Category Archives: Food

PHD Baby Food

Posted by on August 31, 2015 80 comments

Before I get to the recipe, let me play proud papa for a few minutes, and share with you an episode with Luke this weekend that illustrates his spirit and character. I mentioned last week that he had started walking. However, as recently as his birthday, last Thursday, we thought it was impressive if he strung together 20 steps at a time. This weekend, coming out of church Saturday evening, he demanded to be allowed out of my arms to walk. He proceeded to walk almost the entirety of the 3/4 miles home. Here is a short section of his journey; he was already 10 minutes in and starting to get tired:

You can see him refusing any support from me – he wanted to do it all himself – and grinning at his new skill.

It was inevitable that he would take a tumble at some point, and soon after we stopped recording he did. He tripped and landed on all fours, just as in the video; but then he tried to launch himself back to his feet by sheer strength of arms, and didn’t quite make it all the way up. His head came back down first and he got a cut and bump on his forehead. I picked him up and he cried for 10 seconds or so; after 20 seconds he was smiling again:

Luke after fall while walking Aug 30 2015 02

Just seconds after this photo was taken, he demanded to be let back down to the ground, and proceeded to walk the rest of the way home, grinning. When we reached home, he complained at being taken indoors. Nevertheless, he was tired. Forty minutes later, he was asleep, and slept 11 hours.

OK, back to food. When Luke was age 6 months or so, we introduced him to solid food through this recipe. It is essentially a PHD meal suitable for infants, puréed with a blender. As is suitable for a baby, the “baby meal” has less protein and more carbs and fat than would an adult meal.

At first we mixed the purée into his milk. Luke soon came to love this “PHD milk” and started to refuse plain milk. Here he is enjoying his favorite meal:

Lukemilk-08 vfullHe also loves the baby food by itself. When we make it, we give him the mixing bowl and spoon, and he finishes everything eagerly (making a mess along the way).

One note on ingredients. We recommend here that the meat be a mix of beef liver, oysters, salmon, and scallops.However, there’s no need to obtain all of these ingredients for every batch. It is fine to make a batch with one, then the next with another, then the next week with a third. Just balance the proportions over time. Instead of 5 g of each every week, get 20 g of each in over 4 weeks, in whatever fashion is most convenient for you.

A note on allergy risk: There have been some concerns that early introduction of shellfish could pose a heightened risk of allergy. The issue is discussed here. However, evidence has been piling in pointing the other way — that earlier introduction of potentially allergenic foods reduces the risk of allergy. More evidence. Since 2008, earlier introduction of allergenic solid foods has been the recommendation of the American Academy of Pediatrics. Current recommendations can be found here.

Nutritionally, this mix is not perfect, but it’s impossible to make a perfect baby food using natural whole foods. For example, breast milk has a higher zinc content than any natural whole food. Therefore, mixing in a few supplements, such as zinc and vitamin K and pantothenic acid, is a reasonable tactic.

[Further note: If you’re viewing this on the main page, click here to see the recipe.]

The Virtues of Spicy Food

Posted by on August 6, 2015 31 comments

I’ve been blogging recently about gut health, and emphasizing that an impaired gut often leads to systemic diseases (“Disease Begins in the Mucus,” June 23, 2015).

Impairment of the gut most commonly comes from (or is associated with) infections, or what amounts to the same thing, microbial overgrowth. Small intestinal bacterial overgrowth (SIBO) is a very common disorder, afflicting about 5% of younger adults and 15% of older adults. [1]

If SIBO is a precursor to systemic diseases, then any intervention that clears germs from the small intestine should help prevent disease.

