Thursday, August 25, 2011

Finding New Ways With Elecampane




Elecampane is said to be the herb of the fairies and I have no doubt why. Playful and whimsical, it will take up a corner of your garden with it's majestic leaves and bright yellow bursts of flowers. 




I've been growing elecampane in my garden for a few years now. In the fall I harvest the roots to infuse in honey and make into tinctures and elixirs. 




Most people do not adore the taste of the roots. Pungent and bitter, it's strong enough to wipe out intestinal pests. 


I love how it can bring up congested stuck mucus in the chest, wonderful for that winter time crud. Infuse it in honey and the pungent bitter taste is mellowed. 





Elecampane root infused in honey


I also add it in small amounts to digestive blends. It's warmth and pungency can spicen up a digestive bitters blend. 


This year I was especially taken with the flowers. By the end of the season I will have had over fifty blooms on my towering plant. Every time I visit the elecampane I am struck by how voraciously the bees attack the blooms. Literally crawling on top of each other to find the sweetness below. 


I've always wondered about using elecampane flowers as medicine. Thomas Avery Garran tells me that the Chinese use the flowers of different Inula species. And sometimes species are interchangeable and sometimes they aren't. 


As my own mind was full of elecampane flower musings I started to hear other herbalists echo this query. Can we use the flowers? Are they similar to the roots? 




In herbalism some of the best ideas come from following our intuition so today I headed down to the garden with my harvest basket in hand to pick the brightest flowers I could find. 


I had to gently shoo away the bees since they busily buzzed over every bloom. 




Back home I stuffed the flowers into a small jar and covered with this everclear. 



In a few weeks I'll be able to report my initial thoughts on these elecampane flowers. 



Common name: Elecampane
Botanical name: Inula helenium
Family: Asteraceae
Parts used: Root in western herbalism, TCM uses the flower of various species
Plant Energetics: Stimulating, warming, aromatic
Tastes: Bitter, pungent with a little sweetness
Plant Actions: Stimulating diaphoretic, stimulating expectorant, carminative, vermicide
Use for: Colds and flus, fever with chills, bronchitis, intestinal parasites, stagnant or damp digestion, asthma, imbalanced intestinal flora


You can buy your own elecampane plant at Crimson Sage Nursery. They ship all over the US. 


You can buy dried elecampane root at your local apothecary or Mountain Rose Herbs


Try the dried root infused in port! 


Have you used elecampane flowers? Done any experimenting yourself lately? Please share!

Some Recent Meals

 This is a so-called 'century egg,' a Chinese invention.  They take raw duck eggs, pack them in in a mixture of clay, ash, salt, lime, and straw or rice hulls for several weeks to several months, depending on the method of processing.
 When you crack it open, you find that the white has turned gelatinous and black.
 They have a strong flavor.  I cut them into slices like below.  Inside you find that the yolk has turned blue-green, and semi-solid.  The alkalinity of the curing materials above raises the pH of the egg to 9 or more, causing changes in the egg proteins.
 I cut the egg into slices and put a few along with slices of an omelet on top of this miso soup that contained bok choy, bean sprouts, onions, and other vegetables.
On May 30 I had the plate below.  Egg omelet, two types of sweet potato, white potato, and a combination of steamed Asian greens.
On August 12, I had the meal below.  Two grass-fed beef burgers, one raw and one cooked, about 8 ounces total.  On the cooked burger, we had a sauce Tracy created from blended tofu and spices that made it look a lot like cheese.  I had a large sweet potato, a large ear of fresh corn, some cooked kale and onions, and a green salad with quick-pickled cucumbers that Tracy made atop.  To finish I had one of those quarters of a small watermelon.


 On August 22 my first feeding consisted of this bowl of fruit and nuts.  It contained a half banana, 9 grapes, an apricot, half a pint of raspberries, a plum, a quarter-cup of cashews, a quarter-cup of almonds, an a couple of tablespoonfuls of coconut flakes.


 A couple hours later, I had the plate below with about 4 ounces of leftover cod, a pile of kabocha winter squash, steamed kale with some carrot raisin salad atop, half an avocado, and some cole slaw.  The two photos have different dates because it changes date some time in the mid morning (apparently I didn't set it correctly and don't want to take time to fix it).
Later that same day I had  two plates of food.  The first has a ~4 ounce turkey burger under that pile of wilted onions (seasoned with cumin), more kale, slaw, olives, avocado, and green salad.  I ate this while waiting for our potatoes to steam.  Then I had the second plate:  another turkey burger and onions, and two steamed red potatoes with black pepper.  Then I had the bowl of blueberries and banana with coconut milk. 



