So to refresh your memory, here is a drawing of a wheat seed (Genus Triticum) that I have lifted from Wikipedia.

I covered some of this at a general level in Part I, but perhaps its well to repeat some of it for emphasis now.

It’s hard to beat up on wheat too much, after all.

To relate the anatomical parts to food, wheat germ is the embryo – the dormant baby-in-waiting of the next generation of this annual grass. Found in the germ is wheat germ agglutinin (WGA), which is a defensive secondary compound known as a “lectin”. WGA binds to such a wide variety of proteins in our bodies that it is used in biological science and laboratory medicine for exactly that purpose – to label proteins. When eaten, WGA has effects (bad effects) on the gut and gut permeability separate from those caused by gluten proteins. Once it leaks through or around the gut barriers, it also seems to diminish leptin sensitivity and bind insulin receptors – both effects that can help make you fat.

The bran is the relatively indigestible hull of the seed, which is supposed to be good for us for exactly that reason, I am told. I don’t doubt we evolved to get a small amount of fiber along with the veggies, primordial fruit and odd tubers we have eaten along our evolutionary path, but I still can’t see the need to refine the inedible parts of plants and eat them on purpose – especially inasmuch as the hulls of grass seeds will have the highest concentrations of the lectins that plants have evolved to be herbivore defenses. As we are not herbivores, nor even descended from them, (even vegetarian-leaning omnivorous chimps do not eat grass seeds) I think it is best to not eat like them. I recommend avoiding wheat bran. Sawdust would be both cheaper and safer. Don’t laugh - some whole wheat breads have been “fortified” with cellulose.

Finally we get to the largest part of the seed by volume, the endosperm. The endosperm plays egg to the seeds embryo, with the endosperm analogous to the yolk and white of a bird egg.

Sidebar: The eggs of birds are the perfect food. Not so the “egg” of a grass plant. Why not? The egg of a vertebrate contains all the proteins, vitamins and minerals necessary to grow a baby vertebrate from a handful of cells to the point where it can peck or bite it’s way out of the shell, and start eating on its own. So that makes it a pretty reliable source of nutrients for vertebrate predators like us. Not so the egg of a grass seed. Besides the antinutrient issue, the complement of amino acids and fat soluble vitamins in the endosperm is not enough to grow or feed a human without supplementation from other sources.

The endosperm stores carbohydrate and a dizzying variety of proteins to be used as the sources of energy and structural growth for the embryo during its germination, when the embryo must grow into enough of a plant to be able to collect energy and nutrients from the environment, and stand on its own plant feet. It is worth reminding ourselves that this assemblage of protein and carbohydrate is meant to serve the structural and fuel needs of the baby plant, and is in no way a gift from the plant to feed us.

Picture a kernel of wheat, along with its mates, attached to the tip of a slender blade of grass whose sole purpose was to stick the seed up high enough for the wind to blow it somewhere and have the whole cycle start over again. Can you see how plants that evolved mechanisms to protect the tiny germ and its vulnerable, metabolically costly bundle of proteins and starch (the endosperm) would have a better chance of survival?

Shall I remind you of the dictum: “Favor food that is defenseless when dead”.

The corollary of this might be “beware food that appears defenseless while alive”.

So the endosperm represents an investment by the grass, a lifetimes’ worth of plant 401-K meant to be passed on to the next plant generation. The hull therefore contains an array of molecules known as secondary compounds, including lectins and other antinutrients, such that, should an opportunistic animal eat the seed, the animal will be induced, to use the vernacular – to have the shits. This state of affairs will give the seed a fighting chance for the seed to be shat out before digestion occurs, and might also serve as a learning opportunity for the animal, to the mutual benefit of both organisms in the future.

Basically there is one class of animal that has fought the evolutionary arms race with grass seeds enough to be evolved to eat a fair amount of them. These animals are called birds.