Spices: A Natural and Beneficial Antibiotic

The traditional cooking spices, such as onions, garlic, and ginger, are all antimicrobial. [3] So if clearing microbes out of the small intestine is important for health, then eating spicy food should be a good thing. The hotter, perhaps, the better: the hottest spice, chili peppers, are known for their antimicrobial and antiviral properties. [4]

But how large are the benefits of including spices on food? Evidence toward an answer comes from a new study out of China [2] using the China Kadoorie Biobank database. The study asked 487,000 people at baseline, “During the past month, about how often did you eat hot spicy foods?” Then it tracked their health outcomes for 7 years and analyzed death rates as a function of the number of spicy meals consumed per week. In this case, “hot spicy foods” means meals with chili peppers or chili oil.

Interestingly, the mortality benefits of spicing food were large. Here’s a table showing the relative risk of dying from various causes, as a function of chili pepper consumption:

  No spicy meals Spices eaten 1-2 days per week Spices eaten 3-5 days per week Spices eaten 6-7 days per week
Death from all causes 1.00 0.90 0.85 0.83
Death from cancer 1.00 0.96 1.01 0.95
Death from heart disease 1.00 0.83 0.75 0.73
Death from diabetes 1.00 0.77 0.46 0.59
Death from respiratory disease 1.00 0.60 0.59 0.57
Death from infections 1.00 0.87 0.68 0.71
Death from all other causes 1.00 0.90 0.89 0.81

The biggest benefits were for diabetes and respiratory disease, then infectious disease and heart disease. This makes sense:

  • Diabetes is probably often caused by small intestinal infections that spread to the pancreas.
  • Respiratory pathogens infect the mouth and throat, where food spices can kill them; also, they are frequently swallowed, after which they can infect the gut as well.
  • Systemic diseases often enter the body through the gut, so anything that clears pathogens from the gut will reduce infectious disease.
  • Heart disease is also known to have a major infectious component.

In the subgroup analyses, there were some interesting correlations. Here’s Figure 2 from the paper:

virtue_of_spices01

The interesting thing here is that alcohol consumption eliminates the benefits of chili pepper consumption. Alcohol intake is a known cause of SIBO [1], and possibly the alcohol is removing the beneficial effects of the chili peppers.

Another interesting finding was that fresh chili pepper seemed to be more protective than dried chili pepper or chili oil. Probably there are more bioactive and antimicrobial compounds in the fresh peppers.

Neurotoxicity: Pro or Con?

The study authors note that capsaicin in chili peppers has complex biological effects. So it’s possible that not all the benefits of chili peppers were due to antimicrobial action in the small intestine.

Razib Khan, tongue in cheek, suggests another possibility: maybe chili peppers kill off the neurons of the gut. Capsaicin is a ligand for the pain receptor TRPV1 on neurons; this is why eating hot chilis can be painful. In high doses, capsaicin can actually kill neurons. [5]

Now, it happens that TRPV1 knockout mice live 14% longer than wild type mice [6]. If capsaicin could kill off the TRPV1-positive neurons, then maybe the effect on longevity would be the same as in the knockout mice, who have the neurons but not TRPV1.

Entertaining as this idea is, it would require massive chili pepper consumption. Rats lost neurons after intraperiotoneal injection of 125 mg capsaicin per kg body weight, equivalent to 10 g in humans [5]. Since pure capsaicin has a rating of 16,000,000 on the Scoville scale, ten times hotter than the hottest known pepper, this would be like taking 100 grams of the Carolina Reaper, 600 grams per day of habanero chilis, 6000 grams of serrano peppers, or 60,000 grams of jalapeño peppers. I don’t know about you but I would rather not eat a hundred pounds of jalapeño peppers, at least not at one sitting.

Another consideration is that the chili consumption would have to be sustained. Capsaicin can kill neurons, but if you stop eating the chilis, the neurons come back. [5] [7]

More fundamentally, the neurons of the gut are crucial for digestion, gut motility, and tissue healing. Losing those neurons would itself be a potential cause of SIBO and all the diseases against which chili peppers are protective.

Conclusion

Killing off neurons seems an unlikely path to health; nor is it likely a good thing to make your soup so spicy that it burns a hole in your stomach, as happened to one Chinese man.