Tuesday, August 23, 2011

My Ancestral Health Symposium Presentation


"Ancestral nutrition: An alternative approach" by Don Matesz, MA, MS from Ancestry on Vimeo.


You may need to attach speakers or earphones to your computer to hear the audio.

Due to time constraints, I was not able to go into details explaining how each of the items I pointed to as adaptations to a plant-based diet could prove maladaptive for a diet providing a major proportion of energy from meat or fat.   I will expand on one example here and leave the others for others to think through.

Humans as well as other primates have uric acid levels higher than other mammals due to knock-out of the uricase-coding gene at least 15 million years ago. [1] This appears to have occurred as an adaptation to several environmental factors including 1) high dietary vitamin C (which lowers uric acid),  2) low sodium intake, and 3) low dietary fat combined with high fructose intake. 

Elevated uric acid appears to have at least two adaptive functions in such a context:  1) It raises blood pressure in the face of very low sodium and very high potassium intake, and 2) it facilitates the conversion of fructose into fat for adipose storage when vitamin C intake declines (in autumn, when fruits contain more fructose and less vitamin C).

This human/primate feature has positive effects in the context of a diet low in sodium and dietary fat, but high in potassium and fructose. 

However, it is potentially maladaptive when dietary sodium, fructose, or meat increase, and dietary potassium and vitamin C decrease.

Meat typically has a K:Na ratio of ~5:1 or lower, whereas fruits (the presumed main foods of the common ancestor of humans and chimps) have so little sodium, that the ratio is 100:1 or more.   Therefore, simply switching from plant-based to meat-based, without any addition of granular salt, automatically results in a relatively high sodium intake, for an animal adapted to the reverse, a low sodium, high potassium diet.

In addition, meat provides purines, which feed into the production of uric acid.  Elevated serum uric acid can produce overt gout, but before it does that, it can promote general inflammation [2], and elevated uric acid has been linked to chronic heart failure and increased cardiovascular risk [3, 4], metabolic syndrome [5], and elevated blood pressure [6, 7].  It also appears that uric acid increases the storage of body fat [1]:

Specifically, uric acid causes mitochondrial dysfunction with specific effects to increase fat accumulation by both increasing fat synthesis and by blocking fat oxidation (Sánchez Lozada LG et al, manuscript in preparation). Indeed, acutely raising serum uric acid with a uricase inhibitor in rats will result in fat accumulation in the liver within 24 hours, and this is not observed if the rise in uric acid is prevented. Other studies have suggested effects of uric acid on blood pressure, insulin resistance, and adipocyte activation (28, 29). Indeed, Cheung et al recently reported that mice that cannot produce uric acid (XOR knockout mice) have a central defect in adipogenesis and fail to get fat (30).

Vitamin C reduces uric acid concentrations [8].  Therefore, low intake of vegetables and fruits rich in vitamin C, combined with high intake of meat and fat, may promote abnormal elevated uric acid levels and all of the disorders above.

Fructose also feeds the production of uric acid, and vitamin C blocks the undesirable effects of fructose (which explains why eating fruits has a different metabolic effect than eating refined sugars) [9].  In the ancient environment, when our ancestors had diets low in fat but high in fruit, the pathway that converts fructose to fat when vitamin C concentrations are low was adaptive.  In the fall, when wild fruits had an increase in fructose content and a decrease in vitamin C content, the liver converted a higher proportion of the fructose into fat to be stored as adipose, as a combination of insulation against colder weather and a supply of energy to draw on when food supplies declined through the winter.  In the modern environment with a high ratio of fructose to vitamin C, the same system is maladaptive, resulting in increased uric acid levels, body fat accumulation, inflammation, and metabolic syndrome.

So, human uric acid metabolism remains adapted to a diet with a high ratio of potassium to sodium, and a high ratio of vitamin C to fructose.  In the context of a high dietary ratio of animal protein and fat reducing vitamin C intake and the K:Na ratio and providing purines, this system will likely prove maladaptive for at least some individuals.  The imbalance can manifest in variety of ways: inflammation effects, metabolic changes, hypertension, increased cardiovascular disease risk, increased fat storage, gout, etc..

