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Ship of the desert, shaper of human evolution…

Posted in Evolution, Food, Historical, tagged , , , , , , , , , on January 7, 2013| 14 Comments »

Happy New Year!

2012 was a whirlwind year for me. I defended my PhD at the beginning of 2012 and am now almost finished with all the required clerkships of third-year medical school. Phew!

I spent my winter holiday visiting my brother in Dubai, exploring many sites of the United Arab Emirates (UAE). I got to see a lot during my stay, and I’ve been writing a post on some of the interesting things I saw there.  As I was writing about the traditional dietary staples of the Middle East, I took a foray through a lot of literature that is available on camel milk.  It’s interesting stuff, and I found myself heading off on a tangent that I thought I should post as a stand-alone article.

So here we go…

Ship of the desert
Camels were (and still are, but for different reasons) an important part of life in the Middle East. The Arabian camel (the dromedary Camelus dromedarius) is a one-humped beast, and should not be confused with the 2-humped Bactrian camel (Camelus bactrianus) of central Asia.  Dromedaries were the only mode of transportation in the desert before motorized vehicles (walking any substantial distance on foot is out of the question and horses need too much water), and they also were an important form of wealth and source of food. Camel meat was a rare delicacy, while camel milk was a staple of the Bedouin diet. Camel hair was also used to make household necessities and camel dung was often used as fuel (a nice argument against the calories in calories out argument- if biological creatures were bomb calorimeters there wouldn’t be anything worth burning coming out the other end…).

Camel meat was not a staple of the Bedouin diet.  In fact, most nomadic people are reluctant to kill their subsistence animals for meat. Female camels were used for dairy and some males were kept for breeding purposes, but extra young male camels would be slaughtered and eaten for special occasions.

Though definitely not a traditional dish- this seems to be the #1 way to eat camel meat today

Though definitely not a traditional dish, this seems to be the most popular way to eat camel meat today

Camels are uniquely able to provide sustenance for humans in an environment that is generally rather inhospitable. Camels are able to not only survive, but thrive, on the limited and harsh forages that are available in the desert. She-camels can produce enough milk to nurse their offspring and provide liters of milk per day for their owner.

Camel in its native environment. These beasts thrive on the course and sparse forage of the desert.

Camel in its native environment. These beasts thrive on the coarse and sparse forage of the desert.

Camels’ milk is interesting stuff. Unlike the milk of cows, goats, and sheep, it cannot be easily made into cheese.  It doesn’t coagulate with bovine rennet, however recombinant camel rennet is incredibly efficient at coagulating cow milk and can also coagulate camel milk (there is a difference in the camel kappa-casein that makes it more resistant to cleavage) [1, 2].  With the right enzyme the job can be done, and there is at least one company that makes a camel cheese (nicknamed Camelbert!).

Camel milk isn’t much good for making yoghurt either, being much more resistant to lactic acid fermentation than cow milk. The result of camel milk lactic fermentation is very runny, with little microbial growth [3]. Gariss, a traditional Sudanese fermented camel’s milk product, is made with a mixed culture including Lactobacillus, Streptococcus, and yeast [4]. Here’s how it was traditionally made:

fermentation is carried out in two leather bags of tanned goat skin embedded in green or wet grass carried on the bag of camels and subjected to continuous shaking by the jerky walk inherent to camels. Whenever part of the product is withdrawn for consumption, a portion of fresh camel’s milk is added to make up volume and this continues for months [4].

According to one paper I spotted, food scientists can thicken fermented camel milk with gelatin or alginate (a thickener made from seaweed) in order to make a yoghurt-like product that consumers might find acceptable, but I didn’t spot any on the shelves in the stores of Dubai [5].

It seems to me that when it comes to camel milk it might be best to just keep it simple. Plain old milk.

CamelMilk

But camel milk may not be such simple stuff.  There is growing research that explores the use of camel milk for medicinal purposes.

I haven’t gone into the research in depth, but there are a number of small studies looking at the benefits of camel milk for people with diabetes (type 1 and type 2), with rather remarkable results. The addition of 500mL of camel milk on top of usual care for patients with type 1 diabetes resulted in significant improvements in a number of parameters in comparison to people who just received standard care. The camel milk group had a decrease in mean blood glucose levels and hemoglobin A1c.  The study was small, but 3 of the 12 participants in the camel milk group were able to completely stop using insulin (an almost unheard of occurrence for those with type 1 DM).  While the mean amount of insulin used in the control group remained constant, the amount used in the camel milk group dropped rapidly [4].

Abdelgadir et al [4]

Abdelgadir et al [4]

It hasn’t been determined how camel milk affects those with diabetes, but there are a number of hypotheses. Some sources think that insulin from camel milk is uniquely able to escape digestion when ingested or that camel milk contains a unique insulin-like small peptide that is bioavailable when consumed [6]. This is unlikely to be the whole story, however, as camel milk is able to increase endogenous insulin secretion in type 1 diabetics (individuals in standard of care + camel milk groups have higher levels of C-peptide, showing an increase in insulin production) [7].

Some readers may know that I have a fondness for fatty liver disease, so I was particularly interested to learn that, in a rat study, camel milk reversed alcohol-induced liver injury. This was seen histologically, where there was minimal fatty accumulation in the livers of alcohol-treated animals supplemented with camel milk in comparison to those just treated with alcohol alone, and serologically, where animals that were treated with ethanol alone had significantly increased liver enzymes in comparison to controls and those fed alcohol and camels milk [8]. I would postulate that it might have something to do with the high levels of carnitine found in camel milk [9], but that’s a story for another day.

