Primal Wisdom: Potatoes and Protein

Primal Wisdom: Potatoes and Protein

Potatoes and Protein

The Food and Nutrition Board of the National Academies of Science publishes the Dietary Reference intakes, which includes Estimated Average Requirements for Indispensible Amino Acids for Adults Aged 19 years or Older.

I decided to find out whether the average person could meet his or her IAA requirements eating a diet composed solely of white potatoes. I used the USDA nutrient database to find the amino acid delivery of potatoes at 1880 kcal and 2350 kcal, approximate caloric requirements of a 120 pound woman or a 160 pound man, respectively. I created the following table for the purpose:
Click for larger version

According to these FNB and USDA data, the average person can meet all indispensable amino acid requirements eating potatoes as his/her sole protein source. No 'limiting amino acids' nor protein complementing required so long as caloric requirements are met.

Kon and Klein reported in 1927 on The Value of Whole Potato in Human Nutrition. Two healthy adults obtained all of their protein and IAAs from potatoes for 167 days. They maintained nitrogen balance. They reported:

"The digestion was excellent throughout the experiment and both subjects felt very well. They did not tire of the uniform potato diet and there was no craving for change."

The potato provides only about 10% of calories as protein. A mixed diet containing other plant foods providing higher proportions of protein, like green vegetables (20-40% of calories as protein), nuts (~25% of calories as protein), or legumes (~25% of calories as protein) will provide higher levels of the IAAs and total protein.

It seems that humans can obtain all of the protein they require from a food like the potato. What does this tell us about ancestral nutrition?

I decided to compare the IAA delivery of potatoes to that of 95% lean ground beef. I compared the IAA delivery of amounts of beef and potatoes that provide comparable total protein, and created the following table to illustrate:
Click for larger version
Both the beef and the potato provide adequate amounts of total protein and IAAs. The much smaller portion of beef (200 g vs 2500 for the potatoes) provides larger doses of the IAAs, presumably constituting greater excesses of IAAs for the average individual.

The body will deaminate and oxidize these excesses of IAAs, increasing the amount of ammonia the liver must detoxify and sulfuric acid and urea the kidneys must excrete.

Since the beef supplies only about 14% of total energy requirements, the individual who fills in the other 86% of calories with whole foods that also provide protein will automatically consume a higher amount of IAAs than one who consumes a mix of plant foods with a far smaller amount of animal protein.

For those who have concerns about overconsuming methionine because some research suggests that reduced methionine consumption might increase longevity, I find it interesting to note that the ground beef provides about 15 times more methionine+cysteine per unit weight than the potatoes (about 9.5 mg per g cooked beef, versus 0.6 mg per g cooked potatoes).

Let's say someone consumes the half-pound of beef (328 kcal) and gets the remainder of his required 2350 calories from potatoes (2022). He would get 1906 + 0.86(1425) = 3132 mg of methionine+cysteine, compared to 1425 mg (less than half as much) if he ate only potatoes.

I wonder if the body has an internal regulatory mechanism for amino acid consumption, which drives appetite to control total amino acid intake, such that if a person eats a diet rich in animal protein, the sytem drives the appetite toward attempting to fill the bulk of caloric requirements with low protein items like fat/oil, sugar, fruits, some very low protein tubers (e.g. cassava), or some refined starches?

Fat and Diabetes: Bad Press, Good Paper, and the Reemergence of Our Good Friend Glutathione - Chris Masterjohn

Fat and Diabetes: Bad Press, Good Paper, and the Reemergence of Our Good Friend Glutathione | Mother Nature Obeyed - Weston A Price Foundation

Fat and Diabetes: Bad Press, Good Paper, and the Reemergence of Our Good Friend Glutathione

A number of people have asked for my comments on the recent headlines claiming that “high-fat diets cause diabetes,” based on a recent paper published in Nature Medicine (1):

Oshtsubo K, Chen MZ, Olefsky JM, Marth JD. Pathway to diabetes through attenuation of pancreatic beta cell glycoslyation and glucose transport. Nat Med. 2011; Aug 14 [Epub ahead of print].

Robb Wolf and Denise Minger have already critiqued this study, but I have a few things to add about the potential for our good friend glutathione to protect us from diabetes.

It’s Not About the Diet . . .

For those who are concerned that this paper might indicate that traditional, nutrient-dense fatty foods are bad for us, I would echo what Denise has already written. “When it comes to studies like this one,” our approach should always be to “white out the headline” and “read with an open but critical mind.” In this case, we can safely ignore the media headlines and observe that even the title of the paper says nothing about high-fat diets. The authors plant a few token sentences in the paper about the ability of a “high-fat or Western-style diet” to cause obesity and thus predispose someone to diabetes, but the paper is fundamentally about mechanism, not diet.

The investigators fed mice either a “high-fat” or “standard” diet. Both diets contained about 12 percent of calories as maltodextrin, which is a string of an average of ten glucose molecules hitched together like links on a chain, and is recommended for use in these diets to aid in pelleting and to reduce heat damage during the pelleting process. Both diets used casein for protein, a small amount of soybean oil to provide essential fatty acids, and a collection of purified vitamins and minerals. Both of the diets contained hydrogenated coconut oil and sucrose. The only difference between the two diets is that the “high-fat” diet contained an extra 47 percent of calories from hydrogenated coconut oil and the “standard” diet contained an extra 47 percent of calories from sucrose. Since fat packs in more calories per gram than sucrose, the high-fat diet was also 37 percent richer in calories.