This then provides one example where the effect of meat consumption depends on the quantity and dietary context, as well as individual variation in uric acid metabolism.   The higher our ratio of meat and fat to vegetables and fruits, the lower our vitamin C intake and K:Na ratio, and the more purines we have feeding the production of uric acid.  Higher intakes of vegetables and fruits rich in vitamin C and potassium will tend to counter the effects of the purines and sodium, which will delay the appearance of symptoms and reduce their severity. 

If someone eats a diet containing a high proportion of animal protein but also includes a fairly large amount of vegetables and fruits, he or she may not see any adverse symptoms related to excess serum uric acid appear for a long period of time.  The context (high intake of fruits and vegetables) modifies the effect of the high meat intake.  Further, the body's ability to adapt to any stressor (e.g. excess serum uric acid) declines as exposure continues for a longer period of time.  The adverse effects creep in slowly, at a rate as noticable as hair growth, or become more noticable after she or he reduces produce intake, or some other factor (e.g. stress) reduces the body's ability to deal with the excessive uric acid, or, simply, the body's ability to deal with the excess uric acid declines due to long exposure to the overload.  As things change, the person naturally gravitates toward non-nutritive ingestive behaviors that tend to reduce the symptoms. 

For example, she has a premenstrual headache.  She doesn't immediately think, "Oh, this is due to the long accumulation of congesting effects of my diet."  Instead, she takes a nap, or an aspirin, gets relief, and goes on her way.  If another person notices a little extra inflammation in a chronic skin condition that naturally fluctuates anyway, he doesn't immediately think that his food caused this, instead he puts some soothing balm on it, or takes an anti-inflammatory, which reduces the discomfort enough that he loses interest in exploring it further.  The use of non-nutritive ingestive behaviors is evolved and hence the natural approach to discomfort:  We "take something for it"  because our species evolved to use non-nutritive ingestion as an integral part of dietary adaptation.  People start looking deeper only when the non-nutritive ingestive behaviors no longer control the discomfort adequately.  So small things so gradually turn into large things that we often don't figure things out until they have gotten very persistent and distracting of our attention.


Friday, August 12, 2011

Legumes: Neolithic or Not?

Some people have suggested that legumes are a relatively ‘new’ food in human diets, introduced only with agriculture, discordant with human biology, and causes of disease.   Some have raised concerns about a number of secondary plant compounds in legumes, especially isoflavones considered phytoestrogens.

I have decided to view human evolution in the larger context of primate evolution, because we share so many characteristics with other primates and have a genome 98 percent similar to that of our nearest relative, the chimpanzee.  Since modern humans eat legumes, and humans share a common ancestor with chimps, if modern chimps eat legumes, this would suggest that probably the last common ancestor of humans and chimps also ate legumes.

So I decided to find out, do modern wild chimps eat legumes? 

It only took a few internet searches to find that, indeed, non-human primates, including chimps, consume legume seeds, leaves, and flowers.

The most remarkable of the literature I have so far come across on this topic is a paper published in the American Journal of Primatology by Shoeninger, Moore, and Sept, entitled “Subsistence Strategies of Two “Savanna” Chimpanzee Populations: The Stable Isotope Evidence.” [1 pdf]  In this paper, the authors report on Ugalla chimps, living “in open, grassy woodland habitats similar to those in which the last common ancestor of apes and humans probably lived.”  These chimps consumed a diet very rich in fresh legumes, estimated at 50% of total food consumption, certainly a level requiring some level of physiological adaptation. 

This puts fresh legumes in a different class from grains.  So far as I know, we have no evidence of chimps consuming any significant amounts of immature grass seeds (grains).




Green Peas.  Source: Ecosalon
Based on this type of evidence, it seems probable that fresh legumes were part of hominoid diets for millions of years before the advent of agriculture.  This would give plenty of time for hominoid physiology to become adapted to regular intake of fresh legumes and their phytochemical constituents, and also provide an evolutionary pathway to the domestication of legumes.

I know many people feel worried about isoflavones with phytoestrogen properties affecting sexual development, function, and fertility.   They have the idea that plants produce these compounds to disrupt the fertility of animals consuming them.

It is easy to think of the herbivore as the enemy of the plants it consumes, and vice versa, but grazing herbivores provide water, nitrogen, and minerals to plants via saliva, urine, and feces deposited in the field while grazing.  Herbivore hooves also knead and soften the soil.   The plants receive many needed services from their ‘enemies,’  not the least of which is a supply of carbon dioxide, without which they can’t live.  The herbivores need the nutrients and oxygen the plants produce.  Food plants and animals using them form a yin-yang pair, complementary and opposite, but if antagonistic, both sides fail.