The best course, it appears, is to eat chili peppers, but in moderation. Nearly all the benefits are obtained with a couple of hot and spicy meals per week.

Reminder: The Perfect Health Retreat

The October Perfect Health Retreat, taking place October 10-17, still has spots remaining. If you’d like to learn PHD home cooking from Shou-Ching, the science of good health from me, and a course in movement and relaxation from our star trainers Court Wing and Jae Chung, plus health coaching from me, while enjoying a delightful time on a magnificent beach and luxury property with hot tubs and pools, come to the retreat!

For more information, see our web pages or write me at paul@perfecthealthretreat.com.
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References

[1] Dukowicz AC, Lacy BE, Levine GM. Small intestinal bacterial overgrowth: a comprehensive review. Gastroenterol Hepatol (N Y). 2007 Feb;3(2):112-22. http://pmid.us/21960820/.

[2] Lv J et al. Consumption of spicy foods and total and cause specific mortality: population based cohort study. BMJ 2015;351:h3942. Full text: http://www.bmj.com/content/bmj/351/bmj.h3942.full.pdf.

[3] Sherman PW, Billing J. Darwinian Gastronomy: Why We Use Spices. BioScience 49(6) June 1999: 453-463. http://www.nbb.cornell.edu/neurobio/BioNB427/READINGS/ShermanBilling1999.pdf.

[4] Khan FA, Mahmood T, Ali M, Saeed A, Maalik A. Pharmacological importance of an ethnobotanical plant: Capsicum annuum L. Nat Prod Res. 2014;28(16):1267-74. http://pmid.us/24650229.

[5] Czaja K, Burns GA, Ritter RC. Capsaicin-induced neuronal death and proliferation of the primary sensory neurons located in the nodose ganglia of adult rats. Neuroscience. 2008 Jun 23;154(2):621-30. http://pmid.us/18456414.

[6] Riera CE et al. TRPV1 pain receptors regulate longevity and metabolism by neuropeptide signaling. Cell. 2014 May 22;157(5):1023-36. http://pmid.us/24855942.

[7] Gallaher ZR, Johnston ST, Czaja K. Neural proliferation in the dorsal root ganglia of the adult rat following capsaicin-induced neuronal death. J Comp Neurol. 2014 Oct 1;522(14):3295-307. http://pmid.us/24700150.

 

Neu5gc, Red Meat, and Human Disease: Part I

Posted by on January 14, 2015 47 comments

A number of people asked for comments on the most recent red meat scare, including Nicole, Ryan, and Mishkin on the blog, JT Olds on Twitter, and others on Facebook. You probably saw some of the headlines:

The article Nicole linked is a bit more scientifically inclined: “Possible Link Between Red Meat Consumption And Increased Cancer Risk Identified” (IFL Science). Here’s the press release version from UCSD: “Sugar Molecule Links Red Meat Consumption and Elevated Cancer Risk in Mice”. In the blogosphere, Stephan has summarized the issue in the context of a post on red meat and cancer.

The headlines are based on a paper [01] that reported that, in mice genetically altered to lack a sugar (Neu5gc) that humans also lack, feeding Neu5gc and injecting anti-Neu5gc antibodies generates inflammation which can promote the growth of cancers.

Significance of Neu5gc

The paper itself is a rather artificial scenario whose significance will be determined by future work. So analyzing this single paper would not be interesting. But I think it’s worthwhile to look into the broader idea that eating Neu5gc-bearing meats might be inflammatory or a source of autoimmunity.

In terms of PHD recommendations, this could affect the relative emphasis we place on different meats. If Neu5Gc is a true health risk, then we would want to emphasize seafood more and red meat less.

Another benefit to thinking about Neu5gc is that it may give us some insight into what a PHD “autoimmune protocol” should look like.