A lot of people think herbivores are seed eaters. Not really. Herbivores that are ruminants are turning cellulose in the grass stems into fatty acids and are not getting the lion’s share of their nutrition from the seed. See 6s and 3s and the logic of grain avoidance to see why even vegetarian herbivores like cattle are not designed to eat predominantly seeds.

So back to the endosperm. We’ve got a picture of the endosperm as this succulent rich storage depot of protein and starch that the plant has invested its whole life into creating for the benefit of the next generation of the plant.

Sometime in the past (10,000 or 25,000 years ago – who cares exactly – our argument is based first on current medical science, not paleo re-enactment, remember?) after millions of years of no significant caloric contribution from grass seeds in the hominin diet, and only birds being really adapted at all, some homo sapiens hanging around the Levant (middle east) figure out that some of the local grass seeds can be ground up with stone tools, and after soaking with water and cooking, can serve as a source of starch and protein.

In a process of cultural and biological co-evolution, after a few thousand years some of the grasses have been artificially selected to the point where they cannot really reproduce that well naturally without their human cultivators, but the fundamental mechanical operation is the same:

The seed is mechanically crushed, and whether the bran and germ are left in the mix (whole wheat) or separated out (white four) the endosperm contents are made accessible to further processing to make them just edible enough by humans that it enables the founding of what we now call civilization.

So refer back to the pencil illustration. Civilization was founded quite specifically on the bit of the drawing labeled “endosperm”. That is where the nutrition lives, and where two of the three Neolithic agents also are found.

What’s so special (good or bad) about the endosperm of grass seeds like Triticum?

Firstly, to serve as the “egg” and storage depot for the germ, it has to be stable over time without rotting, as the seed may not find itself in a favorable germinating environment for a while. The lectins in the hull discourage consumption by everything from bacteria to molds and herbivores and work so well that grass seeds can still germinate after years of dormancy if supplied with the right conditions. It is this quality – storage of protein and carbohydrate at room temperature- that allowed food to be grown in surplus and stored for later without spoiling. It is this quality – the molecules that make it stable and resistant to rot and predation- that also leads to diseases of civilization as a result of leaky gut, autoimmune diseases via molecular mimicry, and direct effects of lectins like WGA.

As a storage depot to feed the growing grass embryo, the endosperm has a relatively complete complement of proteins and nutrients – not a complete set of amino acids if you are a human, but complete for the plant. So there is a fair amount of protein and carbohydrate in a single package, even if, as we discussed in the sidebar, it is not enough to sustain a healthy life for a vertebrate by itself long-term. So that is good, in the “selfish gene” sense, in that it allows greater fecundity on a population basis. But that is bad, from an individual health perspective, as these seeds have just enough nutrition to keep you alive, but being designed to grow plants, are not ideal sources of nutrition for us.

The fat content in the endosperm is biased heavily toward n-6 polyunsaturated fatty acids – the ratio of 6:3 is an order of magnitude or more higher than found in animal cell membranes. Why is this? I am no botanist, but the predominance of PUFA in plants generally must relate to their needs to store energy. As plants are in most circumstances “cold-blooded”, it would not do to store lipids as saturated fat. Higher energy density with sat fat would be useless if the fat were so solid that it could not be mobilized or accessed.

Sidebar: Of course the exception that proves the rule is tropical plants like coconut and palm, which have indeed evolved the capacity to store fat as saturated. They are still cold-blooded but evolved in warm enough environments to get away with it. In fact, by eating coconut you can avoid excess unsaturates (PUFA) even better than by eating pastured butter (even if you get few n-3s).

So that accounts for the fact that depots of lipid in seeds tend to be PUFA heavy with varying amounts of non-saturated MUFA tossed in. Why this tends to be mostly n-6 rather than n-3 I can only speculate. (Experts on this feel free to chime in) The important point is that if the plant intends to burn it as fuel or beta-oxidize it into two carbon Acetyl-coA units as building blocks for other molecules, the plant does not care that if we eat the seeds or extract the oil it will give us a surfeit of n-6.