It should be evident by now that neither of these diets contains any food.

In “They Did the Same Things to the Lab Rats That They Did to Us,” I discussed the emergence of these purified diets in the 1970s, when they first began to replace the cereal-based (i.e., “food”-based) rodent diets of yesteryear. The animals consuming the new diets developed fatty liver, excessive bleeding, kidney calcification, and greater vulnerability to stress, toxins, and carcinogens. Leading scientists have revised and improved the diets to curb their worst effects, but they still don’t contain any food.

Purified diets are advantageous to scientists because they make it easy to control for single variables and to make comparisons between different studies using the same diets. At the same time, the studies become irrelevant to the dietary choices faced every day by human beings. When we decide whether to choose a fat-rich egg yolk or a sugar-rich orange, for example, our choice has a profound impact on our intake of choline, vitamin C, and dozens or hundreds of other chemicals. Rodents consuming purified diets don’t face these effects because the diets contain a standardized amount of each vitamin and mineral and lack hundreds of other substances found in natural foods.

Even if this were not the case — that is, even if we humans were to eat nothing but casein, sugar, refined fats, and multivitamins — we would still be faced with the fact that we are not and never will be mice.

Quite often we find that certain disease processes exhibit remarkable similarities across species but that the dietary factors that can induce those diseases do not. For example, hypercholesterolemia produces atherosclerosis in baboons, monkeys, cats, mice, chickens, parrots, chimpanzees, pigs, dogs, pigeons, goats, rats, guinea pigs, and hamsters, but some of these animals such as rats and dogs are remarkably resistant to the effects of dietary cholesterol. This would suggest that there might be something universal about hypercholesterolemia that is worth studying, but also that it would be profoundly foolish to generalize dietary factors from rabbits to humans if we can’t generalize them to rats or dogs.

As Denise Minger already pointed out, and as we will see in more detail below, the effect of high-fat refined diets on obesity is difficult to generalize even from one strain of mice to another; it would be all the more profoundly foolish, then, to generalize the effects from mice to humans.

This study provided no evidence that diets made from casein, sugar, and hydrogenated coconut oil cause diabetes in humans, but it did show that some of the mechanisms they observed in mice were active in human cells, so let’s take a look and see if we can learn anything that might be of interest to those of us who walk on two feet.

. . . It’s About the Mechanism

The authors concluded from their work that the following scenario is likely to be involved in the development of diabetes:

  • Dietary and genetic factors lead to obesity and insulin resistance.
  • These conditions elevate concentrations of free fatty acids, which in turn cause insulin resistance to worsen.
  • In the pancreas, elevated free fatty acids decrease the ability of two proteins called FOXA2 and HNF1A to travel to the nucleus and bind to DNA.
  • When these proteins fail to bind to DNA, the cell fails to make an enzyme involved in processing glucose transporters and stabilizing them at the cell surface.
  • The loss of glucose transporters at the cell surface impairs the ability of the pancreas to sense glucose levels in the blood and adequately stabilize these levels. As a result, we lose glucose tolerance and type 2 diabetes begins to emerge.

The investigators obtained pancreatic cells from a very small sample of humans (six healthy donors and two diabetics) and found some evidence to support the belief that this basic mechanism is active in humans just as it is in mice: the cells taken from diabetics had lower binding of the same proteins to DNA, lower production of the same enzyme, and 80-90 percent loss of glucose transporters at the cell surface. Moreover, the researchers were able to reproduce this mechanism in healthy human cells by incubating them with palmitic acid, a free fatty acid.

These results suggest that we may be able to learn something useful to our understanding of human diabetes from these mouse experiments.

What’s With Those Funny Mice?

The authors of this study uncovered a little hint that oxidative stress is critically involved in the aspects of the disease process they studied and that the master cellular antioxidant, glutathione, may offer complete protection against the loss of glucose tolerance.

First, let’s consider the strain of mice they used, C57BL/6J. This strain is often called “B6″ and the “J” indicates these particular mice are a substrain from Jackson Labs, so I’ll call them “B6/J” from hereon out.

The diets these researchers used were named “Surwit diets” after Professor Richard Surwit of Duke University, who had helped Research Diets formulate the diets in 1992. Surwit had shown in the 1990s that B6/J mice are uniquely vulnerable to obesity and diabetes when fed high-fat diets, and that the inclusion of sugar in these diets has little or no effect.

Surwit’s team published several papers comparing the effects of different diets in B6/J mice to the effects of the same diet in A/J mice, which are highly vulnerable to hearing loss and cancer but resistant to obesity, diabetes, and atherosclerosis. I’ve blogged about these studies before. Here is what happened when the team fed these mice high-fat or low-fat diets with or without sugar for four months (2):

If you need to enlarge this or any of the subsequent pictures, you can do so by clicking on it.

The fat in this study was hydrogenated coconut oil. We can see that the high-fat diet increased fat mass in B6/J mice to a much greater degree than it did in A/J mice. Sugar increased adipose mass even further in B6/J mice fed high-fat diets, but reduced adipose mass in B6/J mice fed low-fat diets. It had no effect in A/J mice at all. We should keep in mind that this is absolute fat mass, and not fat mass as a percent of body weight.