Background: Evolutionary History of Neu5gc

All cells in multicellular organisms are coated in carbohydrates, and the carbohydrates terminate in one of 43 sialic acids. In mammals, two forms of predominate: Neu5Ac and Neu5Gc. Each mammalian cell has tens or hundreds of millions of molecules of Neu5Ac and Neu5Gc on its surface. [02]

Neu5Gc is made from Neu5Ac, but the gene for making Neu5Gc was inactivated in the human lineage shortly before the emergence of Homo. The mutation occurred 3.2 million years ago and reached fixation – that is, all ancestral hominids had come to have the mutated gene – 2.9 million years ago. [03] This very rapid fixation indicates there was strong selection in support of the mutation.

In fact, this mutation by itself may have led to a speciation event, after which our ancestors could no longer mate with other apes. From that point on, Neu5gc-less females had difficulty producing children with males who retained the Neu5gc gene, because they would form antibodies against Neu5gc-coated sperm, making fertilization unlikely. [04]

Why was losing Neu5gc selected in our ancestors? Two possibilities are likely:

  • Loss of Neu5gc improved brain function.
  • Loss of Neu5gc (temporarily) reduced vulnerability to (ancestral) pathogens.

It should be noted that Neu5Gc has been lost independently in some other mammals as well – ferrets and new world monkeys. New world monkeys such as capuchins and spider monkeys also experienced a brain expansion, and ferrets are notably smart, so either explanation might be relevant to these cases of “convergent evolution.”

Neu5gc and Brain Function

Carbohydrates are extremely important for intercellular interactions. Indeed, the incorporation of carbohydrates into cell membranes and extracellular matrix is what made possible the rise of multicellular life.

In no organ are intercellular interactions as complex or consequential as in the brain. Not surprisingly, then, carbohydrates including the sialic acids are important to brain function.

The human brain is extraordinarly rich in sialic acids: neural membranes have 20 times more sialic acids than membranes of other human cell types. Animal brains are also enriched in sialic acids relative to their other tissues, but not as much as in humans; the human brain has 2-4 times more sialic acids the brains of other mammals. [05]

Curiously, though, Neu5gc is rare in the brains of all animals. Neu5gc is strongly suppressed, by about 98%, in the brains of all vertebrates, suggesting that its presence inhibits brain function. [06] It appears that Neu5gc is somehow toxic to brain function.

Loss of the gene for Neu5gc completely eliminated Neu5gc from the hominid brain. If Neu5gc does impair brain function, mutational inactivation of Neu5gc would have improved brain function. If so, the mutational inactivation of Neu5gc could have been driven by the same evolutionary forces that, soon after, selected for the tremendous expansion of the hominid brain.

Incidentally, dietary sialic acids — except for Neu5Gc – appear to be nutritious for humans, and especially for the developing infant brain. Breast milk is exceptionally rich in sialic acids, almost all of it Neu5Ac. Formula, by contrast, has much lower levels of sialic acids (0.21 mmol/L compared to 3.72 mmol/L in breast milk). Breast fed infants have nearly twice as many sialic acids in saliva than formula fed infants, confirming that milk sialic acids are taken up by the body and utilized.

Animal studies show that sialic acids in breast milk nourish the brain. Sialic acids facilitate neurotransmission between neurons. When piglet milk is supplemented with sialic acids, brain sialic acid levels are increased, and the piglets learn faster and make fewer mistakes in maze tests. [05] Rodents also perform better on tests of learning and memory after sialic acid supplementation. [07]

Not only does formula have fewer sialic acids than breast milk, cow milk based formulas have some Neu5Gc. [05] It has been observed that formula-fed infants have lower IQs than breast-fed infants. Sialic acids might help explain that. The lack of nourishing Neu5Ac and the presence of toxic Neu5Gc in formula might lastingly impair brain function in formula-fed infants.

Neu5Gc and Infection Risk

As the outermost molecules in the carbohydrate coat surrounding cells, sialic acids are the first contact point for pathogens seeking entry to the cell, and for immune cells seeking to detect whether the cell is native or foreign.

