lost the freshman 30 that had plagued me for for several years.
Still, after my second pregnancy, my body didn’t seem so willing to drop the fat
even with good adherence to low carb.
(I had gained a lot of fat in both pregnancies.)
I knew that a low carb diet was healthy, and that the claims about dangers of eating animal fat, and benefits of eating grains were grossly mistaken.
I had been following the relevant research since I first looked up the papers cited in the Eades’ book.
That body of evidence was ahead of its time, and has since grown enormously.
Nonethless, much of it is still not recognised today, to the detriment of the health of many people.
It was demoralising being fat while eating a diet I knew to be not only healthy but the most effective intervention for fatness.
Moreover, fair or not, I felt like I wouldn’t be taken seriously telling others what I knew to be scientifically true when I looked the way I did [1].
So when I saw people on the internet [2] talking about eating a “zero-carb”, all-meat diet [3],
and the unparalleled success it was bringing them,
I was filled with hope against hope,
and I thought:
“Why not?”

Not even a salad?
Still, I found it intimidating.
Not even a salad?
Wouldn’t I be bored?
Most importantly, would I be able to stick to it?
There is little more demoralising than making a promise to yourself that you can’t keep.
So I thought about it for the first three weeks of 2009.
While I was thinking about it, I decided that I could definitely give my regular low carb diet its best chance.
Having been a low carb dieter for over ten years, it was a long time since I measured every meal.
Perhaps I had allowed some “carb creep”.
I made a New Year’s resolution, and counted carbs to the gram, keeping it under 20 a day.
In those three weeks, I think I lost 2-3 pounds of the 60 or so I wanted gone.
In the meantime I planned out meals of just meat, kept reading about the successes of others, and I set a time frame I could live with:
I would eat just meat for three weeks, taking me exactly to my 36th birthday.
On my birthday I would eat cake as a reward.
That birthday cake was never to be, because by the time those three weeks were up, not only had I lost about 10 pounds, but my mood had stabilised.
The major-depressive-disorder-turned-“soft”-bipolar that had been ruining my life at increasing speed since I was a teen was brought to a sudden standstill.
It was utterly amazing, and
no cake would ever be worth a return to that.

A short detour…

However, shortly after my birthday, I learned I was pregnant again.
I was determined to have a zero-carb pregnancy, but for a variety of reasons, this didn’t come to pass [4].
I did manage to keep my carbs low for most of the pregnancy (a first for me) and even had some zero-carb days in the third trimester.

…and a return.

A week or two after his birth, five years ago now, I restarted my carnivorous diet, and I’ve stayed on it since.
It’s easy [5].
My weight quickly normalised to about 130 lbs — some 60 lbs less than I weighed at the beginning of 2009.
Best of all, my mood has been stable without any medications since then, even under periods of enormous stress.
For example, I have recently experienced intense grief due to life circumstances.
Although the grief has been incredibly painful and difficult, it hasn’t resulted in depression as I know it.
While it hasn’t been easy, it is simply incomparable to the emotional dysfunction of a psychiatric mood disorder.
The difference between the normal mood variations I have now, and those I had then is physiological.
It was correctable not by adding drugs, but by removing the drug-like components of my diet coming from plants.
(Continue to Part II.)

Footnotes:

[1] See my rant about equating people’s personal health with the quality of their theories.
[2] The forum I originally read is now lost, though it can be found in the Internet Archives.
It’s successor is here.
[3] The term “zero-carb” is not technically accurate; there are traces of carbohydrate in animal foods in muscle glycogen, and more than traces in others, such as liver, some shellfish, and cream.
For this reason, I prefer to call the way I eat “carnivory”.
See A Carnivorous Diet for more on how I eat.
[4] One component was that I have a strong family history of hyperemesis gravidarum, and though I have been able to mitigate it with pyridoxine/doxylamine, I still suffered debilitating nausea throughout all of my pregnancies. Therefore, nutrition became a secondary concern after could I look at it without retching.
[5] It may sound like eating this way would be difficult; that it would take willpower to avoid eating things we consider delicious.
However, I am rather a hedonist, and I love to eat.
If this took hunger or deprivation, it wouldn’t be for me.
I never restrict the quantity of food I eat.
It turns out than when I eat this way (and I am told I am not alone),
that is, once all the sugar and fiber is out of my diet,
including the low amounts of sugar in fibrous fruits and vegetables,
and all low sugar sources of sweetness,
I feel completely satisfied and satiated by my food.
I simply don’t want anything else.
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Weight loss advice from fat people