The Surwit team repeated the study a few years later, but excluded maltodextrin from the diet and expressed fat mass as a percent of body weight. Here we see similar effects of fat, but no effect of sugar at all (3):

In the earlier study (2), Surwit’s team also measured glucose and insulin levels. The vulnerability of B6/J mice to diabetes was even more apparent than their vulnerability to obesity:

Here we see that a high-fat diet increased fasting glucose and dramatically increased fasting insulin in B6/J mice, while sugar had no effect in these mice. At the same time, neither fat nor sugar had any effect on either variable in A/J mice at all.

Why would B6/J mice be so vulnerable to the effects of a high-fat diet? Well, it turns out that both strains of mice have a higher caloric intake on this diet, so it’s not that.

There are likely numerous genetic differences between these strains of mice, but one particularly interesting difference was discovered in 2006 (4). It turns out that B6/J mice — but not other sub-strains B6 mice or non-B6 mice — have a deletion in the gene that codes for a critical enzyme in glutathione metabolism. As a result of the deletion, the mitochondria of these mice are unable to regenerate a particular form of the B vitamin niacin, and thus have a seriously impaired ability to recycle the master cellular antioxidant glutathione under conditions of oxidative stress.

Glutathione To the Rescue?

Now, how might this relate to the fat-and-diabetes study we’re trying to pick apart at the moment? Well, these researchers also used B6/J mice. And when they induced the disease process in healthy cells by incubating them with palmitate, they showed they could block the effect entirely if they also incubated the cells with N-acetylcysteine (NAC):

The black bars show that palmitate reduced the ability of these two critical proteins to bind to DNA, while the gray bars show that palmitate no longer had this effect if the cells were simultaneously given NAC.

NAC is best known as a precursor to glutathione, and is used for this purpose not only in experimental science but even in clinical practice. Depletion of glutathione is essential to the mechanism of acetaminophen (Tylenol) toxicity, for example, which accounts for half of all cases of acute liver failure in the United States and Great Britain. Administration of NAC is a highly effective remedy in the first ten hours of overdose, and it is believed to act at least in part by restoring glutathione levels (5).

The authors of this study did not measure glutathione levels, but the hypothesis that glutathione is protective is consistent with a study I wrote about in a post back in January, “Eating Fat and Diabetes.” In that study (6), high-fat diets depleted glutathione and impaired insulin sensitivity and glucose tolerance in rats and mice, but treating the rats with a mitochondrial antioxidant and genetically engineering the mice to make lots of the antioxidant enzyme catalase both reversed these effects. Catalase is an enzyme that converts hydrogen peroxide to water.

How Does This All Fit Together?

When mitochondria are overloaded with more energy than they can handle, they begin making increasing amounts of the free radical superoxide. Superoxide carries out important signaling roles. Among them, it directs excess energy into fat synthesis. But it can also wreak havoc on the cell by forming oxidants that can damage vulnerable proteins, lipids, and other important molecules. Thus, a manganese-dependent enzyme called superoxide dismutase converts it into hydrogen peroxide. Hydrogen peroxide can also damage important molecules, but increasing evidence suggests it also regulates the activity of hundreds of proteins by controlling several “redox switches,” including glutathione.

An interesting picture begins to emerge as a working hypothesis:

  • When the mitochondria’s capacity to burn lipids and fats in order to make ATP is overloaded, it makes signals such as superoxide that will redirect incoming energy to be stored as fat.
  • Superoxide also generates hydrogen peroxide, which oxidizes glutathione and thereby flips a “redox switch” controlling a multitude of proteins. These proteins may then help the cell stop responding to insulin in order to minimize energy overload.
  • This is a desperate attempt of the cell to protect itself from oxidants that would otherwise destroy its basic machinery, and has the unfortunate consequence of increasing glucose and other forms of energy in the blood, and thus contributing to the metabolic abnormalities we associate with diabetes.
  • Supporting the cell’s antioxidant defense network helps it to handle more energy and thereby protects against this entire process. Thus, providing NAC to cells, synthetic mitochondrial antioxidants to rats, or extra catalase to mice all seem protect against the development of diabetes-like features in the face of energy overload.

In my view, the major causative factor in this pathogenic process is energy overload. This, however, does not simply mean “excess calories.” It means that calories are supplied in excess of our body’s capacity to burn them. This capacity is increased by exercise, optimal thyroid status, lack of infection and inflammation, and a variety of vitamins and minerals involved in energy metabolism and antioxidant defense.

If this is correct, does a “high-fat diet” cause diabetes? The obvious question that must follow is “which high-fat diet?” An anti-inflammatory, invigorating, nutrient-dense diet likely protects against diabetes regardless of whether it is low or high in fat.

For more on glutathione, see “The Biochemical Magic of Raw Milk and Other Raw Foods: Glutathione.”

Heretic: Fat disrupts sugar sensors in pancreas causing type 2 diabetes

Heretic: Fat disrupts sugar sensors in pancreas causing type 2 diabetes

About Me

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Buckhorn/Lakefield, Ontario, Canada
(hires pic) I am a physicist, sensor design consultant (website) and embedded software engineer (picture of my lab). This blog is meant to collect essays, articles and debates on optimal human nutrition, science and other topics. This board is for like-minded people who know (or will know) each other and share certain common values. I welcome all heresies and opposing views, and discourage conformity of any kind. I sincerely welcome all people who are creative and like doing things, are self-reliant, have individualistic mindset and do not like wasting too much time on socializing, sport or mainstream entertainment. I am currently interested in the socio-anthropological theory (link) of evolutionary regression in developed countries.