Nutritionally, camel milk is unique. As I just mentioned, it has a more free carnitine as a percentage of total carnitine than other species and higher total carnitine than cow or human milk (though lower than sheep and goat milk) [9]. Camel milk has three-times the vitamin C of cow milk, but a similar amount of vitamin E and considerably less vitamin A and riboflavin [10]. Camel milk is low in short chain fatty acids in comparison to other milks and it has primarily long chain fatty acids, a significant portion of which is linoleic acid [11].  I tend to avoid this omega-6 FA, but I suspect that as part of a traditional diet the amount found in camel milk does not cause a problem.
Camels can carry a number of zoonotic organisms, including Coxiella burnetii (which causes Q fever) and Brucella sp. (which causes brucellosis), which can be transmitted through the milk. In fact, there was a recent brucellosis outbreak in Israel caused by raw camel milk [12].  If you’re drinking milk from an untested camel, it’s probably best to have it pasteurized. All the milk that’s available in Dubai supermarkets is pasteurized and homogenized. There are a variety of brands, and you can get milk in an array of flavors!

I spied plain, chocolate, strawberry, saffron, rose, cardamom, and date flavor! In this pic there's saffron, chocolate, strawberry, date, and plain.

I spied plain, chocolate, strawberry, saffron, rose, cardamom, and date flavor! In this pic there’s saffron, chocolate, strawberry, date, and plain.

Of course I had to try some… I opted for plain milk, and found it slightly sour in comparison to cow’s milk, with a watery mouthfeel. It’s been at least a decade since I drank skim milk, but as I remember the mouthfeel is similar.

Sculptors of human evolution

Camels have played central roles in the lives of desert dwelling people for millennia. They are the “ship of the desert” and their milk has nourished and sustained generations.  Their milk has also shaped the human genome…

The predominance of lactase persistence in populations is a well-known and well-studied example of human evolution. In populations that had access to animal milk, a mutation that allowed for the production of lactase past the age of weaning gave humans access to a rich food source. This was a huge advantage to those that had such a mutation.  Those that could easily consume milk were able to have more children, and the mutation spread throughout the population.  The advantage of having persistent lactase expression is so advantageous it has occurred independently in multiple populations over time.  While some mutations are linked back to the domestication of the cow, there are novel mutations found in Middle Eastern populations that are linked to the domestication of, and subsequent milk consumption from, Arabian camels [13].

The advantage of camel domestication is still present today.  A paper from 1996 looked at child health in three populations of Rendille pastoralists in Northern Kenya. Two of the groups had abandoned their nomadic roots to become settled, while one group remained nomadic.  In wet years (good years) there was a similar number of malnourished children in the three groups; however in a drought year, the children of the nomadic group faired significantly better.  The differences in malnutrition were attributed to food- specifically camels milk.  In drought years, the children in the nomadic group consumed three times as much milk as those from the sedentary group, where the children got more starches and sugar.  Other studies have found that nomadic groups generally do poorly during drought years (because of decreased production of milk from their herd), but because the Rendille maintain a large number of camels, they faired better during hard times [14].

So there you have it… I went diving into pubmed looking for a few fun facts to incorporate into a blog post on my trip to Dubai and found myself swept up in a mess of Dromedary data… I hope you found it as interesting as I did!

Camel

1.            Kappeler, S.R., H.J. van den Brink, H. Rahbek-Nielsen, Z. Farah, Z. Puhan, E.B. Hansen, and E. Johansen, Characterization of recombinant camel chymosin reveals superior properties for the coagulation of bovine and camel milk. Biochem Biophys Res Commun, 2006. 342(2): p. 647-54.

2.            Sorensen, J., D.S. Palmer, K.B. Qvist, and B. Schiott, Initial stage of cheese production: a molecular modeling study of bovine and camel chymosin complexed with peptides from the chymosin-sensitive region of kappa-casein. J Agric Food Chem, 2011. 59(10): p. 5636-47.

3.            Attia, H., N. Kherouatou, and A. Dhouib, Dromedary milk lactic acid fermentation: microbiological and rheological characteristics. J Ind Microbiol Biotechnol, 2001. 26(5): p. 263-70.

4.            Abdelgadir, W., D.S. Nielsen, S. Hamad, and M. Jakobsen, A traditional Sudanese fermented camel’s milk product, Gariss, as a habitat of Streptococcus infantarius subsp. infantarius. Int J Food Microbiol, 2008. 127(3): p. 215-9.

5.            Hashim, I.B., A.H. Khalil, and H. Habib, Quality and acceptability of a set-type yogurt made from camel milk. J Dairy Sci, 2009. 92(3): p. 857-62.

6.            Malik, A., A. Al-Senaidy, E. Skrzypczak-Jankun, and J. Jankun, A study of the anti-diabetic agents of camel milk. Int J Mol Med, 2012. 30(3): p. 585-92.

7.            Mohamad, R.H., Z.K. Zekry, H.A. Al-Mehdar, O. Salama, S.E. El-Shaieb, A.A. El-Basmy, M.G. Al-said, and S.M. Sharawy, Camel milk as an adjuvant therapy for the treatment of type 1 diabetes: verification of a traditional ethnomedical practice. J Med Food, 2009. 12(2): p. 461-5.

8.            Darwish, H.A., N.R. Abd Raboh, and A. Mahdy, Camel’s milk alleviates alcohol-induced liver injury in rats. Food Chem Toxicol, 2012. 50(5): p. 1377-83.

9.            Alhomida, A.S., Total, free, short-chain and long-chain acyl carnitine levels in Arabian camel milk (Camelus dromedarius). Ann Nutr Metab, 1996. 40(4): p. 221-6.

10.            Farah, Z., R. Rettenmaier, and D. Atkins, Vitamin content of camel milk. Int J Vitam Nutr Res, 1992. 62(1): p. 30-3.

11.            Gorban, A.M. and O.M. Izzeldin, Fatty acids and lipids of camel milk and colostrum. Int J Food Sci Nutr, 2001. 52(3): p. 283-7.

12.            Shimol, S.B., L. Dukhan, I. Belmaker, S. Bardenstein, D. Sibirsky, C. Barrett, and D. Greenberg, Human brucellosis outbreak acquired through camel milk ingestion in southern Israel. Isr Med Assoc J, 2012. 14(8): p. 475-8.