That grass-seed endosperm contains concentrations of oils that can be extracted was first good for industry in making industrial oils, paints and lubricants (like the linseed oil that the “food” industry likes to call “flaxseed oil”) for the industrial economy. Then is was good for the post-industrial “food” industry that marketed seed oils that were fobbed off as food, first as a cheap substitute for lard after catalytic hydrogenation (Crisco was so-called because the name is a contraction of “crystallized cottonseed oil”…. As Dave Barry says, I am not making this up) and then as a “healthy” substitute for butter in the wake of that homicidal fraud Ancel Keys and the saturophobia he spawned that we are fighting to this day. That these oils have come to dominate modern lipid consumption to the point where n-6 PUFA alone as a percentage of calories is around 10%, is bad. It is bad because it is totally outside of our evolutionary experience.

Our cells are more or less passively composed with a ratio of n-6 to n-3 based on the ratio of PUFA that we eat. Having never been exposed to artificially extracted n-6 oils in large quantities until less than 100 years ago, we have not had time to evolve a mechanism to regulate the 6:3 ratio at the level of the cell membrane to compensate for this. The result is that excess pro-inflammatory hormone like molecules, with n-6 derived arachidonic acid as a precursor, are produced. This 6:3 imbalance has been linked to increased cancer promotion, disturbed immune function, increased blood clot formation, increased death from coronary atherosclerosis, increased incidence of mental illness, etc. These consequences of artificially extracting and eating the oils found in endosperm of seeds are all bad. Pubmed "Lands" for details.

But the altered 6:3 ratio is only part of the story. Whether “bad” 6s or “good” 3s, there are consequences to consuming a large percentage of dietary calories from PUFA. PUFA are polyunsaturated. This means, unlike saturated fat that has no unsaturated positions, they are unsaturated at two positions. Each site that has a double bond that is not “saturated” with hydrogen atoms, has the potential to react with other molecules, including oxygen. Eating PUFA can therefore lead to consumption of lipids that react with other molecules in your body in ways that cause damage. Excess PUFA can cause damage to the liver, may damage gut integrity and contribute to leaky gut with all of those consequences, and may contribute either directly or via activation of inflammatory cytokines to atherosclerosis with resulting coronary artery disease and strokes.

So you really have two reasons to keep total PUFA low:

1)   Total PUFA of any kind is bad. The EM2 is less than 4%

2)   You need to keep your dietary intake in the range of the EM2, which is around a ratio of 1:2 to 4:1 of n-6:n-3.

If you try to accomplish #2 via megadoses of fish oil to balance eating “healthy oils” like flax and even olive, to get to a 4:1 ratio you will be consuming well over 10% of calories as PUFA, which totally blows out goal #1. We want less than 4%. Hence we first eat ruminants and fish, favor ghee butter coconut and cream as sources of fat, go easy on the nuts, and never eat or cook with extracted plant oils other than coconut.

Ever.

Don’t cook with non-coconut plant oils, don’t eat fried food in restaurants and don’t eat “food” that comes in a box. Ever.

It is better to eat potatoes, corn and white rice than vegetable oil.

It is better to eat potatoes, corn and white rice than vegetable oil.

That is so important to emphasize I have repeated it.

So my recommendation is to focus on goal one of low total PUFA first, as it accomplishes all of goal #1 and most of goal #2, then add 1- 2 TEASPOONS  of Cod Liver Oil or equivalent. This will give one to two grams of DHA and EPA to optimize your ratio wihout blowing goal #1.

Sidebar Quiz: Although it has corn and wheat as the carbohydrate source, what snack food in a bag is actually still fried in coconut oil rather than industrial vegetable oils?