Tuesday, August 16, 2011

Fat disrupts sugar sensors in pancreas causing type 2 diabetes

That's why a diet simultanously high in fat and carbs is detrimental, but a diet high in either one and not both, is not!

See on BBC health:


(Source: "Pathway to diabetes through attenuation of pancreatic beta cell glycosylation and glucose transport")

This is important finding that clears a lot of confusion. I used to answer countless of questions from diabetics (on other forums), the most frequent was this, paraphrasing:

"Why should I eat high fat diet if we know that it would increase my already high insulin resistance?"

This article is telling us that the answer to this is that it won't!

It will make pancreas stop reacting to blood glucose while you are eating fat AND carbohydrates at the same time. This won't matter you eat fat on its own with very little or no carbs! On the other hand, diabetic insulin resistance appears in this light to be a totally different phenomenon - related to body tissues and organs being permanently resistant to insulin that is already produced by pancreas and circulating throughout the body!

Will fat affect the tissue insulin resistance as well? Yes - probably by reducing it! As me and millions of other people who tried Dr. Jan Kwasniewski's Optimal Diet, have found!

We are probably dealing here with two opposing effects:

1) Detrimental effect of dietary fat upon pancreas preventing it from reacting to blood glucose
(Which matters if and only if one consumes significant amount of carbohydrates together and simultaneously with fat).

2) Positive long term effect of dietary fat upon body tissues and organs

Can a fatty meal impair cardiovascular health? Absolutely, since it can lead to hyperglycemia due to (1) if the meal is also high in carbs (I will pass that carrot cake, thank you...)

Can a high fat meal reduce the risk of cardiovascular disease (see this)? Absolutely! If it is low in carbohydrates!

This clarifies also another issue, namely Dr. Kwasniewski's claim that a diet with 35-45% fat by calories is the most detrimental to one's health (for adults). It makes a lot more sense in the light of this article. (Note: since a diet typically would contain 10-20% protein, therefore 35-45% fat means 35-55% carbohydrates, by calories).

Bottom line:
- Do not mix high carbohydrate diet with high fat nutrition!

------------ Update 30-Aug-2011 -------------------

Read this:

Fat and Diabetes: Bad Press, Good Paper, and the Reemergence of Our Good Friend Glutathione

Fasted exercise - Matt Metzgar

Matt Metzgar

Fasted exercise - Matt Metzgar
September 18, 2011

Running on Empty

I've noticed a couple curious things lately in regard to eating and exercise. First, I've noticed that if I ocassionally skip dinner, or just have some carbs like potatoes but no meat for dinner, that I actually feel better upon waking the next morning. Of course, I'm not doing this every day, but if I do this once or twice a week, then I am virtually guaranteed to feel better the next morning. This points to how occassionally restricting calories in the evening, or perhaps restricting protein in the evening seems to yield benefits.

Today, I noticed how this carried over into exercise. I have been exercising fasted in the morning, going for an intermittent run on the nearby trail. Last night, I just had some potatoes instead of dinner, and this morning I ran before eating anything. This combination seemed to really prime my body for running. I don't know if it put me in "fat-burning" mode or something, but I was just really cruising on the trails today.

It's amazing how good you can run on an empty fuel tank. I wish someone would have told me about this 15 years ago. I remember reading Runner's World for a few years straight back in my twenties. Never once did I see an article that recommended running while fasted. Guess it wasn't the expert publication it was supposed to be!

Archevore Diet Version 3.0 (2.0 revisited) - Dr Kurt Harris

Archevore - Archevore Diet

The Archevore Diet - A pastoral whole foods diet that can improve your health by more closely emulating the evolutionary metabolic milieu (EM2) and avoiding the hazards of industrial foodways.

Kurt Harris MD

"An Archevore is someone who eats based on essential principles, and also someone who hungers for essential principles. Take your pick."

(Last revised as of 9/13/2011)

This diet is a practical framework using whole foods easily available in the 21st century. It is designed to be as universal as possible. The average person who adopts it in preference to the standard american diet should be healthier in every respect, and will usually settle at a more optimal body composition spontaneously.

The diet minimizes putative neolithic agents of disease (NADs) and ensures adequate micronutrition.

The diet is designed to be healthy and sustainable as long as you are alive and to offer plenty of satisfaction, while minimizing food reward effects that lead to overeating.

Historically, many find this diet results in spontaneous reduction in caloric intake and in health-improving fat loss, with no measuring, weighing or special supplements. I eat this way myself, of course.

Although this diet is a framework designed to work well for as many people as possible who are starting with a western diet, it will not necessarily work well enough, or completely enough, for everyone who needs to lose fat or for anyone afflicted with any particular disease. For fat loss, more radical maneuvers might be necessary, depending on the etiology of your obesity.

This information is offered as a free piece of educational information to anyone who finds it useful and is not to be considered individualized dietary or medical advice.

Your health is your responsibilty. If you have any doubts about the advisability of any dietary maneuver that might affect your health, consult a competent physician.