13.            Enattah, N.S., T.G. Jensen, M. Nielsen, R. Lewinski, M. Kuokkanen, H. Rasinpera, H. El-Shanti, J.K. Seo, M. Alifrangis, I.F. Khalil, A. Natah, A. Ali, S. Natah, D. Comas, S.Q. Mehdi, L. Groop, E.M. Vestergaard, F. Imtiaz, M.S. Rashed, B. Meyer, J. Troelsen, and L. Peltonen, Independent introduction of two lactase-persistence alleles into human populations reflects different history of adaptation to milk culture. Am J Hum Genet, 2008. 82(1): p. 57-72.

14.            Nathan, M.A., E.M. Fratkin, and E.A. Roth, Sedentism and child health among Rendille pastoralists of northern Kenya. Soc Sci Med, 1996. 43(4): p. 503-15.

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Guest Post: Observations from the field

Posted in Evolutionary Medicine, Food, Guest post, Historical, Life, Med school, tagged , , , , , , , , , , , on November 25, 2012| 3 Comments »

As an evolutionarily minded medical student, you can sometimes feel a bit alone in the crowd of conventionally minded medical practitioners and students.  I’ll admit that I’ve been repeatedly impressed with the interest that many of my fellow med students (as well as residents and even some attendings) show the ancestral/evolutionary ideas that I sometimes talk about, but most generally find an evolutionary approach to health and wellness interesting, rather than integral, in the consideration of health, wellness, and disease. 

 

I am not, however, alone.  There are a number of MDs and DOs who are interested in bridging the gap between ancestral health and western medicine.  There is a budding new organization of Physicians and Ancestral Health (with a winter meeting in February that I hope to attend), and there are other medical students who share a passion for thinking about modern medicine in the context of ancestral health. One such medical student is Angela Arbach, a student at Cornell Medical School currently doing research during a year long sabbatical between her third and fourth years of medical school, who I had the pleasure of meeting at the Ancestral Health Symposium in Boston in August.  There we had a long chat about our shared interest in evolutionary and ancestral medicine, as well as our specific areas of focus (she is passionate about women’s health and infectious disease).  I didn’t know it at the time, but Angela would soon be winging her way to Africa, where she would be involved in an international nutrition research project. When we recently caught up over e-mail I asked if she’d be interested in sharing her experience on my blog.  Her travels and observations are something that so few get to experience but so many could benefit from pondering. 

 

With out further ado: an ancestrally minded med student abroad.

Fresh from the Ancestral Health Symposium (AHS), after several days home in NYC and then a national boards exam in Philly, I was on a 4-hour bus trip to upstate New York to finalize plans for a research project in international nutrition.  A month later, I was on a plane to Northern Uganda: a nation in the global south, devastatingly resource poor, with an uncomfortably recent history of conflict.  [Check out the doc Uganda Rising, on youtube, for more history and a quick but imperative summary of colonialism in Africa].  It’s also a beautiful place.  From polychromatic garb to the giant layered sky underscored by the surrounding savannah, there is no shortage of images to appreciate.  The Acholi people, the dominant ethnic group of Northern Uganda, are still close to their traditional roots despite colonization and the recent influx of modern technologies.  When the English arrived, they left their development plans out of the north, making it easier to forcibly enlist Acholi men in the security forces.  And then, after independence (50 years, last month!), the north remained isolated and underdeveloped due to the LRA insurgency.  The Nile River, separating Acholiland from the rest of the country, only aids in this political and cultural divide.  For these reasons, an AHS-primed brain finds many cultural practices as fodder for rumination, along with prompts for contemplating our role in a global context.  Below, I will describe some of my earliest observations in this complicated milieu.

First, of course, the food.  It starts with starchy staples, mostly sweet potatoes, millet, rice, maize, sorghum, cassava, squash, and plantains.  These starches are used to scoop up, usually by hand, some combination of beans, peas, sesame seed paste, and, if you’re not incredibly food insecure, goat, fish, chicken, beef, or offal. The modicum of nonstarchy vegetables is nearly always cooked: the beans and meat stews are boiled with small pieces of tomato, green pepper, and onion, and a common side dish is boiled leafy greens.  I recently read an account of a Ugandan grandmother’s reaction to Western salads, laughing and asking how people can be healthy eating these raw foods since humans are not goats or cows.  The author explained how cooking all vegetables is a protective tradition, as soil and water is often contaminated by waste, but I wonder if there is more to it.  Fruit is eaten raw, however, and the most common fruits I see are bananas, oranges, jackfruit, mangos, avocado, passion fruit, and watermelons.  In terms of ferments, I’ve only heard of bongo (fermented milk) and the various alcoholic homebrews, usually from banana, maize, sorghum, or millet.

Example meals:  a plate of sweet potato and posho (stiff maize porridge) with a bowl of beans in a sesame paste sauce; kwan kal (stiff millet porridge) with boiled greens, tahini mixed in the green water; rice with a bowl of smoked goat meat stew.

fresh fish, sesame pasted greens, stiff millet porridge, sweet potatoes

One of my favorite meals, also an Acholi staple, is sesame paste mixed with mashed, cooked pigeon peas (dek ngoo) drizzled with dark shea nut oil (moo yaa).  Eat this by dipping in pieces of sweet potato or kwan kal.  These are typical lunches and dinners.

dek gnoo and moo yaa, with stiff maize porridge rice on the right

Breakfast is varied.  Some skip it, especially if they live in poverty and work all day (sure, call it a “feeding window, or just malnutrition).  Milk tea and milk instant coffee are very popular, with a milk-to-water ratio of 1:1 loaded up with table sugar.  The milk here is delicious– largely local and grassfed, it tastes so rich and sweet (a Ugandan colleague’s wife, who lived in the US for a year, told me “American milk doesn’t taste like milk”).  Millet porridge is served in some schools for breakfast.  A popular drink for children is milk, fermented or fresh, mixed with some kind of grain (I’ve heard millet or corn).  More common outside of the north, but still present here, is katogo:  stewed plantain or banana with offal or groundnuts.  Groundnuts are very similar to peanuts, and people buy them roasted for breakfast or snacking.  Groundnut stew (similar to a mild peanut sauce) is common elsewhere, but sesame paste stews are more common here.  Overall, the food variety is less than other places I’ve traveled, and the dishes are quite plain with little spice or herb additions– low food reward, perhaps.