Answer: Bugles

I have built this indictment of grass seeds on wheat, but I’ve tried to show generally how the endosperm of seeds, sitting at the nexus of technology-wielding man looking for things to eat and the development of diseases of civilization, is the source of two of the three Neolithic agents in the PaNu scheme:

Wheat

Linoleic Acid

By extension, many of the same arguments can be made for other cereal grains. In some cases, like corn, the oil argument is stronger (we don’t see commercially available wheat oil much, but corn oil is everywhere), the antinutrient argument real but weaker. For legumes, the arguments are about the same on the oil front and mildly weaker on the poison issue (unless you get anaphylaxis with peanuts) Legumes is lower in the “eliminate” scheme of the 12 steps simply because legume consumption in north America is less ubiquitous than wheat flour.

Most seed and legumes will come out somewhere between corn and gluten grains like wheat.

Not worth the effort.

I posted a shorter version of this explanation of the difference between Type I and II diabetes on Paleohacks and thought it might be of more general interest.

Technically, diabetes mellitus is just hyperglycemia (High blood glucose) that spills into the urine if it gets high enough - that was how it was originally diagnosed.

Type I and II are actually completely different diseases that just both have the common end result of hyperglycemia - high serum blood glucose or high "blood sugar".

I consider both types of DM to be diseases of civilization related to the neolithic agents.

Type II diabetes is a late consequence of the metabolic syndrome where the primary defect is in the liver - likely due to the neolithic agents fructose and n-6 PUFA injuring the liver and causing both liver and systemic inflammation.

Impaired insulin sensitivity in the liver means the pancreas must secrete more insulin to communicate with the liver (control blood sugar, etc) - peripheral insulin resistance follows, likely as a defensive response to hyperinsulinemia and hyperglycemia (hyperglycemia that the pancreas has trouble controlling despite increased insulin secretion). So initially, in Type II there is more hyperinsulinemia than hyperglycemia. This the reason why by the time Type II is diagnosed, so much damage is already done. Not only is the threshhold for fasting BG too high, the post meal spikes are not tested for routinely and the high insulin levels are flying completely beneath the radar.

Ultimately, the hyperinsulinemia cannot keep up with the hyperglycemia, and when serum BG gets high enough, you get diabetes. The beta cells that make insulin fail, and in fact one of the things that damages them is hyperglycemia itself which is toxic to the beta cell. So you get B cell damage/death in type II eventually as well.

Type I diabetes and LADA (Late onset autoimmune diabetes) or type 1.5 have autoimmune destructon of the islet islet B cells that make insulin. Insulin sensitivity is usually normal.

Relevant to the theme of this blog, you should know that Type I DM is an order of magnitude more common in those with celiac disease and is more common in those with other autoimmune disorders like Hashimoto's thyroiditis, etc. Type I DM is an autoimmune disease that usually has onset in childhood. I believe it relates to leaky gut - with foreign proteins or peptides inducing an immune response via molecular mimicry in the context of an immune system that is likely impaired by excess n-6 linoleic acid and consequent 6:3 imbalance.

In type I DM, the initial damage is caused by the hyperglyemia - excess glycation leads to kidney, nerve and eye damage and inflammation, etc. Later, the damage is also caused by the excess injected insulin required when the patient is put on the ADA diet and the spikes in glucose that inevitably occur due to the inherent lack of precision of injected insulin. As an alternative to the insanity of the ADA, this can be minimized with VLC - a fatty acid/ketone -based metabolim that requires just enough insulin just to tell the liver to hang on the glycogen stores and facilitiate peripheral uptake, not the massive doses of insulin required to compensate for 6 times a day tsunamis of glucose arriving from the gut to keep the glucose from putting you in a coma.

In type II, the initial damage can be thought of as prior to both the hyperglycemia and the the hyperinsulinemia. The initial damage is the suite of early metabolic defects like liver inflammation, steatosis (fatty liver), elevated inflammatory cytokines like IL-6 and TNF-a and likely systemic inflammatory and immune effects that contribute to cancer and immune disorders and atherosclerosis - (you can have these effects as well even if you never develop diabetes and are thin and apparently healthy on the SAD).