Go as far down the list as you can in whatever time frame you can manage. The further along the list you stop, the healthier you are likely to be. Earlier steps, in my clinical experience, will give more bang for the buck.

There is no counting, measuring, or weighing. Calories count, but why bother counting?* (Hat tip Nigel)

1. Get plenty of sleep and deal with any non- food addictions.

Laird Hamilton sleeps 9 hours. Can you surf Teahupoo?

If you're drinking a 12-pack a day, or chain-smoking, diet may help but is hardly your first priority.

2. Eliminate sugar and all caloric drinks.

Drink water, tea or coffee. No sodas, sports drinks, juices, or milk. Don't add sugar to your food or eat things made with sugar or high fructose corn syrup.

3. Eliminate gluten grains and wheat flour.

No cake, cookies or pastries. No bread or pasta, whole grain or otherwise.

This rule and rule #1 pretty much eliminate anything that comes in a box.

White rice and whole meal corn products are reasonable sources of starch if tolerated, but not as nutritious as plant storage organs (root vegetables).

4. Eliminate seed oils - grain and seed derived oils (cooking oils) Eat or fry with with ghee, pastured butter, animal fats, or coconut oil. Avoid temperate plant oils like corn, soy, canola, flax, walnut, etc. Go easy on the nuts, especially soy and peanuts.

5. 2 or 3 meals a day is best. No snacking. You're not a herbivore. Whole foods prepared at home should be the rule. Low meal frequency is a powerful tool if you have weight to lose.

6. Whole foods from animals. Eat them for the protein, the micronutrients and the fuel.

Favor grass-fed ruminants like beef and lamb for your red meat. These meats have excellent n-6/n-3 ratios and their saturated and monounsaturated fats are a great fuel source. Wild game is good if you can process it yourself- but commercial venison and bison is too lean and is expensive.

Eat fish a few times a week and pastured eggs if you like them.

Eat offal for the vitamins and choline- some fresh beef liver 1-2 times a week is plenty. Mix it with your ground hamburger if you prefer. Pastured butter is good source of K2.

7. Choose fuels from the EM2. Both animal fats and starchy plant organs are time-tested fuel sources for humans.

Animal fats are an excellent dietary fuel and come with lots of fat soluble vitamins. It can work very well to simply replace your sugar and wheat calories with animal fats. If you are not diabetic and you prefer it, you can eat more starch and less animal fat. A low carb diet can rely more on ruminant fat and pastured butter.

Plant storage organs like potatoes and sweet potatoes are nutrient laden and well tolerated by most people. Bananas and plantains are convenient starchy fruits. The soluble fiber in all these starchy foods is very likely beneficial, unlike the insoluble fiber in bran.

If you are not diabetic, there is no reason whatsoever to avoid either animal fats or starches in whole food form.

8. Make sure you are Vitamin D replete. Get daily midday sun in season or consider supplementation if you never get outside.

9. Vegetables and fruits - Besides starchy plants for fuel and micronutrients, eat a variety of different colored plants of whatever you like and tolerate. Think hormesis. Some is better than none, but neither big salads nor fruit to excess will save your life. You're not a gorilla, you're an omnivore

10. Get proper exercise - both resistance and "aerobic" exercise have benefits, including mental. Think hormesis again- the recovery periods are where you get the benefit. Lift weights every day or run marathons for "fun", but not for your health.

11. You won't get too much fructose eating reasonable quantities of fruit, but don't make it your staple. Most modern fruits aren't really just bags of sugar. That was hyperbole, folks, a rhetorical technique. Bananas rich in starch and citrus fruits are preferred. Don't go nuts with watermelon and agave, which are nearly pure fructose. Beware stone fruits like peaches and apricots if you have IBS - the polyols are fermented in your colon.

A diet based on beef and potatoes is healthier than one based on granny smiths or 30 bananas.

12. If you are allergic to milk protein or concerned about theoretical risks of casein, you can stick to butter and avoid milk, cream and soft cheeses. Aged cheeses 6 months and older may not have beta-casomorphin and are good sources of K2.


No counting, measuring or weighing is required, nor is it encouraged.

I am agnostic on macronutrient ratios outside of very broad parameters.

Archevore eaters typically range from 5-35% carbohydrate, from 10-30% protein and from 50 to 80% fat (mostly from animals) but wider ranges are entirely possible if you are not dieting and you are meticulous about the quality of your animal food sources.

If you are trying to lose weight, really minimizing fructose and eating 50-70g a day of carbohydrate as starch is recommended. Skipping breakfast or at least no carbs for breakfast can be very helpful.

If you are at your desired weight and healthy, 20% of calories as carbs is plenty for most very active people.

It is perfectly acceptable if you don't gain fat with it to eat more starch and less animal fat.

Note that the 19th century categories called "Fat" and "Carbohydrate" are each broad macronutrient categories that contain both good and bad.

Saturated and monounsaturated fat is generally good. A lot more than 4% of calories from PUFA (whether n-3 or n-6) is likely bad.

For healthy non-diabetics, starch is good. Excess fructose (added sugar) may be bad.

In wheat, the carbohydrate starch is probably not the major problem. It is the gluten proteins and wheat germ agglutinin that come along with the starch that are suspect.

So forget "carbs vs fat".

It is neolithic agents of disease versus everything else. And consider that the way food is prepared and its cultural context (food reward) may itself prove to be a NAD.