That all sounds wonderful, but I left out a big part of the common diet:  wheat, vegetable oils, and soft drinks.  All new additions to the food tradition, sometimes supplanting old foods.  Indian influence means chapati and samosas are common street foods, cooked in vegetable oils, of course.  Loaves of bread are becoming a staple, as well, and some people eat it with a schmear of sesame seed butter for breakfast.  I was happy to discover how common eggs are, but if I eat out, they are always fried brown in veg oil.  So it goes.  Within the ubiquity of food insufficiency in a context of very limited healthcare, I fear the implications of substituting already meager dietary items with these industrial foods.

Modern staples: vegetable oils, toilet paper, and soda

Walking around, I see people in positions that could be in Gokhale’s book.  The women work hard– constantly bent over to cook, wash dishes, do laundry, and clean floors (brooms are 2-3 feet long and made from reeds, mops are rags that you move with your arms).  They stay bent at the waist with perfectly straight backs, motivating me to keep stretching the hammies…

Women at work

 Some of these chores are done squatting, too.  Otherwise, the women can be seen transporting heavy objects on their heads, from 5 gallon jugs of water to sacks of grain.  This is all done with a baby wrapped to their backs.

I could be wrong, but perhaps these practices are the reason I see less postural kyphosis in the elderly ladies.  Also, I should mention that gyms are nearly nonexistent, and the only time I see running is when people get caught in the rain, are playing football (soccer), or are white people doing aid work or research (that’s me! But my research involves too much time at a desk).  Strenuous jobs are the norm, and most people don’t have cars.  Walking and bicycling are the rule.  Most of the footwear I see are thin sandals (minimalist), and it’s common to see barefooted people walking around, especially outside the towns (poverty).

About 100 years old, but I’m told these are still made in some villages

The lack of street lamps, along with daily power outages, and the fact that the vast majority of homes don’t have access to electricity, means that people generally experience natural darkness as the sun sets.  I’ve been heading to bed much earlier, especially since I cannot sleep past 5 or 6 am due to the roosters.  If I go to bed early enough, I often wake up in the middle of the night for an hour or so before a “second sleep”.  One of my colleagues (a Ugandan) does this, too, but I cannot generalize beyond us.  He and his family sometimes take a little siesta after lunch, too, which I can certainly get behind.  I can also check off items from the recent MDA post on hormesis.  I already mentioned the exercise and calorie restriction, and sunlight exposure is a given in a country on the equator.  Also, without modern conveniences such as electricity and hot water heaters, all showers are cold showers!

Another topic I want to touch on is Acholiland’s continued tribal culture.  Traditional dance and music is at the heart of this.  I frequently hear drums in the distance as I walk, and I’ve seen groups of students in universities meet up for dances in the grass.  For more on the healing power of traditional music and dance, track down the 2007 film War Dance, an incredibly beautiful but heartbreaking story about school children in Northern Uganda.  I have yet to read my book on the history of the Acholi tribes, so the majority of my info is from conversations with Ugandan friends, one of whom is the designated leader of his clan.  The presence of tribal culture is strong, the sense of belonging is crucial, and excommunication from your clan is considered a punishment worse than death.  Clan leaders are still called upon to resolve disputes or offer advice.  [See the Al Jazeera documentary, Bitter Root, for how these traditional practices lead to reconciliation, rather than retribution, for former abducted-children-turned-rebel-soldiers, taking the justice system from the hands of the government to the realm of tradition].  Distant relatives are sometimes described using nuclear family nouns– the son of your grandpa’s cousin’s kid is your brother– and everyone feels a sense of responsibility and goodwill towards other members of their clan.  This sounds like ubuntu, the topic of Frank Forencich’s talk (Africa reference?) at AHS, which I missed because I had to run back to New York that day.  I should mention that everyone here was thrilled when Obama won, and they often cite that sense of brotherhood they get from him, along with his more skillful way of taking care of the poor.

That’s my account so far, but remember that some of this information came from people who may want to tell the foreigner something interesting, rather than common, and then that data is filtered through my biased brain.  And of course, I can’t talk about these things without sprinkling in some political, economic, and social issues facing the Acholi.  An ancestral health picture is nice, but it’s not complete.  Acholi tradition has been undermined by forced migration into internally displaced peoples camps for over a decade, ending merely a few years ago, preventing the practice of many cultural rituals.  They were without land, independence, and other means to continue traditional livelihoods.  On a few occasions, I’ve been able to informally talk with Acholi elders.  They never fail to remind me how the IDP camps destroyed their peoples’ culture and morals, as well as fostering drug abuse, rape, and disease.  And yes, the foodways and hormesis sound great, but people are starving here.  Naturally active livelihoods are awesome, but not when they are the result of extreme gender inequality where women have no choice.  It’s sweet and heartwarming that man-on-man handholding is so common– brotherhood, right?  But it’s scary that the same affection towards your wife is risqué, or that you could be killed or imprisoned if you engage in love outside the bounds of heteronormativity.  Blame it on the proximate lack of education, former colonialism, or widespread Christianity, but it’s happening.  And let’s not start on the infectious diseases, government corruption, illiteracy rates, motor vehicle accidents, and lack of good healthcare.