There is an assumption that is easy to make about health advice:
that the health of the person giving advice is a good test of the correctness of their theories.
This is a terrible mistake.
Here are a couple of reasons why it is a mistake:

  • It conflates what people advocate with what they do.
    This goes in two directions. Someone could advocate something that they don’t adhere to, or they could adhere to it but do something else that, known to them or not, changes the outcome.
    For example, someone could claim to gain fat on a very low carb diet, but not realise that those high-protein peanuts they are eating have signficant carbohydrate in them.
    Or, on the other hand, they could claim great loss, but not mention that were also taking a hormone that turned out to have made all the difference.
  • It doesn’t take into account what the person is struggling with.
    Someone with a strong genetic propensity to gain fat and who has been obese for a long time is simply never going to have the results from a fat loss intervention that someone with a more moderate genetic risk who has not ever been fat.
    A hard gainer is never going to get as bulked up as a natural bodybuilder type, even if they find the perfect protocol.

This latter problem would even seem to suggest that people who struggle or have struggled with health problems are better judges of what works and what doesn’t.
There is some truth to this:
If someone with a health problem manages to improve it, that positive outcome suggests that someone else in the same position might also see improvement following the same plan.
Moreover, sick people, fat people, people who can’t meet their goals through mainstream advice are often more likely than others to hit upon fundamental scientific misconceptions that are holding them back, or new therapies that are incredibly effective.
And yet, a person who has recovered from severe diabetes, for example, may still have health measurements that don’t inspire great confidence in someone who is starting out with less severe issues.
However, this is also a mistake!
If you want to evaluate whether someone’s health advice is good,
comparing where they started with where they are is a good starting heuristic,
but it doesn’t take the place of evaluating scientific research.
There can always be coincidences, or relevant information you are not aware of.
People who do health research and promote their conclusions are aware that their own health is under scrutiny.
They can hold themselves up as positive anecdotes of what is possible, and they should.
Anecdotes, like observational correlations, are useful for generating hypotheses.
A randomised controlled trial that refutes the hypothesis must be considered better evidence than an anecdote or even a correlation generated from a large data set.
On the other hand, a negative anecdote can single-handedly refute certain kinds of scientific claim.
It bothers me when people criticise the theories of public figures based on their personal successes.
It equally bothers me when people applaud those who have lucked out genetically, and who can basically do no wrong: they will look fantastic under a variety of abuses.
Take advice from fat people, if the advice is scientifically tenable.
Ignore advice from thin people if it doesn’t stand up to scrutiny.

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Dangerous Mistakes of Reading the Internet

Zooko and I get a lot of questions here and on ketotic.org about our work, or about ketogenic diets. That’s encouraging, and we like hearing from you!
However, we often don’t have time to answer questions in depth.
I’ve decided to answer this one, because my answer to it has some common themes that transcend the particulars of the topic.
On Eat meat, not too little, mostly fat, Matthew Blanchard asked:

I have been reading through your blogs, and I find them interesting. I am considering doing the 30 day challenge. Then I found this webpage: http://www.poliquingroup.com/ArticlesMultimedia/Articles/Article/1143/Eight_Common_but_Dangerous_Mistakes_of_A_High-Fat_.aspx A lot of this information seems to contradict your research. Have you seen this before? What are your thoughts on some of this?

Here are my thoughts.