Most Archevores only know macronutrient metrics in retrospect, as they don't target numbers just like wild humans didn't target numbers.

Your mileage may vary!

So eat what you want. This is simply free advice that has worked very well for me and at least hundreds of patients and readers. I'm not trying to save the world, as I find it generally does not want saving.

Note: The order of the steps is arrived at by balancing my best guess at the noxiousness of each neolithic agent or food with the prevalence of each agent in the north american diet and the effort/reward ratio of the step. If your culture has a different diet the order of the steps might change. For instance, Chinese who fry everything they eat in soybean oil and don't eat much wheat would move step three up to the step two position.

* If you prefer to suffer with a calculator and scale without trying this first, knock yourself out, but why not try it first? If it doesn't work, go to 70g of carbs a day and take out whatever foods you are "enjoying" the most. If that doesn't work, then you might indeed have to count calories. You might have lost the genetic lottery or it may just be too late.


companion article..........

Archevore Diet Revised

The all vegan version is now up.

Not really.

But I did just spend several hours doing a needed update. I think this is about version 3.0 since the original back-of-the-envelope diet I first put on the web in June 2009. That was a diet I had been using successfully clinically for more than two years.

The emphasis on animal products remains.

The emphasis on real whole foods - kill it or dig it up with a stick - remains and is enhanced.

Macro ratios had already been de-emphasized in v 2.0, but that has now been made even more explicit in the steps, and not just in the coda.

Things which in my mind were "givens" but had been pointed out to me were not clearly emphasized have been made more explicit, like sleep and eating some offal.

I've deleted references to legumes other than avoiding soy and peanuts, as other legumes seem more and more benign to me.

It remains congruent with, and is perhaps now more so with other whole foods diets that I consider "Paleo 2.0" approaches, like that of Chris Kresser, Paul Jaminet, Chris Masterjohn (he won't force you to eat wheat) and J Stanton, and with more potatoes and less steak, Stephan Guyenet.

I've not had a chance to do big blog posts about food reward yet. Those who might have seen some comments of mine elsewhere will see I find merit in the idea, but I don't know its ontological status yet.

Whether reducing food reward is restoring the EM2 or whether it is just a useful fat loss maneuver I am not sure. Either way, I think that is part of how diets like mine and maybe all diets may work, so I have emphasized that a bit more in the rank ordering.

There is also a notable but not strictly scientific bias I have used for this re-write.

It could fairly be called data mining or reverse engineering, but I've tried to write the steps such that most of the weight optimization failures that I know of would have not been following the new steps.

For example, I know of people who failed despite eating very low carb, but I cannot think of many that actually ate only twice a day with no snacks, never ate from a box, avoided restaurants and never ate ANY liquid calories, including milk and cream. So this has resulted in modifications that make my own current diet noncompliant in a few ways (I still add cream to my coffee), but I think these changes make it more universal.

This does seem to work well for many people, but nothing works for everyone. If it optimizes your weight and health and you are satisfied, you can always break a few rules and see what you can still get away with.

I'll try to do a re-write of "how to lose weight" sometime soon and add more therapeutic tricks for when the whole foods low-NAD idea is not enough.

How to Make Beef Jerky - wikiHow

How to Make Beef Jerky - wikiHow

Article Edit Discuss History
Make Beef Jerky

For most of human history the only way to preserve meat was to dry it into jerky. While new methods of meat preservation have now been developed (freezing, chemicals, and so on) many people still enjoy the flavor and convenience of jerky, which, in the U.S., is most commonly made from beef. Because moisture and fat must be removed from the meat, it can also be a healthy source of protein. Follow these steps and make your own!

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Edit Steps

  1. 1
    Select a cut of meat.
    Select a cut of meat.
    Select a cut of meat. Choosing a lean cut like sirloin, top round, or eye round will save time later.

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  2. 2
    Remove all noticeable fat, as this will cause the jerky to spoil much faster.
    Remove all noticeable fat, as this will cause the jerky to spoil much faster.
    Remove all noticeable fat, as this will cause the jerky to spoil much faster. Slice your meat into very thin strips less than 1/20`` thick (sometimes a butcher will do this for you for $10 if you ask). To make it easier to slice, freeze it for about 5 hours before slicing. You can cut with or against the grain; some find that strips cut against the grain are easier to chew. Trim the fat as you go along, since fat does not dry.
  3. 3
    Marinate the meat in a solution of olive oil and vinegar sea salt, or according to a recipe of your preference.
    Marinate the meat in a solution of olive oil and vinegar sea salt, or according to a recipe of your preference.
    Marinate the meat in a solution of olive oil and vinegar sea salt, or according to a recipe of your preference. Place in the refrigerator for 10 - 24 hours to allow the meat absorb the flavor. This step is optional; the additional moisture can make dehydration take longer and the resulting jerky may be stickier. [You can also mix with soy sauce or soy sauce powder and paprika for a teriyaki taste] Brown sugar is a great addition.
  4. 4
    Coat the meat in the seasonings of your choice.
    Coat the meat in the seasonings of your choice.
    Coat the meat in the seasonings of your choice. Don't be afraid to use salt. Salt will aid in dehydrating.
  5. 5
    Dehydrate the meat. Leave enough room between pieces to allow air to flow around the meat. Avoid letting the meat separate if possible.