If a plant slightly limits the fertility of an animal grazing upon it, this actually serves the animal species.  Sure, some individuals may complain because they don't get the litters they want, but by keeping the animal numbers within limits, this reduces the chance that the animal population will overshoot its resource base and crash, while also increasing the amount of food/nutrients available for each individual animal, increasing the quality of life for the grazier.  The plant helps the animal maintain a sustainable population size, and by grazing, the animal helps the plant maintain a sustainable population size.   In the big picture, this is synergism, not antagonism.

The synergism and mutuality of plant-animal nutrition relationships is especially evident in human interactions with plants.  When humans like a plant, usually because the plant helps them thrive and reproduce,  the people take on the task of feeding, protecting, and promoting the reproduction of that plant.  Humans help plants that help humans thrive, so plants that help humans have become among the dominant plant species on the planet.

When thinking about evolutionary plant-animal interactions, I feel it is important to realize that organisms adapt not only to ‘beneficial’ but also to challenging aspects of their habitats, if given enough time. 

Let’s assume that at some point in the past, some herbivores were grazing on plants rich in phytoestrogens.  Let’s also assume that, initially, the herd grazing on these plants does have reduced fertility.  Nevertheless, within the herbivore herd a range of susceptibility to the phytoestrogens’ effects on fertility.  That is, some of the animals may be rendered completely infertile, some will have reduced fertility in varying degrees, some will have no reduction in fertility, and it is possible that in some animals the increase of phytoestrogens will actually increase fertility. 


If this process continues for several generations, gradually the animal population will move toward adaptation to the isoflavones.  The animals resistant to the anti-fertility effects of the isoflavones will have more offspring than those not resistant.   Eventually, the entire herd will have resistance to the effects of the typically encountered levels of isoflavones.  

Now, let’s suppose that the mechanism of action of the isoflavones is to reduce hormone levels in the animals.  In this situation, the animals resistant to the anti-fertility effects of these phytochemicals will be those who have an endogenous production of hormones high enough to counter the negative effects of the phytoestrogens.  Over several generations, the evolutionary result will be a species adapted to a phytochemical drain on its endogenous hormone production by virtue of a higher endogenous output of hormones to compensate for the losses induced by the phytochemical.

Now, if you take this species off of the diet to which it is adapted, removing or greatly reducing the ‘hormone disrupting’ phytochemicals, the animal’s usual hormonal output might be excessive.  As a consequence, the animal might develop disorders due to excessive levels of its own hormones.  Adding the phytochemicals back to its diet will reduce those hormone levels, producing a more balanced physiology, because the animal is genetically adapted to a diet containing chemicals that ‘disrupt’ its hormones.   It may actually need the ‘hormone disrupters’ to maintain hormone balance. 




Edamame.  Source:  Dried-edamame.com
I suggest that this may provide part of an evolutionary explanation for the growing body of research suggesting that consumption of legumes and other plant foods containing phytoestrogens may have positive effects on human health. 

I discussed here some research that supports the idea that plant-rich diets and specific whole plant foods can reduce the excessive sex hormone levels present in premature menarche, premenstrual symptoms, menstrual pain, polycystic ovary syndrome, hirsutism, menopausal syndrome, and reproductive system (breast, ovarian, etc.) cancers in women.

Tham et al of the Stanford Center for Research in Disease Prevention and the Department of Medicine discuss the growing evidence for potential health benefits of dietary isoflavones and lignans, two types of phytoestrogens  including prevention of cardiovascular disease, promoting bone health, and regulating hormone levels across the life cycle, in both men and women, to prevent sex hormone-linked reproductive system cancers. [2

World-wide patterns of human population growth seem to lend little support to the idea that phytoestrogens make people infertile.  Historically, growth rates have been luxuriant in nations consuming more plant-based diets (India, China, Asia in general) rich in phytoestrogens. 

Legume proteins may also have unique benefits.  For example, multiple studies have shown that substituting soy protein for animal protein might improve kidney function in type II diabetics with nephropathy [3, 4, 5, 6, 7, 8].  This may not be a property unique to soy, but an effect of legume protein versus animal protein, due to legume proteins having a different ratio of amino acids.  It certainly does not indicate lack of adaptation to legume proteins. 

I find it hard to fit this data into an picture of human evolution that considers legumes discordant with human biology, but it makes sense in a view that includes legumes among human ancestral foods. 
 