So what can we learn from these people, a group so geographically close to the Hadza, Batwa, and Karamojong, close to some of the earliest human remains in the archaeological record?  The answer seems largely irrelevant.  We have a lot of the answers we need about diet and lifestyle.  Perhaps this is a case where we should ask:  what can we give of ourselves?  The ancestral health community has gained a lot from the study of indigenous groups, so what can we do in return?  How will we enable empowerment and protect culture?  American health trends have a global effect, so how can we be the example of doing this in a positive way?  Why was the apropos panel on Reclaiming Latino Health so under-attended, compared to the lamentable, stale debate on… potatoes?  Were we fighting with the Pima to protect their water?  Has anyone heard of the Decolonizing Diet Project?  And for the egocentric: more preservation of cultural heritage means more research opportunities to figure out the perfect post-workout meal…  I mentioned missing Forencichs’ talk, but when I read how greatly he inspired people, I looked him up and found this relevant post.  Adele Hite, a speaker at the symposium, gave a list of ways to become more involved than just frequently-commenting-on-blogs.  Her examples largely involve the USA, but I don’t see why our scope cannot transcend self-created national borders.  This already happens in research and blogging, so why not in action?  Involvement in other cultures demands care and scrutiny (you want to avoid dead aid), but I think this community is smart and thoughtful enough to create a significantly net-positive effect.  We’re crafty people, and we’ve already accomplished so much.  Some organizations are doing exciting, ancestral-health-minded things, like this medical clinic in Burundi.  They started a native foods garden, along with the administration of agriculture education programs, to combat widespread food insecurity that took place after the civil war and genocide– a nice solution to what many food aid programs stick a bandaid on by creating relationships of dependency using their culturally inappropriate bags of wheat and jugs of vegetable oil.

I’m merely a student, so I cannot provide all the answers, but I hope the bulk of my career will work on these issues.  I think this community is also up for the challenge, as evidenced by the last symposium.  The blogging about micro/macronutrients is dying down, and our focus is getting bigger:  public policy, remarkable research projects, interventions, activism, creation of med student electives, and the introduction of evolutionary health into workplaces and grand rounds.  I’m not saying that global issues and cultural preservation need to supplant the other amazing endeavors born from the synergy in the ancestral community, but I look forward to more attention to these topics.  They are not tangential, but fundamental, to progress for us all.

Angela is a medical student at Cornell in NYC. If you’d like to read more of her observations (with less focus on ancestral health) you can check out her travel blog, I highly recommend it!  

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An ode to the soft-boiled egg…

Posted in Food, Life, tagged , , , , , , on November 2, 2012| 6 Comments »

Sandy has come and gone (at least in my part of the country- last I heard she was still making her presence felt somewhere in the middle of the country), but for me (and many fellow New Jerseyans) power has gone and not yet come back.  I weathered the storm in my apartment near school, and stayed there for the following day. When word came that my school would be closed for the entire week (the associated hospitals have remained open throughout), I decided to pack up my freezer and head back to my parents’ place (also without power) where there was storm damage that needed to be handled.

All things considered, my family and I were very fortunate with this storm. We are not on the coast and as such were spared the coastal flooding that has damaged so much of our Jersey Shore. We faired much worse with Irene last year, where flooding led to serious damage at our house and at our farm.  While Irene brought us water, Sandy brought us wind.  The majority of the damage after this storm (at least in our area) is due to downed trees or direct wind.

Of course, with downed trees come downed power wires.  As I write this, we approach 100 hours without power*.  At my apartment, while I lacked power, I had water (and while it lasted, the bit of hot water that remained in the tank). My parents’ old farmhouse is on a well, and as such lacks running water when the power goes out.  Luckily there is a stream that can be accessed for water to flush the toilets and we stockpile water in tanks for occasions such as this. We have lots of firewood stashed (and a good old wood-burning stove), so while the temperatures continue to drop we are able to keep ourselves warm the old fashioned way.  The biggest concern with extended power cuts (for us at least) is the risk of our 2 big freezers defrosting. With hundreds of pounds of beef, lamb, pork, and fish (not to mention veggies and berries), an extended outage gets a bit concerning.  Fortunately we have very generous neighbors who have a generator, and after a couple days without power they bring their generator over so we can plug in and recharge our freezers for a bit (as I write this, we’re on round 2 of recharging- so far so good).

At times such as this there are a number of things for which I’m very grateful .

1-    Health. If you aren’t physically well and physically able this manner of glorified camping could turn into hell.

2-    A gas stove. Seriously. The power may go out, but at least I can still cook. What do people with electric stoves do?

3-    Firewood. And after this storm we’ll be set with firewood for many more years to come

4-    Friends with generators (who not only recharge out freezers, but also offer warm showers… saints!)

5- Merino clothing. Cozy and  stink free… need I say more?

With a limited water supply and a desire to keep dirty dishes to a minimum, I keep my cooking simple. Dinners have been big one-pot numbers (I cooked up a good beef shin bone 2 nights ago and I have lamb shanks on the go at the moment), and breakfasts have been soft-boiled eggs.

“Eggs and soldiers” (soft-boiled eggs served with slivers of toast for dipping) was a regular breakfast when I was a child.  While I haven’t had toast in years, soft-boiled eggs remain a regular part of my diet.  They’re quick, they’re easy, they require no preparation or clean up, and despite this I’m not sure I’ve ever met another American that eats them (my parents are English).  Soft-boiled eggs seem to be quite popular in Europe.  Not only are they part of English culinary history (Go to work on an egg), but I’ve seen them at a number of breakfast buffets while traveling in Germany.

I have no intention of writing a food blog. There are much more capable chefs (with much fancier cameras) who cook and write about delicious and nutritious healthful food (here’s a good example), but I’ll take this opportunity to introduce this tasty treat to my readers (and if I’m completely wrong and Americans are eating soft-boiled eggs like mad, please let me know!).

If you can boil water, you can boil an egg. The difficulty with making soft-boil eggs is getting the timing right.  I’ve sometimes heard soft-boiled eggs referred to as “4-minute” eggs, as 4 minutes is about as long as it takes to cook.  Some variables interfere, such as altitude, size of the egg and freshness of the egg (there’s nothing worse than overcooking a beautiful fresh egg still warm from the chicken!), but 4 minutes is a good estimate.