There has been a “Red Queen” evolutionary arms race in which pathogens evolved ways to utilize sialic acids for cell entry, or to hide from the immune system; and animals evolved changes to their sialic acids to frustrate the pathogens. [08]

Many pathogens interact with sialic acids in order to adhere to and gain entry into the cell. Pathogens generally rely on a single specific endocytic route for cell entry. This often requires binding to a specific sialic acid as the initial point of attachment.

Pathogens that specifically utilize Neu5Gc to enter cells include canine and feline parvoviruses [09]; pathogens that specifically utilize Neu5Ac include adeno-associated viruses and the minute virus of mice (MVM) [10].

A human pathogen that uses sialic acids to enter cells is the malaria protozoan. Plasmodium falciparum causes severe disease in humans and enters cells via Neu5Ac; Plasmodium reichenowi causes milder disease in chimpanzees and gorillas and enters cells via Neu5Gc. Plasmodium falciparum appears to have evolved recently – possibly reaching its current form only 10,000 years ago when the rise of agriculture and animal husbandry brought humans and mosquitos into closer proximity – while Plasmodium reichenowi is thought to resemble the ancestral form that would have afflicted hominids and apes 3.5 million years ago.

Possibly, the gene for Neu5Gc was inactivated to protect ancestral hominids from malaria. With the loss of Neu5Gc, hominids would have become immune to P. reichenowi. [11] [12]

Unfortunately, after P. falciparum’s adaptation to Neu5Ac which is overabundant in humans, we now suffer from more severe malaria than chimpanzees or gorillas (the “malignant malaria” mystery). [13]

In addition to entry points for microbes, sialic acids can be entry points for microbial toxins. For example, Shiga toxin from shigatoxigenic E. coli binds to Neu5Gc. [14]

Sialic Acid Concealment and the Gut Microbiome

The immune system is sensitive to the composition of the carbohydrate coat on a cell. White blood cells have a number of sialic acid detectors on their surfaces (called Siglecs, for sialic acid Ig-superfamily lectins). Some, which bind to human sialic acids, inhibit immune responses. Others, which bind to non-human sialic acids, activate immune responses.

Thus, when white blood cells contact a cell bearing human sialic acids, the immune system interprets it as “self” and tamps down immunity. When it detects foreign sialic acids, the immune system treats the cell as “foreign” and is more likely to attack it.

Some microbes – including commensal gut microbes – have been living in humans long enough that they have learned to take up sialic acids, chiefly Neu5Ac, and incorporate them into lipopolysaccharides on their cell membranes. This suppresses immunity toward them. [15]

A number of human pathogens have learned the same trick. Pathogens that incorporate sialic Neu5Ac into their cell membranes for the purpose of mimicking human cells and evading human immune defenses include Escherichia coli K1, Haemophilus influenzae, Pasteurella multocida, Neisseria spp., Campylobacter jejuni and Streptococcus agalactiae. [16]

Due to this “molecular mimickry” of human molecules, it has been suggested that these bacteria – especially Haemophilus influenzae and Neisseria spp. – may be sources of autoimmunity. [17]

While some bacteria can synthesize sialic acids themselves, most obtain it from their environment. These bacteria release enzymes called sialidases to cleave the sialic acids from food in the digestive tract, from surrounding cells, or from mucus. [15] Bacteria can obtain Neu5Ac from human tissue and mucus as well as food, but Neu5Gc only from food, chiefly beef and pork.

Neu5Gc in Human Tissue

Although humans can no longer synthesize Neu5Gc, we still have all the cellular machinery for utilizing it. When dietary Neu5Gc is absorbed into the body and enters cells, it can be incorporated into glycoproteins bound for the cell surface glycocalyx, just as Neu5Ac is.

As a result, Neu5Gc of dietary origin appears at low levels on the surface of human cells.