Then, when the pancreas is pumping insulin like mad to control BG in the face of liver and increasingly, peripheral, insulin resistance, we are now adding the bad effects of hyperinsulinemia like promotion of more atherosclerosis, degenerative diseases like osteoarthritis, tumor promotion, etc.,etc. Once the pancreas fails, we add the effects of hyperglycemia - the same ones that a Type I can get, like neuropathy, cataracts, damage to the kidneys, and yet more additive effects on inflammation, glycation with increased tissue stiffness, more atherosclerosis and thrombogenesis, etc.

Finally, if you are treated with the ADA diet as a type II, your sBG may be brought under control, but often only at the expense of treating you with EVEN MORE OF THE SAME INSULIN that is causing about half the damage in the first place.

This is the best explanation for the failure of trials of tight glycemic control to show mortality benefits. They do it with drugs that are hepato- or cardio- toxic or with supra-physiologic doses of INSULIN and not by simply having you eat less of the glucose in the first place. The point being, it does you little good to decrease the damage from glucose if you balance with more damage caused by exogenous insulin.

In my opinion, Type II diabetes can actually be cured if it is caught and treated before there is too much beta cell destruction or burn-out. If one fixes the diet and allows enough time for the primary defect in liver sensitivity (and liver inflammation, NAFLD, etc) to heal, this metabolic defect should be reversible. Even if some damage has been done, one can usually avoid medication and especially insulin by lowering carbs to whatever it takes to allow your pancreas to just be occupied with "talking to your liver"

I am aware of at least one young woman who had type I DM diagnosed, and eating a paleo diet, the autoimmune reaction was arrested and she now no longer has diabetes. Usually type I is not diagnosed early enough for this to happen, but it could (and in the one case I am aware of did) reverse if caught right away and treated with a paleo diet

So - Type I low insulin - high sBG - normal insulin sensitivity - can't be cured usually. VLC paleo is the treatment of choice as it allows more stable BG with less exogenous insulin.

Type II - late effect of metabolic syndrome - damage if treated via ADA principles is as much due to hyperinsulinemia as hyperglycemia. Can often be essentially cured with diet. If caught early enough, you are cured if your liver heals and the pancreas recovers or is not that damaged. If caught later and the metabolism remains broken or pancreas is irreversibly burnt out, then VLC PaNu (Bernstein level of carbs or lower) is the treatment of choice

Hat Tip to Peter for the "talking to your liver" metaphor.

Some of you are no doubt too young to remember them.

They came in two forms when I was a kid in the late 60’s. The first was a hard white candy stick the same length as a standard filtered cigarette but just a bit thinner. No particular flavor, unless “sucrose” is a flavor. There was a red, actually pink, smudge painted onto one end to simulate the ember of a real smoke.

The other kind was the one I preferred. It was actually a stick of pink bubblegum. Nude, this faux cancer-stick was not too realistic and certainly did not make you look tough, as it was pink, but if you could resist the urge to chew it right away, the dimensions were closer to a real cigarette and it had a white paper wrapper, the mouthward inch or so embossed with a printed pattern that made it look like a filter.

At least one of these – I know for sure the hard candy ones and I believe the gum ones as well - had a coating of fine confectioner’s sugar that, with a sharp puff outward, you could imagine for about two puffs that you were part of the sophisticated world of those who fit in – the smokers.

After those two puffs, you could become a regular gum-chewing or candy crunching kid, or you could go for another “smoke”.

The idea that a 9 year-old kid feigning a bad habit is more likely to take up the real and very deadly one it is modeled on makes a good libertarian roll his eyes- now what, even candy cigarettes are bad?

But there may be something to the idea. It turns out that no tobacco company has ever sued a candy company for using their brand names on candy cigarettes. It seems obvious that candy companies counted on Junior’s emulation of Dad and Big Tobacco allowed trademark infringement to enable candy companies to socialize the new recruits. 

Does this remind you of anything?