I’ll admit I almost never time my eggs. I invested in one of these gadgets a few years ago, and can’t recommend them highly enough. If you’re lazy like me and sometimes cook tons of eggs at a time, this little device can tell you when they’ll all be done better than any timer.  Worth every penny (I get no kickbacks, I assure you)!

Once your egg is cooked you can stick it in cold water to stop it from cooking too much or just eat it right away. Soft-boiled eggs are best enjoyed warm and are most easily eaten using an eggcup.  Here’s my favorite:

This was the eggcup my Nan would give me as a child when I visited her in England. I reminisced about it and she kindly gave it to me!

The next step is cracking the egg. This too, is easily done!

Once whacked, you can get to work and open up the egg. If all went according to plan, you’ll have a perfect soft yolk!

Mmmm…. Brains

I like mine with a bit of salt (and sometimes some pepper).

I’d like to thank my hens for eating such a nutritious diet and for having such lovely yolks!

It seems as though Brits are pretty keen on soft-boiled eggs (or at least they have been in the past). Maybe it’s because soft-boiled eggs are delicious, or maybe it’s because eggcups are kind of fun. There are lots of options, from cute little pants sets to fine silver.

An antique silver eggcup set- also from my Nan (I can’t believe anyone ever used these!)

Soft-boiled eggs are not only quick to cook with minimal cleanup (usually just a spoon) but they’re also excellent emergency food.  They’re very nutritious, and they can be cooked in water that wouldn’t otherwise be potable (love that shell!). I remember my good friend Jamie Scott  making that point when he wrote about his experience with the earthquakes of Christchurch.

In college I toured Iceland, including a visit to the geysers. I remember hearing that you could cook a soft-boiled egg in the sulfurous hot springs if you were so inclined (talk about Waste not, want not!), and I tracked down a video of some guys doing just that.  The kitchen method might be easier- no hot spring required!

(As the pictures might suggest, I am going a but stir-crazy, though I have to admit that life without power is not without its charms. I’ve read a big book of EKG interpretation cover-to-cover, dismembered a fallen old maple, fixed a chicken house, and taken the dog for a number of walks over the last few days. I’m also rather enjoying the darkness-imposed early bedtimes (now that it no longer sounds like the wind will rip the roof off from over me!)  More science to come- I do plan to get back to liver and lipids shortly!)

 

*This post is up courtesy of the photons and electrons of a local coffee spot… Thanks Riverside Coffee!

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Liver saving saturated fats

Posted in Disease, Food, Lipids, Liver, tagged , , , on August 2, 2012| 25 Comments »

As my last post started to explore, different types of dietary fats have different effects on the progression of alcoholic liver disease. This post will further explore the protective effects of saturated fats in the liver.

 

For many, the phrase “heart healthy whole grains” rolls off the tongue just as easily as “artery clogging saturated fats”. Yet where is the evidence for these claims? In the past few decades saturated fats have been demonized, without significant evidence to suggest that natural saturated fats cause disease (outside of a few well touted epidemiological studies). Indeed, most of the hypothesis-driven science behind the demonization of saturated fats is flawed by the conflation of saturated fats with artificial trans fats (a la partially hydrogenated soybean oil).

 

In the face of a lack of any significant scientific evidence that clearly shows that unadulterated-saturated fats play a significant role in heart disease (and without a reasonable mechanism suggesting why they might), I think the fear-mongering “artery clogging” accusations against saturated fats should be dropped. On the contrary, there is significant evidence that saturated fats are actually a health promoting dietary agent- all be it in another (though incredibly important) organ.

 

Again (from my last post), here is a quick primer on lipids (skip it if you’re already a pro). For the purpose of this post, there are two important ways to classify fatty acids. The first is length. Here I will discuss both medium chain fatty acids (MCFA), which are 6-12 carbons long, and long chain fatty acids (LCFA), which are greater than 12 carbons in length (usually 14-22; most have 18). Secondly, fatty acids can have varying amounts of saturation (how many hydrogens are bound to the carbons). A fatty acid that has the maximal number of hydrogens is a saturated fatty acid (SAFA), while one lacking two of this full complement, has a single double bond and is called  monounsaturated (MUFA) while one lacking more (four, six, eight etc.) has more double bonds (two, three, four, etc.) and is called a polyunsaturated fatty acid (PUFA).

 

Next time you eat a good fatty (preferably grass-fed) steak, or relish something cooked in coconut or palm oil, I hope you will feel good about the benefits you are giving your liver, rather than some ill-placed guilt about what others say you are doing to your arteries. From now on, I hope you think of saturated fats as “liver saving (and also intestine preserving) lipids”. Here’s why:

 

In 1985, a multi-national study showed that increased SAFA consumption was inversely correlated with the development of liver cirrhosis, while PUFA consumption was positively correlated with cirrhosis [1].  You might think it is a bit rich that I blasted the epidemiological SAFA-heart disease connection and then embrace the SAFA-liver love connection, but the proof is in the pudding- or in this case the experiments that first recreated this phenomenon in the lab, and then offered evidence for a mechanism (or in this case many mechanisms) for the benefits of SAFA.

 

The first significant piece of support for SAFA consumption came in 1989, when it was shown in a rat model that animals fed an alcohol-containing diet with 25% of the calories from tallow (beef fat, which by their analysis is 78.9% SAFA, 20% MUFA, and 1% PUFA) developed none of the features of alcoholic liver disease, while those fed an alcohol-containing diet with 25% of the calories from corn oil (which by their analysis is 19.6% SAFA, 23.6% MUFA, and 56.9% PUFA) developed severe fatty liver disease [2].