Lignans are another type of phytoestrogen.  As shown in this table, lignans occur in fruits and vegetables as well as seeds, nuts, legumes, and grains.  Although the seeds typically have the highest concentrations, sweet potatoes, carrots, asparagus, and garlic have levels comparable to pinto beans, peanuts, and several grains. 


Legumes like clover naturally occur in grasslands, and farmers grow clover as part of their pastures and fodder for ruminants.   Consequently, products from either pasture- or grain/legume-finished animals also can contain phytoestrogens, although in lesser amounts than in plants.  Hence, human ancestors probably would have gotten exposed to these compounds through eating wild game meat as well as plants.

Of course, as with every other item we ingest, dose and context affects outcome.  Nature never delivered isoflavones in concentrated pills or isolated legume proteins, absent counter-balancing compound present in the whole foods, nor did it give isoflavone-rich soy formula (based on soy protein isolate) to human infants.  Obviously, substituting soy infant formula for human breast milk is discordant with human biology.  

Now on to one of America's favorite beans.  



Coffee Bean.  Source: Whos3d3n

Did you know that coffee supplies the same isoflavones found in soybeans, albeit in smaller amounts? 


"This paper reports the isoflavone contents of roasted coffee beans and brews, as influenced by coffee species, roast degree, and brewing procedure. Total isoflavone level is 6-fold higher in robusta coffees than in arabica ones, mainly due to formononetin. During roasting, the content of isoflavones decreases, whereas their extractability increases (especially for formononetin). Total isoflavones in espresso coffee (30 mL) varied from 40 μg (100% arabica) to 285 μg (100% robusta), with long espressos (70 mL) attaining more than double isoflavones of short ones (20 mL). Espressos (30 mL) prepared from commercial blends contained average amounts of 6, 17, and 78 μg of genistein, daidzein, and formononetin, respectively. Comparison of different brewing methods revealed that espresso contained more isoflavones (170 μg/30 mL) than a cup of press-pot coffee (130 μg/60 mL), less than a mocha coffee (360 μg/60 mL), and amounts similar to those of a filtered coffee cup (180 μg/120 mL)."


Tuesday, August 9, 2011

The Ancestral Health Symposium

Last Thursday Tracy and I drove to L.A. from Phoenix so that we could participate in the Ancestral Health Symposium at UCLA.  I feel grateful that Aaron Blaisdell and Brent Pottenger invited me to speak at the conference nearly a year ago. They put together an awesome event.

We got a bit of a late start Thursday morning.  Mapquest says the drive takes a little over 6 hours.  We were right on track until we got to Pasadena and hit rush hour traffic at about 6 p.m.  It took something like an hour and a half to cover the last 20 miles.  At one point, we waited about 20 minutes just to traverse an exit from one road to another.  Welcome to L.A.!

We were hoping to arrive at Aaron's home shortly after the Thursday evening presenter gathering started but didn't get there until about 7:30 p.m.  The party was still in progress though we unfortunately missed a presentation by Denise Minger.

We were very hungry, having eaten very lightly since our pre-trip breakfast at about 9:30 that morning.  There were hardly any vegetables and fruits left, but they had some nice red wine, the first thing Tracy got for us, and they still had salmon and steaks on the grill.  After the wine, Tracy and I split a small steak, had a little salmon, and shared a small bowl of strawberries with new friends.

At the party and the symposium, I was pleased to meet people I previously knew only via electronic communication.  When I first walked in, I saw a young man I thought looked a little familiar, but couldn't place his face.  It was Stephan Guyenet, he put a name to my face before I could identify him.

Next I met Jimmy Moore in the kitchen while Tracy was getting the wine.    Next came Denise Minger (yes she is a real person, contrary to vegan myths), then Richard and Bea Nickoley, and Chris Masterjohn. I really enjoyed talking with Richard and Chris as Tracy and I waited for the food.  As the evening progressed, we met Rob Wolf, Mark Sisson, Loren Cordain, Paul and Shou-Ching Jaminet, Staffan Lindeberg, Gary Taubes, Mike and Mary Dan Eades, Seth Roberts, and Dr. BG

The next morning Tracy and I walked down 14 flights of stairs of the Palomar hotel then 15 minutes to the Ackerman hall on UCLA campus to check in.  There I was pleased to meet Doug McGuff.  I had in mind to ask him a question about some recent research I saw on retention of training effect from resistance training in older people, but got distracted because there was some problem finding Tracy's admission ticket in the electronic data base.  The kind fellow at the door waved at me, saying "Don, you're okay, come on in," but I said "not without Tracy." Fortunately I had brought the hard copy of the ticket.