The article is called Eight Common but Dangerous Mistakes of A High-Fat, Low-Carb Diet.
The authors have done something frustrating, but not uncommon. They have placed most of the burden of research on the reader. They have made a swath of claims in an authoritative voice followed by over a dozen references of mixed origin: from peer reviewed papers to blogs. There is no way to tell which articles and which parts of those articles are supposed to support a given claim. That means that to verify a given point, you basically have to read all or most of the articles cited (and often further the articles those articles cite!), and then you still can only guess at why the authors think it supports the claim. On ketotic.org, we aim to show the full trace of every claim we make, which we call “end-to-end citations”. This allows the reader to know why we think something is true, and encourages them to look at that evidence critically. See the Apologia for more on our approach.
This approach also, unfortunately, takes much more work. I would say the vast majority of the time I spend writing an article comes from finding papers that clearly support what I’m claiming, even after I can find many sources that merely make the same claim. I try not to rely on authority, and I take into account the type of experiment used. On several occasions, I have found that I could not find clear support of something I assumed was true.
For example, as of last time I looked, there is no clear published research showing that lowering protein increases ketosis. I’m pretty sure that it’s true: clinicians in the field say it is true, many anecdotes report it, and I’ve experienced it myself! However, I don’t have the kind of evidence that meets my standard to claim it. Contrast my article Protein, Ketogenesis, and Glucose Oxidation with the glib statements made in Dangerous Mistake #2. One of those statements is “if you go overboard and eat too much protein than the body needs [sic], some of the amino acids in the protein will be turned into glucose via a process called gluconeogenesis”. I’m quite sure the causality implicit in this statement is wrong, and I’ve written a series of articles exploring that, starting with If you eat excess protein, does it turn into glucose.
All that said, the particular article of ours in question suggests eating an all-meat diet, which is not a well-studied variation of a ketogenic diet. We’ve tried to be quite explicit about that. We’re well aware that few ketogenic dieters do it this way all the time, and we don’t have anything even approaching a randomised controlled trial to back it up with. That’s why we’ve phrased it as an experiment; as a way to learn about how diet affects you by removing almost all confounds, including the variation in tolerance many people have to carbs. It is also true that I (and a handful of others I know) feel much healthier eating no plants, and eat essentially only meat all the time. Nonetheless, it is not very much different from the induction phase of most versions of low carb diets, which are extra restrictive for many of the same reasons as those we cite. See Wait, why eat only meat? for more on how this trial is similar to induction phases, and why we advocate it.
The main statements that I disagree with in the Dangerous Mistakes article are the ones about meat and vegetables in particular. I will briefly address “Dangerous mistakes” #3, #4, and #8.

#3. Poor gut health due to a diet high in animal protein and low in indigestible fiber

There are two claims here. First that “low-fiber, higher animal protein diets have been found to increase inflammatory gut bacteria.”
I have been working on a post about the inflammatory gut bacteria hypothesis (which is all it is, the claims of the scientists who report it notwithstanding).
So I don’t have much to say about it here, except that the claims vastly outweigh the evidence, and the scientists making them appear to assume that which they are trying to prove.
The second claim is that “these bacteria release a compound called TMAO after you eat animal protein, which increases plaque buildup in the arteries, elevating inflammation.”
For this claim I will simply refer you to work by a researcher cited elsewhere in the Dangerous Mistakes article, Chris Masterjohn, who has shown the main problem with that claim:
Meats produce no more TMAO than fruits and vegetables, or assorted grains and dairy, and the primary source of TMAO is seafood, not beef or other red meat.
See his article for details about that, and more reasons to question that claim.