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 pride yourself on being a nice person. You are happy with your progress and pleased if people ask you how you lost weight, maybe more when they seem to look at you funny – a little jealous, maybe even suspicious. 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 pulling up your shirt to point at your gentle washboard, 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, not having been clinically diagnosed as having celiac disease, when the rectangular slab of Hy-Vee or Piggly Wiggly birthday cake – frosted 3/8” thick and a stratum of oily granular sugar running through the middle to boot – is proferred, you say “thank you”, flash a non-Duchenne 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?

Even if you are not Philip Morris, are you the candy company?

What do the kids think? Well, they probably think nothing at all. It’s a birthday party after all and presents and sugar buzzes and juice and soda and treats are the sea they swim in.

All the time.

They will have no opportunity to say to you, “How come you don’t want cake?” or to their parents – “how come that skinny man doesn’t eat cake?”.

OK, young children probably wouldn’t notice one way or another, but what if you said, “No, thanks” to the cake offer? What if mom is serving, and asks “Why not?”.

Is there not a small but finite probability that you could give an answer that might lead to a discussion – a discussion that might change someone’s life, even if it’s not the questioner’s.

Maybe an image conscious teenage girl notices an adult male who from the neck down looks fitter than all the boys at her school who don’t play sports, and some of the ones that do. Maybe she hears you talk about your lack of hunger and maybe, being a teenager, after all, she is attracted to the transgressive notions you hint at – carnivory, saturated fat -that obviously horrify her parents.

How can this scenario, however unlikely, ever occur if we all keep pretending that we eat agricultural food like everyone else. Food that is constructed or manufactured instead of killed, food that is not real, food that everyone thinks is just fine for people to eat, as long as it goes easy on the “fat”.

Maybe your response to me is “Hey, lighten up, man. I do my part. I preach paleonutrition and the virtue of real food and animal fats on a selective basis.  I can’t be expected to ruin everyone’s day all the time.”

OK, you wear the Real Food Uniform often enough to do some good. No one expects you to get fired over diet advocacy at the office picnic.

If you nibble the cake to be neighborly, maybe the only damage you’ve done is some minimal aiding and abetting – The minions of Ancel Keys and the harpies of Ornish and Campbell have a little less work to do.

You’ve helped them just a little with your vignette of The Thin and Fit Old Guy Who Proves It’s Fine To Eat a Bunch of Sugar.

But what happens when you go home?

Do you doff the uniform of the Real Food Army and join Keys’ agricultural army reserve? Do you train yourself to crave the manufactured food of the dominant paradigm? Do you make and eat food with the modifier “paleo” in front of it?

Food that is designed to look and taste like signal dishes of 19^th and 20^th century industrially-inspired and manufactured food?

Paleo pancakes?

Paleo cupcakes?

Try a google search of neolithic treats with the prefix “paleo-” stuck on.

Here’s one:

You can make pancakes without flour? Yes! Recipe from xxxxxxxxx:

1. Beat/Mix:

1-2 eggs

1-2 table spoons of crushed almonds (or nut butter ... no peanut butter though .... peanuts are beans, not nuts)

cinnamon to taste

2. Fry the batter as you would a pancake on greased pan.

3. Top with fresh fruit. I usually heat up frozen mixed berries from Costco. When you heat them up they get all juicy and act as a syrup. I also like to add a little bit of honey even though this is not true paleo because of it's likeness to sugar.

Crushed nuts mixed with eggs? Who thinks this is not just a vehicle for sugar?

“Frozen mixed berries……get all juicy and act as syrup”

You bet they do!

Honey has a likeness to sugar ….well I suppose if likeness means “is”.

Here is another:

Paleo Pancakes Ingredients:

         1 1/2 Cups Pecan Flour (or almond flour)

         1/4 Cup Heavy Cream

         4 Eggs

         1/4 Cup Butter, melted

         1/8 Cup Agave Nectar

         1 tsp. Vanilla

         1/2 tsp. Baking Soda

Combine all ingredients in a blender. Cook pancakes in a non-stick skillet.

Serve with natural fruit spread or pumpkin butter.