    • In a dehydrator, spray the racks with non-stick cooking spray and place your prepared meat on the racks.
      In a dehydrator, spray the racks with non-stick cooking spray and place your prepared meat on the racks.
      In a dehydrator, spray the racks with non-stick cooking spray and place your prepared meat on the racks.
    • In an oven, set the temperature to 165 degrees F (70 degrees C), any less may cause early spoilage as it not hot enough to kill bacteria in the meat, and will only incubate the bacteria already present in the meat, and allow it to preheat. (Heat is not intended to cook your jerky; gentle heat aids in the dehydration process by causing the moisture to evaporate.) Place your prepared meat on a wire rack.
  6. 6
    Wait and watch.
    Wait and watch.
    Wait and watch. Making jerky is a quick process. Since temperatures, humidity levels, and slice thickness will vary, there can be no set time for the process to complete. Usually it will take between 2 - 6 hours. Check the consistency of the jerky regularly after 6 hours until it meets your satisfaction. Cut into the jerky to ensure that it is not raw inside. Jerky should turn a deep brown or burgundy color.
  7. 7
    Place the fresh jerky in plastic bags and store in the refrigerator or freezer until ready to eat.
    Place the fresh jerky in plastic bags and store in the refrigerator or freezer until ready to eat.
    Place the fresh jerky in plastic bags and store in the refrigerator or freezer until ready to eat. Enjoy the homemade jerky within 2 weeks of its preparation.

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Edit Tips

  • If you wish to store your jerky for longer, use glass mason jars. Plastic bags tend to accumulate moisture which encourages the growth of bacteria. In jars, jerky can be kept for months.
  • Be swift. The meat should be dried as quickly as possible, to limit bacterial growth. Cutting the meat into thin slices dramatically shortens drying time. Placing the meat in a freezer for an hour or two before cutting will make it easier to cut thinly.
  • Do not allow the jerky to become too dry or it will become hard and unpleasant. It should be the consistency of rubber.
  • Traditionally, jerky was smoked or salted to preserve and flavor the meat at the same time.
  • Ideally, the jerky should be vacuum sealed in plastic with a pouch of oxygen absorber in order to retard spoilage, but this is not practical in most home situations.
  • For a vegetarian version of this, try using seitan (wheat protein) or marinated tofu.
  • Use liquid smoke and you will have the best jerky you have ever had. Only use a few drops, as it's very strongly flavored.
  • Try a soy sauce based marinade. Some excellent flavoring agents include Adobo seasoning, red pepper flakes, cayenne pepper, powdered ginger, sesame oil, cajun seasoning
  • When drying in an oven, keep the door open a few inches with a couple of wooden spoons. This help the drying process and helps prevent the jerky scalding before it is dry.
  • You can also buy home jerky making kits if you are unsure of the whole process.
  • Use 3/4 cup of soy sauce, 3.5 oz of liquid smoke, and 1/2 cup of brewed coffee for your marinade.

Edit Warnings

  • This is not commercial jerky and therefore does not contain preservatives. Please take proper precautions to preserve your jerky (i.e. refrigerate or freeze) and consume it promptly.
  • Sun drying can lead to spoilage, and you will have a difficult time keeping the insects away.

Edit Related wikiHows


Historical Origins of Food Preservation - National Center for Home Food Preservation | NCHFP Publications

National Center for Home Food Preservation | NCHFP Publications

Historical Origins of Food Preservation

Brian A. Nummer, Ph.D.
National Center for Home Food Preservation
May 2002



The astonishing fact about food preservation is that it permeated every culture at nearly every moment in time. To survive ancient man had to harness nature. In frozen climates he froze seal meat on the ice. In tropical climates he dried foods in the sun.

Food by its nature begins to spoil the moment it is harvested. Food preservation enabled ancient man to make roots and live in one place and form a community. He no longer had to consume the kill or harvest immediately, but could preserve some for later use. Each culture preserved their local food sources using the same basic methods of food preservation.

Another reason you shouldn’t go nuts on nuts - Chris Kresser

Another reason you shouldn’t go nuts on nuts

Another reason you shouldn’t go nuts on nuts

September 23, 2011 in Food & Nutrition | 88 comments

picture of mixed nuts

In a previous article1, I suggested that nut consumption should be limited or moderated because of the high levels of omega-6 fat many of them contain. But there’s another reason you shouldn’t make nuts a staple of your diet.

One of the main principles of the Paleo diet is to avoid eating grains and legumes because of the food toxins they contain. One of those toxins, phytic acid (a.k.a. phytate), is emphasized as one of the greatest offenders.

But what is often not mentioned in books or websites about the Paleo diet is that nuts are often as high or even higher in phytic acid than grains. In fact, nuts decrease iron absorption even more than wheat bread2. This is ironic because a lot of people on the Paleo diet – who go to great lengths to avoid food toxins – are chowing down nut like they’re going out of style.

What is phytic acid and why should we care?

Phytic acid is the storage form of phosphorus found in many plants, especially in the bran or hull of grains and in nuts and seeds. Although herbivores like cows and sheep can digest phytic acid, humans can’t. This is bad news because phytic acid strongly inhibits mineral absorption in adults3 – especially iron and zinc. Studies suggest that we absorb approximately 20 percent more zinc and 60 percent more magnesium from our food when phytic acid is absent4.