#4. Chronic inflammation from high intake of fat and protein and few fruits and veggies

The support for this comes in the form of the following logical chain:

  1. In one study from Tufts, the lean mass in young people was positively associated with increased oxidative stress and inflammation.
  2. The best explanation of the association the scientists could come up with was that these young people must have been eating fewer fruits and vegetables, because, the Dangerous Mistakes authors claim, “people who eat more animal protein tend to eat fewer plants”.
  3. Therefore, you should eat more of the particular plants that are fruits and vegetables (as opposed to, say, grains and legumes, which are also plants, I’ve heard…)

I didn’t look up the Tufts study, but this is terrible reasoning.
The authors of the Tufts study presumably know that lean mass is usually associated with good health, which is why they were compelled to make something up after the fact to explain their results.
(As an exercise for the reader, do an Internet search to figure out what lean mass is typically associated with.)
Don’t get me wrong. Making up stuff is a fine activity—scientists are expected to offer an interpretation of unexpected results—but it is irresponsible to make strong claims based on untested hypotheses, especially when you are in a position of authority.

#8. A chronic acid load that degrades lean tissue and increases cancer risk

The paper in the reference list that seems to go with this claim is called Diet-induced acidosis: is it real and clinically relevant?
I took the time to look at it briefly.
The authors of this paper do point out that the human body keeps pH tightly regulated, and that diet can only effect pH to a small degree, which stays within normal range.
They then speculate that this chronic small amount of acidity might lead to problems such as bone loss.
They further cite some studies that associate acid-forming foods with bone loss.
They also discuss the problem of kidney stones and its potential relationship to bone loss.
I don’t have time to thoroughly respond to this paper right now, but I’ll touch on two points.
First, diets with high-normal amounts of protein do not lead to bone loss [1], and in fact the physiological changes that happen under ketogenic conditions are lean mass preserving.
These facts alone should lead you to think that the associations cited here may not apply to a carnivorous ketogenic diet.
Second, some children on ketogenic diets for epilepsy have had problems with kidney stones.
However, the epilepsy diet has usually been based on KetoCal shakes (full of vegetable oil), not on meat.
The best remedy for kidney stones appears to be high intake of potassium citrate.
Plant advocates like to note that plants are high in potassium, which is true.
However, it is also true that meat has potassium, but when we cook, it is mostly lost to the drippings.
Eat the drippings.
Drink the broth.

[1] See for example, this review. It discusses this unsupported myth, and others. Note that it does reiterate the idea about alkalizing fruits and vegetables
“Despite a widely held belief that high-protein diets (especially diets high in animal protein) result in bone resorption and increased urinary calcium, higher protein diets are actually associated with greater bone mass and fewer fractures when calcium intake is adequate. Perhaps more concern should be focused on increasing the intake of alkalinizing fruits and vegetables rather than reducing protein sources.”
but note that it is the potassium content of fruits and vegetables that leads them to that conclusion:
“[N]et renal acid excretion can be predicted from the ratio of dietary protein to potassium because the dietary intake of potassium occurs mainly as salts of weak organic acids and therefore has an alkalizing effect (30, 33). This relationship may explain the reported beneficial influence of fruit and vegetables, the major dietary source of potassium, on bone health”
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Killjoy vs. Freak Flag

I read a recent story by Julia Llewellyn Smith about John Yudkin, an early proponent of the theory that sugar (not fat) is likely to be the main culprit behind many modern diseases.
It contained the following paragraph:

“One of the problems with the anti-sugar message — then and now — is how depressing it is. The substance is so much part of our culture, that to be told buying children an ice cream may be tantamount to poisoning them, is most unwelcome. But Yudkin, who grew up in dire poverty in east London and went on to win a scholarship to Cambridge, was no killjoy. “He didn’t ban sugar from his house, and certainly didn’t deprive his grandchildren of ice cream or cake,” recalls his granddaughter, Ruth, a psychotherapist. “He was hugely fun-loving and would never have wanted to be deprived of a pleasure, partly, perhaps, because he grew up in poverty and had worked so hard to escape that level of deprivation.””