Once in we went to the table to get our name tags, where we also met Rob Wolf's wife Nicki.  

After check in, we walked rapidly back to the hotel to change our clothes.  We were right on time to get to other presentations, until we got to the parking kiosk.  The attendant tried to show me on a map how to get to the only lot still having empty spots.  I thought I had it, but the UCLA roads were under construction and not well marked, so I couldn't really follow the map.  I got lost at some turn, and ended up at a lot for student dorms, a ways from the Ackerman hall.  We asked some one for re-directions, which again were difficult to follow because of the construction.  We found some students who finally gave us directions that took us off campus for a short drive, circumventing the construction, and found the lot. Unfortunately, by that time we had missed Loren Cordain's presentation.

We finally got to the hall shortly before Staffan Lindeberg gave his presentation on his work with the Kitavans.  Well worth watching.  I wanted to ask him a question, but I had to leave before the end of his presentation in order to get to the other hall where I was scheduled to speak.  I got the impression that he said his team has found no Kitavans on their native diet with atheroma, and apparently no one has found atheroma in any wild animal living on its native diet.  This contrasts with some human tribes, such as the Masai, who have extensive, although apparently stable atherosclerosis.  I found this supportive of my developing ideas on human dietary adaptation. 

I did my presentation Friday morning at ~11 a.m.:  Ancestral Nutrition: An Alternative Approach.  When the video link is available I will let you all know.  It seemed well received.

At my presentation, and later, we were glad to see our friends from Phoenix, Marty Wilson (Ecotone Wellness), Cathy Pisano and Karen Marco (Fooditude), and Keven Kula (Ready State Fitness).

After my presentation, there was a lunch break, but most of it I spent talking with people who had questions after my presentation.  Then we went back to the main hall for an interview, which didn't happen during the break because we couldn't find the video camera guy.  He appeared with the camera just before Stephan started his presentation.  I was very sorry to miss it.   The interviewers, Tess and Alyssa, the Planetary Girl, spent the length of Stephan's  presentation interviewing me, very interested in my approach to paleo, sustainability, and perspective on adjusting dietary proportions to male vs female metabolism using an evolutionary context.

After the interview we attended Linda Frasseto's talk on her work using paleo diet, one of the few clinical studies on paleo diet published in peer-reviewed literature.  Her paleo diet approach was very high in plant foods to supply, if I remember correctly, a ~12g/d intake of potassium and a 12:1 K:Na ratio.  It produced some remarkable improvements in metabolism and blood pressure, but was more effective in salt-sensitive individuals than in 'normal' people.  Since the diet she used improved insulin function,  I asked her if she knew of any research connecting K:Na ratio to insulin function.  She did not, but Loren Cordain said he did.  I will follow up on that.

By the way, her version of 'paleo' was 45% carbohydrate and much of that from carrot juice (essentially simple sugars), and only 30% fat.  She also worked to keep the caloric intake up at maintenance levels, which was difficult according to her report.  It was among the facts that got me thinking again, there is no universal application of 'paleo' diet (just as there is no universal vegetarian diet).   In contrast to her study, this one produced a 'paleo' diet that was low in calories (1445 on average), 24% protein, 39% fat, and 32% carbohydrate.  This might be fine for people wanting to lose weight, but we can't assume that this diet will have identical or beneficial effects for someone maintaining weight and eating 2500 calories per day, because increasing caloric intake at the same proportions will result in greater absolute intakes of fat, protein, and carbs.  Especially in the case of protein, the more you eat, the more toxic waste you produce (acids, ammonia and urea), which puts additional burden on detoxification systems.

One of the challenges I had with meat-based, low-carb paleo revolved around how to get 2500 calories daily without eating above 25% carbohydrate.  The nub for me involved the nausea and appetite loss that I would get whenever eating a large amount of fat.  Sometimes I would get such bloating and discomfort from high fat meals that I would  be unable to eat much but fruit and juice for a couple of days, completely negating the temporary increased caloric intake I got from the extra fat. This is an accepted effect of high fat meals (even Peter at Hyperlipid mentions it fairly often), not unique to me, which some might consider a benefit for people trying to limit energy intake, but it is certainly undesirable when it prevents adequate energy intake. At one point I decided to try drinking milk to fill in the calorie gap, adopting a 'pastoral' diet, despite my previous experience that milk increased my sinus congestion and allergy difficulties, hoping that in the context of a grain-free diet, milk would have a different effect on me.  Alas, it did not.