Neu5gc is found at high levels in all mammals except humans, ferrets, and new world monkeys; birds and reptiles do not produce Neu5Gc at all, and fish and shellfish produce only low levels. So, of the four major meat groups – beef, pork, chicken, and fish – Neu5gc is obtained predominantly from the red meats, beef and pork.

Among human cells, Neu5Gc appears at highest levels on tumor cells, especially metastatic cells. [21] This makes Neu5Gc a potential target for cancer therapy.

Neu5Gc as an Immunogen

Neu5gc expressed on cell walls is a potential immunogen. When pig organs are transplanted to humans, Neu5Gc is the second most important cause of rejection, after the α1,3-galactose (αGal) epitope. [20]

Anti-Neu5gc antibodies have been found in 85% of humans. [18] It is thought that antibodies form in early childhood after dietary Neu5Gc is incorporated by certain gut bacteria into lipooligosaccharides that can generate antibodies. Some of these antibodies may cross-react with compounds human cells form from dietary Neu5Gc; these human molecules are then known as “xeno-autoantigens.” [21]

Summary

Neu5Gc from mammalian meats, such as beef and pork, is incorporated into the cell surface coats and walls of gut microbes and some human cells, mainly in the gut and in tumors. Neu5gc in bacterial walls is immunogenic and 85% of people have detectable antibodies to Neu5Gc. Eating beef and pork supplies antigens for these antibodies, potentially triggering inflammation. There are concerns that this inflammation may have negative health effects.

Next up: Neu5Gc and autoimmunity.

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References

[01] Samraj AN et al. A red meat-derived glycan promotes inflammation and cancer progression. Proc Natl Acad Sci U S A. 2014 Dec 29. pii: 201417508. [Epub ahead of print]. http://pmid.us/25548184.

[02] Kraemer PM. Sialic acid of mammalian cell lines. J Cell Physiol. 1966 Feb;67(1):23-34. http://pmid.us/5327858. Was 21

[03] Hayakawa T, Aki I, Varki A, Satta Y, Takahata N. Fixation of the human-specific CMP-N-acetylneuraminic acid hydroxylase pseudogene and implications of haplotype diversity for human evolution. Genetics. 2006 Feb;172(2):1139-46. http://pmid.us/16272417. Full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1456212/. Was 22

[04] Ghaderi D et al. Sexual selection by female immunity against paternal antigens can fix loss of function alleles. Proc Natl Acad Sci U S A. 2011 Oct 25;108(43):17743-8. http://pmid.us/21987817. was 2

[05] Wang B. Molecular mechanism underlying sialic acid as an essential nutrient for brain development and cognition. Adv Nutr. 2012 May 1;3(3):465S-72S. http://pmid.us/22585926. Full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3649484/. Was 31

[06] Davies LR, Varki A. Why Is N-Glycolylneuraminic Acid Rare in the Vertebrate Brain? Top Curr Chem. 2013 Mar 8. [Epub ahead of print] http://pmid.us/23471785. was 8

[07] Wang B. Sialic acid is an essential nutrient for brain development and cognition. Annu Rev Nutr. 2009;29:177-222. http://pmid.us/19575597. was 32

[08] Varki A. Colloquium paper: uniquely human evolution of sialic acid genetics and biology. Proc Natl Acad Sci U S A. 2010 May 11;107 Suppl 2:8939-46. http://pmid.us/20445087. was 51

[09] Löfling J et al. Canine and feline parvoviruses preferentially recognize the non-human cell surface sialic acid N-glycolylneuraminic acid. Virology. 2013 May 25;440(1):89-96. http://pmid.us/23497940. was 54

[10] Wu Z et al. Alpha2,3 and alpha2,6 N-linked sialic acids facilitate efficient binding and transduction by adeno-associated virus types 1 and 6. J Virol. 2006 Sep;80(18):9093-103. http://pmid.us/16940521. was 55