2 tablespoons of Agave nectar would give 18-27 grams of fructose, plus whatever is in the arbitrary quantity of “natural” fruit or sugar-laden pumpkin butter you put on it. A small pack of M&Ms candy has 12 g fructose.

1 ½ cups of almond flour is about 6 or 7 ounces. Almonds are about 17% PUFA, nearly all n-6 linoleic acid, probably well-oxidized after frying in a skillet hot enough to give the “pancake” that golden hue we all like.

That seems like a pretty big oxidized linoleic acid dose to just to manufacture a sugar vehicle.

Does anyone agree that “paleo pancakes” taste like complete shite unless absolutely smothered in hepatotoxic sucrose/ and or butter?

Why not just have 4 eggs fried in butter, cream in your coffee, and a few ounces of unfried almonds?

Why mash it together into a “pancake” if it’s not about the sugar?

If it’s because your kids will scream without a sugar vehicle (we all know 4-year-olds are more physically powerful than crossfitters and are messed with at your peril!), what will your kids do the first morning at University in the breakfast line when there is pile of all-you-can eat pancakes? Will they know there’s wheat flour in place of the ground-up almonds you’ve been conditioning them with?

Would it not be better to train your kids, and yourself, to avoid Neolithic food by the simplest expedient there is? So simple a child could manage it?

Something as simple as a simple rule.

A rule like:

Don’t eat anything that looks like Neolithic food, especially Neolithic food.

What is the point of all this? I just don’t get it, and I don’t think it is because I am just too lazy to make this stuff. 

It’s easy to make fun of commercial junk in a box like “low carb” pasta, zone and atkins bars, etc. All stuff that may be gluten free or have sawdust in place of of high GI starch, but whose real reason for existence is just to appropriate what should properly be freestanding, honest, real food back into the maw of corporate big-agra commercial interests.

How about this:

I am not making this up.  A “Paleo” chocolate cake loaded with Stevia, price $45 US. Note the high-end Barbara Barry tile in the background. I suppose that explains the price.

I am on record as stating that eating anything sweet should be totally avoided if you do not want to have difficulty avoiding sweets. I cannot prove it, but it seems plausible that eating and drinking artificial sweeteners is a physiologic version of “smoking candy cigarettes”. There is likely to be some neuro-hormonal conditioning along with three diet sodas a day. Is there any way a diet soda habit makes it easier to avoid the hyper-ubiquitous sweets we are surrounded by?

I think “cheat days” make just as much sense as a weekly Marlboro red for ex-smokers or lines of coke once in a while after you have left Hazelden. But I admit that is a mere common sense observation, and if it “works” for you to go hyperglycemic or have an extra BM once a week, go for it.

But this “paleo food” thing is bogus. If your food needs a prefix, it is not “paleo” in either the historical or the metabolic sense, and it is, more emphatically, not paleo in the sense that it is helping to keep alive the reigning agricultural paradigm – the one that wants our food to look like agricultural food so that we still crave agricultural food.

Manufacturing simulacra of grandma’s comfort food in your kitchen is either:

1)   Pointless work to make something awful tasting

2)   A veiled excuse to make a sugar vehicle

3)   An unconscious exercise in the service of Ancel Keys’ Neolithic Food Army Reserve. Keep that big-agra-supplied uniform pressed and hanging in the closet, waiting for the call-up. For the day when the paleo-pancake is not doing the trick, and hell, why not have just one real pancake?

If you’re not as evil as the tobacco company or as cynical as the candy company, are you still unconsciously the kid at school sharing cigarette –shaped treats with his playmates at recess?

Are you nurturing the seed of the dominant agriculture-based dietary paradigm, an unconscious conscript in Ancel Keys’ sugar-is-innocent reserve army?

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.

History of childhood candy cigarette use is associated with tobacco smoking by adults.

BMJ article on candy cigarettes

Where to get them

Lustig video on fructose

Top photo by Sally Mann - Candy Cigarette - 1989 - reproduced under fair use doctrine

I like to respond to comments and questions, but we do not live our lives at the quantum level (where time can go backwards) and I am starting to run up against some physical limits.