We had to leave the symposium shortly after that because we were hungry and had to drive back to Phoenix, because Saturday I started teaching at Phoenix Institute of Herbal Medicine and Acupuncture.

But before we left, we had another chance to chat with Richard Nickoley and Bea.  We also met Erwan LaCorre of MovNat, and a few people who follow my blog. 

Before leaving we went down stairs to the student food concession.  We got a grilled chicken salad and an order of black beans from a Rubios concession. 

I was sorry to have to leave early and miss the presentations given on Saturday.  We had a wonderful time and look forward to the next opportunity to participate.  Thanks again to Aaron Blaisdell and Brent Pottenger, and the dozens of volunteers who pulled this off.





Thursday, August 4, 2011

Follow-up on Farewell to Paleo, and Comments on Confirmation Bias

Seems that many people did not understand my Farewell to Paleo post.

I wrote that blog after ~14 y of tinkering with paleo principles under the common assumption that we (humans) are fully adapted to a meat-based diet, i.e. that a 'paleodiet' should supply most of its energy and protein from meat and fat.

My experience didn't confirm this belief.  Tracy and I, and many of my clients and students,  had increasing problems with inflammation, accumulation, congestion and stagnation while eating a meat-based diet supplying ~50-60 percent of calories as fat, despite avoiding the dreaded neolithic foods and also eating a large amount of produce.

It seems paleo has for many people become synonomous with meat-based, high-fat nutrition, and so many 'paleo' and 'primal' people are also endorsing and including processed meats (bacon, sausages, etc.) or dairy products (cream, butter, etc.), that it has become little more than a kind of rehashed Atkins.

I regret having contributed to that.

It is to that 'paleo' that I said good bye.

After looking at research ignored by advocates of meat-based and high-fat nutrition, thinking things through, and experimenting a bit, I now have a different understanding of paleo diet.  I leave the details for the follow-up on the Ancestral Health Symposium.

For now, in case you didn't notice, people in the media have already pegged 'paleo' as rehashed Atkins in the 'caveman diet' guise.  If anything will destroy paleo, it is this.

Now, I have also noticed that people in the paleosphere have taken to accusing me of confirmation bias.  I find that very rich indeed.


Confirmation bias means only seeing evidence that supports your beliefs, and not seeing evidence that contradicts your beliefs.




In the paleo- and low-carbo- spheres, confirmation bias looks like this:









  • Only focusing attention on or considering as important those physiological features that make humans different from other primates, and ignoring the many nutrition-related physiological features that humans share with other primates.
  • Only seeing/accepting evidence that meat-eating has benefits, while ignoring, refusing to accept, or denying good evidence that meat-eating can in some quantities and contexts be harmful.
  • Only seeing/accepting evidence that saturated fats are neutral or beneficial, refusing to accept good evidence that excess dietary SFs have harmful effects in certain quantities and contexts.
  • Only seeing/accepting evidence that unsaturated fats are harmful, while ignoring contrary evidence.
  • Only seeing/accepting evidence for the positive effects of cholesterol, while ignoring a mountain of contrary evidence showing adverse effects of excess dietary and serum cholesterol.
  • Only seeeing/accepting evidence that grains and legumes are harmful, refusing to acknowledge evidence that they can be neutral or beneficial.
  • Only seeing/accepting evidence that 'vegetables are useless or unnecessary,' while refusing to acknowledge evidence that they have benefits.
  • Only seeing/accepting evidence of potential harm from eating nuts (e.g. so-called antinutrients), while ignoring or belittling evidence that they provide benefits.
And so on.

I was caught up in that confirmation bias for quite a while.

But as I have increasingly broken away from it, and written blogs discussing evidence contradictory to the popular 'paleodiet' and high-fat/low-carb perspectives, I get attacked for confirmation bias?

It reminds me of the old adage:  When you point a finger at someone else, you have several pointing back at yourself.

As I said in the 'Farewell to Paleo' post, I said farewell after tolerating cognitive dissonance for too many years. 

I forgot to write that I came to meat-based 'paleo' diet after ~14 years eating a primarily vegetarian, grain-based, macrobiotic diet.  That diet, combined with herbal medicine, had provided me with many health benefits, not the least of which being control of my constitutional tendency to respiratory allergies and inflammatory skin conditions (diagnosed as eczema and psoriasis, labels I don't necessarily accept).