Phytic acid interferes with enzymes we need to digest our food, including pepsin, which is needed for the breakdown of proteins in the stomach, and amylase, which is required for the breakdown of starch. Phytic acid also inhibits the enzyme trypsin, which is needed for protein digestion in the small intestine.

As most people following a Paleo diet will probably have heard by now, diets high in phytate cause mineral deficiencies. For example, rickets and osteoporosis are common in societies where cereal grains are a staple part of the diet.5

How much phytic acid should you eat?

Before you go out and try to remove every last scrap of phytic acid from your diet, keep in mind that it’s likely humans can tolerate a small to moderate amount of phytic acid – in the range of 100 mg to 400 mg per day. According to Ramiel Nagel in his article “Living With Phytic Acid”6, the average phytate intake in the U.S. and the U.K. ranges between 631 and 746 mg per day; the average in Finland is 370 mg; in Italy it is 219 mg; and in Sweden a mere 180 mg per day.

If you’re on a Paleo diet you’re already avoiding some of the higher sources of phytic acid: grains and legumes like soy. But if you’re eating a lot of nuts and seeds – which a lot of Paleo folks do – you still might be exceeding the safe amount of phytic acid.

As you can see from the table below, 100 grams of almonds contains between 1,200 – 1,400 mg of phytic acid. 100g is about 3 ounces. That’s equal to a large handful. A handful of hazelnuts, which is further down on the list, would still exceed the recommended daily intake – and that’s assuming you’re not eating any other foods with phytic acid, which is not likely. Even the Paleo-beloved coconut has almost 400 mg of phytic acid per 100 gram serving.

[Disappointing side note for chocolate lovers: Raw unfermented cocoa beans and normal cocoa powder are extremely high in phytic acid. Processed chocolate may also contain significant levels.]

In milligrams per 100 grams of dry weight

Brazil nuts 1719
Cocoa powder 1684-1796
Oat flakes 1174
Almond 1138 – 1400
Walnut 982
Peanut roasted 952
Brown rice 840-990
Peanut ungerminated 821
Lentils 779
Peanut germinated 610
Hazelnuts 648 – 1000
Wild rice flour 634 – 752.5
Yam meal 637
Refried beans 622
Corn tortillas 448
Coconut 357
Corn 367
Entire coconut meat 270
White flour 258
White flour tortillas 123
Polished rice 11.5 – 66
Strawberries 12

Can you prepare nuts to make them safer to eat?

Unfortunately we don’t have much information on how to reduce phytic acid in nuts. However, we know that most traditional cultures often go to great lengths prior to consuming them.
According to Nagel7:

It is instructive to look at Native American preparation techniques for the hickory nut, which they used for oils. To extract the oil they parched the nuts until they cracked to pieces and then pounded them until they were as fine as coffee grounds. They were then put into boiling water and boiled for an hour or longer, until they cooked down to a kind of soup from which the oil was strained out through a cloth. The rest was thrown away. The oil could be used at once or poured into a vessel where it would keep a long time.50

By contrast, the Indians of California consumed acorn meal after a long period of soaking and rinsing, then pounding and cooking. Nuts and seeds in Central America were prepared by salt water soaking and dehydration in the sun, after which they were ground and cooked.

Modern evidence also suggests that at least some of the phytate can be broken down by soaking and roasting. The majority of this data indicates that soaking nuts for eighteen hours, dehydrating at very low temperatures (either in a food dehydrator or a low temperature oven), and then roasting or cooking the nuts would likely eliminate a large portion of the phytic acid.

Elanne and I have been preparing nuts like this for a few years, and I personally notice a huge difference in how I digest them. I used to have a heavy sensation in my stomach after eating nuts, but I don’t get that at all when I eat them after they’ve been prepared this way.

Another important thing to be aware of is that phytic acid levels are much higher in foods grown using modern high-phosphate fertilizers than those grown in natural compost.

So how many nuts should you eat?

The answer to that question depends on several factors:

  • Your overall health and mineral status
  • Your total intake of phytic acid from other foods
  • Whether you are soaking, dehydrating and roasting them nuts before consuming them

One of the biggest problems I see is with people following the GAPS or Specific Carbohydrate Diets, which are gut-healing protocols for people with serious digestive issues. Most GAPS and SCD recipe books emphasize using nut flour to make pancakes and baked goods. This is presumably because many people who adopt these diets find it hard to live without grains, legumes and any starch.

Unfortunately, nut flours have not been soaked and prepared properly, so they’re likely to be loaded with phytic acid. The same is true – I hate to say – for coconut flour, which is now all the rage in the Paleo/GAPS community. Soaking nut or coconut flour for 18 hours before using it can help, but it does change the texture significantly – which many find undesirable.

It’s also best to avoid most commercial nut butters, which are made with unsoaked nuts. However, some health food stores do carry brands of “raw, sprouted” nut butters that would presumably be safer to eat.

In the context of a diet that is low in phytic acid overall, and high in micronutrients like iron and calcium, a handful of nuts that have been properly prepared each day should not be a problem for most people. However, for more vulnerable populations – like those suffering from tooth decay, bone loss or mineral deficiencies, pregnant women, children under 6 years of age, or those with digestive malabsorption issues or serious illnesses – it’s best to consume as little phytic acid as possible.