 

More recent studies have somewhat complicated the picture by feeding a saturated fatty-acid diet that combines beef tallow with MCT (medium chain triglycerides- the triglyceride version of MCFAs). This creates a diet that is more highly saturated than a diet reliant on pure-tallow, but it complicates the picture as MCFA are significantly different from LCFA in how they are absorbed and metabolized. MCFA also lead to different cellular responses (such as altered gene transcription and protein translation). Nonetheless, these diets are useful for those further exploring the role of dietary SAFA in health and disease.

 

These more recent studies continue to show the protective effects of SAFA, as well as offer evidence for the mechanisms by which SAFA are protective.

 

Before we explore the mechanisms, here is a bit more evidence that SAFAs are ‘liver saving’.

 

 

A 2004 paper by Ronis et al confirmed that increased SAFA content in the diet decreased the pathology of fatty liver disease in rats, including decreased steatosis (fat accumulation), decreased inflammation, and decreased necrosis.  Increasing dietary SAFA also protected against increased serum ALT (alanine transaminase), an enzymatic marker of liver damage that is seen with alcohol consumption [3].  These findings were confirmed in a 2012 paper studying alcohol-fed mice. Furthermore, these researchers showed that SAFA consumption protected against an alcohol-induced increase in liver triglycerides [4].  Impressively, dietary SAFA (this time as MCT or palm-oil) can even reverse inflammatory and fibrotic changes in rat livers in the face of continued alcohol consumption [5].

 

But how does this all happen?

 

Before I can explain how SAFA protect against alcoholic liver disease, it is important to understand the pathogenesis of ALD. Alas, as I briefly discussed in my last post, there are a number of mechanisms by which disease occurs, and the relative importance of each mechanism varies based on factors such as the style of consumption (binge or chronic) and confounding dietary and environmental factors (and in animals models, the mechanism of dosing). SAFA is protective against a number of mechanisms of disease progression- I’ll expound on those that are currently known.

 

In my opinion, the most interesting (and perhaps most important) aspect of this story starts outside the liver, in the intestines.

 

In a perfect (healthy) world, the cells of the intestine are held together by a number of proteins that together make sure that what’s inside the intestines stays in the lumen of the intestine, with nutrients and minerals making their way into the blood by passing through the cells instead of around them. Unfortunately, this is not a perfect world, and many factors have been shown to cause a dysfunction of the proteins gluing the cells together, leading to the infamous “leaky gut”. (I feel it is only fair to admit that when I first heard about “leaky gut” my response was “hah- yeah right”. Needless to say, mountains of peer-reviewed evidence have made me believe this is a very real phenomenon).

 

Intestinal permeability can be assessed in a number of ways.  One way is to administer a pair of molecular probes (there are a number of types, but usually a monosaccharide and a disaccharide), one which is normally absorbed across the intestinal lining and one that is not. In a healthy gut, you would only see the urinary excretion of the absorbable probe, while in a leaky gut you would see both [6]. Alternatively, you can look in the blood for compounds such as lipopolysaccharide (LPS-a product of the bacteria that live in the intestine) in the blood. (Personally, I would love to see some test for intestinal permeation become a diagnostic test available to clinicians.)

 

Increased levels of LPS have been found in patients with different stages of alcoholic disease, and are also seen in animal models of alcoholic liver disease.  Increased levels of this compound have been associated with an increased inflammatory reaction that leads to disease progression.  Experimental models that combine alcohol consumption and PUFA show a marked increase in plasma LPS, while diets high in SAFA do not.

 

 

But why? (Warning- things get increasingly “sciencey” at this point. For those less interested in the nitty-gritty, please skip forward to my conclusions)

 

Cells from the small intestine of mice maintained on a diet high in SAFA, in comparison to those maintained on a diet high in PUFA, have significantly higher levels of mRNA coding for a number of the proteins that are important for intestinal integrity such as Tight Junction Protein ZO-1, Intestine Claudin 1, and Intestine Occludin.  Furthermore, alcohol consumption further decreases the mRNA levels of most of these genes in animals fed a high-PUFA containing diet, while alcohol has no effect on levels in SAFA-fed animals.  Changes in mRNA level do not necessarily mean changes in protein levels, however the same study showed an increase in intestinal permeability in mice fed PUFA and ethanol in comparison to control when measured by an ex-vivo fluorescent assay. This shows that PUFA alone can disturb the expression of proteins that maintain gut integrity, and that alcohol further diminishes integrity. In combination with a SAFA diet, however, alcohol does not affect intestinal permeability [4].

 

Improved gut integrity is no doubt a key aspect of the protective effects of SAFA. Increased gut integrity leads to decreased inflammatory compounds in the blood, which in turn means there will be decreased inflammatory interactions in the liver.  Indeed, in comparison to animals fed alcohol and PUFA, animals fed alcohol with a SAFA diet had significantly lower levels of the inflammatory cytokine TNF-a and the marker of macrophage infiltration MCP-1 [4].  Decreased inflammation, both systemically and in the liver, is undoubtedly a key element of the protective effects of dietary SAFA.

 

This post is already becoming dangerously long, so without going into too much detail, it is worth mentioning that there are other mechanisms by which SAFA appear to protect against alcoholic liver disease. Increased SAFA appear to increase liver membrane resistance to oxidative stress, and also reduces fatty acid synthesis while increasing fatty acid oxidation [3]. Also, a diet high in SAFA is associated with reduced lipid peroxidation, which in turn decreases a number of elements of inflammatory cascades [5]. Finally- and this is something I will expand on in a future post- MCFAs (which are also SAFA) have a number of unique protective elements.

 

I realize that this post has gotten rather lengthy and has brought up a number of complex mechanisms likely well beyond the level of interest of most of my readers…

 

If all else fails- please consider this:

 

The “evidence” that saturated fats are detrimental to cardiac health is largely based on epidemiological and experimental studies that combined saturated fats with truly-problematic artificial trans-fats. Despite the permeation of the phrase “artery clogging saturated fats”, I have yet to see the evidence nor be convinced of a proposed mechanism by which saturated fats could lead to decreased coronary health.