Currently, I am logging about 12-15  hours a week just moderating and responding to comments.

I enjoy this, but time is finite and I need to spend much more time reading primary sources (the ones I already have a giant stack of) and putting up more substantive posts - substantive essays are the raison d'etre of this blog and i would rather have a few substantive posts than a whole bunch of trivial ones.

The blog is at the point where new posts and comments are going to take more than 25 hours a week.

This is gratifying, but the reality is that this project simply has to start paying the freight in my own life.

I don't have a book for sale yet, and frankly, maintaining the blog will probably add another year 'til the completion of the first one - an accessible scientifically based guide to the 12 steps.

I sell no supplements.

I don't peddle my essays as ebooks.

I only have affiliate links if you buy books through amazon from my list - this has earned me about $78 so far.

I abhor the idea of cluttering the site with advertisements, especially the useless junk and scams that pop up with google adsense.

Charging a subscription fee for access will limit growth and exposure of new souls to the blog and paleonutrition in general.

I have considered doing skype-enabled personal consultations but have some medicolegal and logistical issues to research before I start that.

So I have decided to add a "donate" button - which you will now see on the right.

I'll come right out and say it - I encourage contributions as large and as frequent as as you are comfortable with.

Maybe you can put the contribution amount in the context of your annualized cable TV bill, your $150 per month Crossfit membership, or relative to the cost/usefulness ratio of a 15 minute appointment with medical specialists who know nothing about nutrition :)

If the blog has value in your life, you will know what do.

There is a lot of mention of dairy being insulinogenic. Anecdotally, this is what I have seen as a type 1 diabetic. Beef causes my blood sugars to rise very high about 7-8 hours post prandial. So does cheese - in similar quantities. Butter and cream and full-fat yogurt do not. But the difference is a serving of cheese might be 1-3 oz. A serving of beef on a low carb or paleo diet might be 8-16 oz. So eating small amounts of cheese are not a problem, insulin-wise. However eating large portions of beef in particular, and other meats as well, require more insulin than 30g of carb - it's just much later on. In an attempt to lose weight I need to keep my insulin dosages low - therefore I must limit my protein. Ditto on carbs. If I don't eat more fat and calories I am worried about stunting my metabolism. It seems very difficult to up your fat intake without dairy (cream, butter). That's just my pragmatic rationalization as to why I'm eating dairy. I do try to choose organic cream and pastured butter to minimize the hormonal gunk though.

She has shown nicely how large protein meals require more insulin or her blood sugar will rise.

She also got me to thinking about how I see the term "hyperinsulinemia" used at times.

In the blogosphere, I occasionally see some conflation of the terms hyperglycemia and hyperinsulinemia. On a chronic basis, they are part of the same pathology of metabolic syndrome, but as part of normal homeostasis they are not.

Insulinogenic means "Induces an insulin response".

Rising blood sugar does not automatically equate to rising insulin -in fact, as any Type I knows all too well, hypergyclemia is due to inadequate insulin response. Your serum blood glucose (BG) can rise in the presence of an insulin response or without it - it depends on glucagon and epinephrine and other foods eaten as well.

It is of course true that there is an insulin response to amino acids- and this is roughly an order of magnitude smaller than the response to glucose on a molar basis. It is also true that if more glucagon is released relative to insulin with the protein meal, that serum BG can rise even with the insulin increasing.

If you are type I, your BG is rising due to the lack of an increase in insulin in the presence of increasing glucagon liberating glucose from your liver, not due to the "insulinogenic" effect of 16 oz of beef. In fact, if there were not glucagon released after eating protein, a non-diabetic could become hypoglycemic from the insulin response to the protein.

When Cordain complains that dairy protein is "insulinogenic", he means (or should mean) that a given amount of dairy protein raises insulin more than an equimolar amount of, say beef protein.

The question is not whether this occurs, but if it a large enough effect to be clinically significant.

Thank You, Dee