[11] Varki A, Gagneux P. Human-specific evolution of sialic acid targets: explaining the malignant malaria mystery? Proc Natl Acad Sci U S A. 2009 Sep 1;106(35):14739-40. http://pmid.us/19717444. was 57

[12] Martin MJ et al. Evolution of human-chimpanzee differences in malaria susceptibility: relationship to human genetic loss of N-glycolylneuraminic acid. Proc Natl Acad Sci U S A. 2005 Sep 6;102(36):12819-24. http://pmid.us/16126901. was 58

[13] Rich SM et al. The origin of malignant malaria. Proc Natl Acad Sci U S A. 2009 Sep 1;106(35):14902-7. http://pmid.us/19666593/.

[14] Byres E et al. Incorporation of a non-human glycan mediates human susceptibility to a bacterial toxin. Nature. 2008 Dec 4;456(7222):648-52. http://pmid.us/18971931.

[15] Varki A, Gagneux P. Multifarious roles of sialic acids in immunity. Ann N Y Acad Sci. 2012 Apr;1253:16-36. http://pmid.us/22524423. Full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3357316/

[16] Severi E, Hood DW, Thomas GH. Sialic acid utilization by bacterial pathogens. Microbiology. 2007 Sep;153(Pt 9):2817-22. http://pmid.us/17768226. Full text: http://mic.sgmjournals.org/content/153/9/2817.long.

[17] Harvey HA, Swords WE, Apicella MA. The mimicry of human glycolipids and glycosphingolipids by the lipooligosaccharides of pathogenic neisseria and haemophilus. J Autoimmun. 2001 May;16(3):257-62. http://pmid.us/11334490.

[18] Zhu A, Hurst R. Anti-N-glycolylneuraminic acid antibodies identified in healthy human serum. Xenotransplantation. 2002 Nov;9(6):376-81. http://pmid.us/12371933.

[19] Takahashi T et al. N-glycolylneuraminic acid on human epithelial cells prevents entry of influenza A viruses that possess N-glycolylneuraminic acid binding ability. J Virol. 2014 Aug;88(15):8445-56. http://pmid.us/24829344.

[20] Park JY et al. α1,3-galactosyltransferase deficiency in germ-free miniature pigs increases N-glycolylneuraminic acids as the xenoantigenic determinant in pig-human xenotransplantation. Cell Reprogram. 2012 Aug;14(4):353-63. http://pmid.us/22775484.

[21] Samraj AN, Läubli H, Varki N, Varki A. Involvement of a non-human sialic Acid in human cancer. Front Oncol. 2014 Feb 19;4:33. http://pmid.us/24600589.

Chilled Avocado Soup

Posted by on July 6, 2014 22 comments

The avocado is a favorite PHD ingredient: it is a fatty subtropical fruit with a fatty acid profile similar to that of olive oil (only about 14% omega-6). Native to the Americas, its wild ancestor, a small, black-skinned berry, is still found in southern Mexico and Central America. The avocado has been cultivated since at least 10,000 BC, making it one of the first domesticated plants in the Americas. After the European colonization of America, it spread slowly: Wikipedia says it was introduced to Indonesia in 1750, Brazil in 1809, South Africa and Australia in the late 1800s, and the Levant only in 1908.

Like all agricultural crops, the avocado has undergone extensive breeding. Over 80% of supermarket avocados are Hass avocados, which descend from a single “mother tree” on the La Habra Heights, California farm of mail carrier Rudolph Hass. Hass patented his tree in 1935.

In addition to their excellent (grade B in our book) fatty acid profile, avocados are nutritious. They have 35% more potassium per unit weight than bananas, a diverse range of vitamins and minerals, and are fiber-rich: 78% of the carbohydrate in avocados is fiber, totaling 7 g of fiber per 100 g serving.

This chilled avocado soup is a great summer food. Because it is so fatty, it is best paired with low-fat foods, such as a white fish like halibut or cod, shellfish, and potatoes.

Here is the recipe. Happy holiday weekend, everyone!