As a graduate of the American Academy of Nutrition, and after 14 years as a vegetarian, I could martial plenty of evidence for a vegetarian, low-fat diet.  When I encountered the evidence for meat-based 'paleo' I of course found it was totally contrary to my expectations,  but after serious consideration it appeared strong enough to me that I could no longer ignore it, so I switched from macrobiotic to meat-based, intellectually convinced that the change might improve my health even further than I had gotten with macrobiotics.

I'm not one to try things lightly then dismiss them.  If I think 'paleo' should work, and I find glitches, I will go back to re-evaluate the basics.  If I still think the basic plan is correct, I will try some adjustment within the framework, like decreasing protein and increasing fat, or some other.  I might be stubborn, but I don't give up on what I think is correct until I seem to have exhausted all possible variations, OR I notice that I am ignoring evidence that the basic plan has some important flaw.

When I see evidence contrary to my expectations repeatedly coming to my attention, I can't keep ignoring it, or explaining it away, to satisfy my preconceptions.

In my life, not only me, but people I love were putting into practice the ideas that increasing intake of meat and saturated fat will improve health, and they were suffering:  Gaining body fat, rising blood lipids, congestion, malaise, low energy, etc.

Meanwhile, I could no longer ignore or consider invalid all of the literally thousands of epidemiological, clinical, and animal studies linking modern degenerative diseases to excessive intake of meat and fats, including saturated fats, in modern nations.

Nor could I continue to ignore or belittle all of the hundreds of well-designed studies showing positive health effects of increasing the plant: animal ratio or particular plant components of modern diets.

And that's why I finally said farewell to meat-based, high-fat 'paleo.'   I just couldn't keep ignoring evidence hitting me in the face, contradicting my belief that a diet providing a high proportion of energy from meat and fat  promotes health.

I could no longer accept a flat earth, when the evidence for a sphere hit me in the face.


Which led me to realize, that if the paleo principle is correct, there must be some evidence for strong human adaptation to plant-based diets that the meat-based paleo crowd has either overlooked or ignored.

And I think I have found that evidence.  

Its complicated.  The effect of any nutrient or food on human health depends on quality, quantity, and context of consumption. 

I can no longer allow myself to fall into simplistic thinking like  'meat good, grains bad,' 'fats good, carbs bad,' and such. 

Meat can have benefits in some quantities, qualities, and contexts, and cause harm in other quantities, qualities, and contexts.

Ditto for fats, carbs, grains, everything.

Done with nutritional dualism. 

Everything is relative.

Anything can be medicine or poison, depending on quality, quantity, and context.

Monday, August 1, 2011

Ancestral Nutrition: An Alternative Approach

I gave that title to the talk I will give at the Ancestral Health Symposium this Friday morning at UCLA.

I wrote this description of it:


For about 65 million years our primate ancestors consumed plant-dominated diets. Humans developed the technological ability to consume meat-based diets only within the last 2 million years, so at least 98 percent of the evolution producing our basic primate physiology occurred before humans could obtain meat-based diets.
Condensing the 65 million years of primate evolution into a 24 hour period, our ancestral diet was plant-based for at least 23 hours and 30 minutes, and animal-based diets emerged only within the last 30 minutes.

Ninety-eight percent of the human genome is identical to the nearest primate relative, chimpanzees, who eat a 95 percent plant diet.  Recent hunter-gatherers consume up to 20 times more meat than chimpanzees on a percent energy basis, a substantial deviation from the primate baseline.     

Similar to other primates, humans retain many physiological and behavioral features displaying adaptation to a plant-based diet, some of which are potentially maladaptive for diets supplying a high proportion of energy from meat, fat, or refined carbohydrates.  Recent hunter-gatherers and pastoralists appear protected from maladaptive responses to animal-based diets by their baseline body composition, ecological context, low total energy intake, and evolved non-nutritive ingestive behaviors. 

Modern people adopting meat-based ‘paleo-facsimile” diets may differ from recent hunter-gatherers in lifetime caloric balance, body composition, ecological context, and non-nutritive ingestive behaviors.   By comparing hunter-gatherers and modern people, I show how the quality, quantity, and context of meat consumption will affect the outcome for any individual. 

Plant and animal foods generally have opposite yet complementary nutritional characteristics.  I present an integration of Chinese medical yin-yang theory with Western nutrition that can enable us to understand the relation each type of food (plant or animal) to modern diseases of deficiency or excess,  and can help guide us to identify an appropriate dietary plant-animal ratio for any individual.
 Time permitting, I plan to post a preview sometime later this week, and after the symposium, I will present the lecture in blog form.