While I am glad that such stories are gaining prominence,
I object to the idea that saying no to ice cream, or keeping a sugar-free household makes one a killjoy.
If it were shown that the link between routine sugar consumption and heart attacks or Alzheimer’s or breast cancer was, for example, even a fraction as strong as that between smoking and lung cancer, would you feel that turning down a piece of cake, or not keeping ice cream in the house, indicated insufficient desire for and approval of pleasure?
Or contrary-wise, if you went to live in a place where children were normally given a cigarette after supper, would you just let it go in the name of good fun?
Such a strong link has yet to be shown, but the body of evidence of such links has increased.
I contrast this idea with an essay by Kurt Harris a few years ago, containing this passage:

“When you go to the birthday party for your neighbor’s kid, and you eat the birthday cake, what message does that send?
You show up looking trim and fit. You are pleased if people ask you how you lost weight. After eating this way for a few years, though, you are perhaps most comfortable if no one says anything at all.
You are weary of the reactions -the incredulity, the mockery, the eye-rolling. Pushing 50, you’ve tried explaining how a diet high in animal fats and low in grains works to keep you slim, but you’ve learned that the segue to explaining why you are not just cultivating an attractive corpse due to all that arterycloggingsaturatedfat that you live on is tedious and it gets you nowhere.
So, when the rectangular slab of Hy-Vee or Piggly-Wiggly birthday cake – frosted 3/8” thick with a stratum of oily granular sugar running through the middle to boot – is proferred, you say “thank you”, flash a smile that only a trained psychologist would question, and accept it, holding the flimsy paper plate and plastic fork with both hands to keep it from tumbling onto the ground.
You repair to some corner of the party where you can nibble at the cake, maybe spill a few crumbs, and eventually hide the paper plate, now soggy with vegetable oil absorbed from the corpus of the cake.
Who are the agents of acculturation here?”
[…]
“If you are a vector for cultural change, which way is the arrow pointing?
Wear your Real Food Uniform.
Active Duty.
Fly your freak-flag high.
Say no to the cake.”

Ruth may not have been deprived of sugar in her grandfather’s presence, but perhaps she was deprived of something after all.
As Yudkin was the author of a book entitled “Pure, White and Deadly”, I am left wondering at the power of acculturation to affect our choices.

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Response to Mark Sisson’s assertion that vegetables are necessary for health

Mark Sisson is the author of The Primal Blueprint, and the blog Mark’s Daily Apple.
His blog is a great reference, and I like his work.
However, I take exception to the article he posted this week entitled Do You Really Need to Eat Vegetables to Be Healthy?
Although he admits at the end that you probably don’t need them, this admission has much less prominence than the section near the top where he says

“Yes. Yes, you do. Maybe not a huge amount, necessarily. But you do need some.”

Then he goes on to make some arguments for eating vegetables that I’d like to address.

  1. Modern Hunter-Gatherer diets:
    First he argues that three of the four known modern hunter-gatherers that are purported to be carnivorous (Inuit, Masai, and Sami — leaving out Plains Indians) weren’t actually.
    I don’t think that’s really settled, but more importantly it doesn’t matter.
    Even if it were true that all modern primarily carnivorous societies ate some plants, that doesn’t and couldn’t prove we need them.
  2. Plants as medicine:
    A second argument that is weaved throughout the post is that plants have medicinal compounds, and therefore should be eaten.
    But this doesn’t make sense.
    This is an argument for growing plants and extracting compounds so that we can isolate and concentrate medicine into useful portions, while removing the toxins that accompany the source. It’s no argument for taking daily minute doses of medicine along with a bunch of other random stuff that grew with it.
    I’ve addressed that more fully in the post Biochemical Warfare
  3. Missing nutrients:
    Another argument is about getting some particular nutrients.
    It is argued that modern meat may be depleted of some minerals and vitamins that are dependent on the diet of the animal.
    That is, there are wild plants that are part of the diet of wild animals, that they use to make vitamins that we then eat, and modern meat may be inadequate.
    This may well be true, but insofar as it is, it does not make a convincing argument for eating those plants ourselves, along with whatever other matter they contain, any more than it argues for taking supplements.
    Even if modern meat is insufficient, that is no argument for eating vegetables.
    Moreover, a similar argument is sometimes made about plant vitamin and mineral content due to soil depletion, so eating plants may not even solve it.
    (I’m ignoring the part of that section that suggests we only need plants if we refuse to eat offal or reserve the cooking water, since they support the ability to get those nutrients from meat.)
  4. Feeding gut bacteria:
    Finally, the argument is made that we should eat fermentable fiber to feed our gut bacteria.
    Although there is much interesting research into the role of gut bacteria in health, it is far from conclusive what the best health practice is with respect to them.
    As a researcher aptly pointed out in an editorial last year:

    “This considerable increase in the number of [publications devoted to the study of digestive microbiota] has generated assumptions and speculations on the role of digestive microbiota in human and animal health are likely far beyond our current knowledge.” — Didier Raoult. Digestive microbiota and its influence on health: Facts and myths. Microbial Pathogenesis. 2013 Aug-Sep;61-62:A1. doi: 10.1016/j.micpath.2013.05.008. Epub 2013 May 27.

In sum, I respectfully disagree with Mark Sisson’s statement that the question “Do You Really Need to Eat Vegetables to Be Healthy” can be answered definitively, let alone with a “yes”.
I am more inclined to agree with the points he makes along the way: that if you do not eat vegetables, then you should consider eating offal, drinking broth, eating wild game, or taking supplements. In fact, I think those are worth consideration even if you do eat vegetables.

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Red Light, Green Light: responses to cortisol levels in keto vs. longevity research

How a scientist interprets outcomes often depends on whether she thinks the outcome should be good or bad.
Cortisol levels make a good example.
In the context of low carb, ketogenic diets, the finding of slightly higher cortisol levels have been interpreted as a warning sign. In a recent post on our blog, Zooko and I attempt to explain why the “red light” that Boston Children’s Hospital gave low carb diets is not justified.

Boston Children's Hospital graphic (with our markup in black). Click for the original.

It is interesting to note that while cortisol sends up red flags for ketogenic diets, which mainstream medicine actively disapproves of, it sends up green flags in another context: longevity research.
Time and again I have come across glib statements in longevity papers saying that the beneficial, health-enhancing and lifespan-increasing effects of caloric restriction probably come in part from the moderately increased cortisol that is consistently seen in calorie restricted animals. The intuitiveness of the beneficial effects of cortisol is usually based on cortisol’s known anti-inflammatory action.
Here are just a few such quotes:

  • “The mechanisms responsible for calorie restriction–mediated beneficial effects on primary aging observed in rodents probably involve the metabolic adaptations to restriction itself, including… a modest increase in levels of circulating cortisol, which result in a reduction in systemic inflammation.”
    — Aging, adiposity, and calorie restriction. Fontana L, Klein S. JAMA. 2007 Mar 7;297(9):986-94.
  • “Even short-term DR can attenuate inflammation and affect metabolic and DNA repair pathways. Mechanisms by which DR suppresses peripheral inflammation include the elevation of glucocorticoids, lowering of glucose and activation of PPARs. Although the effects of DR are less understood in the brain, common pathways are emerging that link many normal aging inflammatory processes with age related diseases such as AD, cancer, diabetes and cardiovascular disease.”
    — Anti-inflammatory mechanisms of dietary restriction in slowing aging processes. Morgan TE, Wong AM, Finch CE. Interdiscip Top Gerontol. 2007;35:83-97.
  • “Glucocorticoids are yet another class of hormones that may contribute to the anticarcinogenic action of DR [101, 102]. Total and/or free glucocorticoid levels are increased by DR [103–105]. Glucocorticoids suppress cellular proliferation and enhance apoptosis in a number of cell types, including osteoblasts, lymphocytes and keratinocytes (for reviews, see Weinstein [106], Herold et al. [107] and Budunova et al. [108]). In humans, glucocorticoids are effectively used for treating lymphoid neoplasms [109]. Importantly, adrenalectomy abolishes the protective effect of DR on skin and pulmonary carcinogenesis, while glucocorticoid replacement restores this protection [110–112].
    — Can short-term dietary restriction and fasting have a long-term anticarcinogenic effect? Klebanov S. Interdiscip Top Gerontol. 2007;35:176-92.
  • Another mechanism by which CR may selectively exert it’s anti-inflammatory effects is via enhanced endogenous corticosteroid production (Sabatino et al. 1991). Chronic CR potentiates the diurnal elevation of plasma corticosterone. CR mice and rats have “moderately” but significantly higher daily mean plasma free corticosterone concentration than mice fed “ad libitum” throughout their lifespan…
    It is well known that the hypothalamic–pituitary–adrenal axis and glucocorticoids in particular are essential in limiting and resolving the inflammatory process (Sapolsky et al. 2000). Glucocorticoids have pleiotropic inhibitory effects on the immune system and inflammatory gene expression (Rhen and Cidlowski 2005). In addition, treatment with pharmacological doses of exogenous glucocorticoids has been used to block many inflammatory and autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus, Graves’ disease, thyroiditis, glomerulonephritis, multiple sclerosis, and psoriasis.”
    — Neuroendocrine Factors in the Regulation of Inflammation: Excessive Adiposity and Calorie Restriction Luigi Fontana, Exp Gerontol. 2009; 44(1-2): 41–45.

I particularly like that last one, because of the use of the word “enhanced”, which connotes that the thing that has increased is surely a Good Thing.
Now of course, the longevity researchers can’t pick up on a significant difference between the animals that lived longer and those that didn’t and say: Well, the diet might be good for some things, but this difference warrants caution.
They can’t do that because the end outcome is definitive.
It’s true that there is a significant school of thought that says that longevity is a result of hormesis. The hormetic explanation amounts to “what doesn’t kill you makes you stronger.” That way a researcher gets to say that phenomenon X is bad for you, and that things that are bad for you improve your health. It is a way out of a paradox, as expressed nicely here:

“One well-known, exemplified response to stress is the hormonal increase in adrenal corticosterone levels in plasma during aging, where increases in these levels appear to be proportional to the degree of stress. Aged animals appear to have a diminished ability to attenuate the increase, causing the aged to have continually elevated plasma levels of corticosterones. These authors suggested that increased levels of corticosterone in aged rats result in hippocampal neuronal cell death, that is, the stage of exhaustion. However, this scenario in the glucocorticoid cascade hypothesis is obviously not applicable in the case of the CR paradigm, because CR results in an increased life span in spite of chronically elevated diurnal levels of serum corticosterone. This apparent contradiction makes the interrelation of glucocorticoid and aging far more complex than one might want to narrowly define it and needs other mechanistic explanations like stress resistance to resolve the disparity in responses.” — Stress resistance by caloric restriction for longevity. Yu BP, Chung HY. Ann N Y Acad Sci. 2001 Apr;928:39-47. (my emphasis)

As Carol Loffelmann recently said on twitter: Scientists who discover paradoxes should examine their initial assumptions.
So supposing we have a study showing that a group that looks healthier than the other groups in essentially every measure also has higher levels of cortisol.
We can reason, as Ebbeling et al. do, that since higher cortisol is associated with bad health outcomes, the ketogenic diet may be dangerous, despite the other measures.
Or we can reason, as the longevity researchers do (and as Zooko and I did), that since the group is healthier, higher cortisol must be exerting or reflecting a healthy process, and this may present a paradox that we as researchers have to resolve.
Allow me one further point:

The findings of higher cortisol in calorie restricted animals is itself a body of literature of relevance here.
Anyone finding that their intervention moderately elevates cortisol can and should now say: Higher cortisol levels are found in animals whose lifespans have been increased experimentally by dietary intervention, and so this finding in our intervention could be indicative of a longevity-inducing effect.