 

ON THE CONTRARY…

 

There is significant evidence, founded in epidemiological observations, confirmed in the lab, and explored in great detail that shows that saturated fats are protective for the liver. While I have focused here on the protective effects when SAFA are combined with alcohol, they offer protection to the liver under other circumstances, such as when combined with the particularly liver-toxic pain-killer Acetaminophen [7].

 

Next time you eat a steak, chow down on coconut oil, or perhaps most importantly turn up your nose at all things associated with “vegetable oils” (cottonseed? soybean? Those are “vegetables”?), know that your liver appreciates your efforts!

 

 

1.            Nanji, A.A. and S.W. French, Dietary factors and alcoholic cirrhosis. Alcohol Clin Exp Res, 1986. 10(3): p. 271-3.

2.            Nanji, A.A., C.L. Mendenhall, and S.W. French, Beef fat prevents alcoholic liver disease in the rat. Alcohol Clin Exp Res, 1989. 13(1): p. 15-9.

3.            Ronis, M.J., S. Korourian, M. Zipperman, R. Hakkak, and T.M. Badger, Dietary saturated fat reduces alcoholic hepatotoxicity in rats by altering fatty acid metabolism and membrane composition. J Nutr, 2004. 134(4): p. 904-12.

4.            Kirpich, I.A., W. Feng, Y. Wang, Y. Liu, D.F. Barker, S.S. Barve, and C.J. McClain, The type of dietary fat modulates intestinal tight junction integrity, gut permeability, and hepatic toll-like receptor expression in a mouse model of alcoholic liver disease. Alcohol Clin Exp Res, 2012. 36(5): p. 835-46.

5.            Nanji, A.A., K. Jokelainen, G.L. Tipoe, A. Rahemtulla, and A.J. Dannenberg, Dietary saturated fatty acids reverse inflammatory and fibrotic changes in rat liver despite continued ethanol administration. J Pharmacol Exp Ther, 2001. 299(2): p. 638-44.

6.            DeMeo, M.T., E.A. Mutlu, A. Keshavarzian, and M.C. Tobin, Intestinal permeation and gastrointestinal disease. J Clin Gastroenterol, 2002. 34(4): p. 385-96.

7.            Hwang, J., Y.H. Chang, J.H. Park, S.Y. Kim, H. Chung, E. Shim, and H.J. Hwang, Dietary saturated and monounsaturated fats protect against acute acetaminophen hepatotoxicity by altering fatty acid composition of liver microsomal membrane in rats. Lipids Health Dis, 2011. 10: p. 184.

What is “Fatty Liver”? Well here’s a slide from my research showing a slice of liver from a control-fed rat on the left and an alcohol-fed rat on the right. Arrows mark macrovesicular lipid accumulations (other models can show much more impressive lipid accumulations).

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Liver and lipids

Posted in Disease, Food, Lipids, tagged , , , , on July 23, 2012| 7 Comments »

My research background, at least as far as my PhD is concerned, is in pharmacology and physiology.  Specifically, I studied the effects of chronic alcohol consumption on signal transduction in the liver. Simply, I explored the ways in which chronic alcohol consumption affects how liver cells “talk” (both to each other, and how individual cells transmit a signal from an extracellular stimulus into an intracellular response).  If I were to go all “alphabet soup” on you, I would talk about my explorations into IP3-Ca2+ signaling, or my real area of expertise, cAMP-PKA signaling and CREB phosphorylation. Luckily (for all of us) that’s not what I want to write about.

 

What I want to write about is the role of various fats (aka lipids) in the development of fatty liver. Before I delve into the land of lipids, a bit of background is in order.

 

Fatty liver is the first phase of a process that in some people ends with cirrhosis and liver failure.  Most people associate this progression (from fatty liver, to fibrosis, and finally to cirrhosis) with chronic alcohol consumption, however recently the prevalence of nonalcoholic fatty liver disease (NAFLD) has grown. In fact, when I first started my PhD research, sources were saying that alcoholic fatty liver disease (AFLD) was the #1 cause of fatty liver. By the time I was writing my thesis (and I didn’t take THAT long), sources were claiming that AFLD had been overtaken by NAFLD. As the name suggests, fatty liver disease (aka liver steatosis) is the accumulation of fat in the liver. Microscopically this is evident as micro or macrovesicular fat accumulations within the cells of the liver (hepatocytes), while grossly a fatty liver appears enlarged, soft, oily, and pale (foie gras anyone?).

 

Fatty liver- both alcoholic and nonalcoholic – is generally asymptomatic, and requires a liver biopsy or radiology (such as CT, MRI, or ultrasonography) for diagnosis, though blood tests for liver markers are used to detect non-specific changes in liver health (you also might notice this while looking around someone’s insides during a surgical procedure, as I noted during a laparoscopic gallbladder removal during my surgery clerkship).  The prevalence of fatty liver is unclear, however the percentage of heavy drinkers that have fatty liver changes is probably quite high, with some studies showing that up to 90% of active drinkers have fatty changes [1]. Again, because of the relative “silent” nature of NAFLD, it’s hard to determine the prevalence of the condition, however it is strikingly (and increasingly) common, with sources suggesting that it may affect 20-30% of the US population [2]. Scarily, it is estimated that over 6 million CHILDREN in the US have this condition today, with this number continuing to grow [3].

 

Fat can accumulate in the liver in five different (though often simultaneous) ways. There can be (1) an increase in uptake and storage of dietary fats, (2) an increased uptake of free fatty acids (FFA) from other stores (from your fat tissue to your liver), (3) increased de novo lipogenesis (making lipids from scratch), (4) decreased consumption (b-oxidation to those in the trade) of fats, or (5) impaired export of triglycerides from the liver [4]. It is likely that a number of these mechanisms work in concert to produce fatty liver disease, but the precise reasons WHY they occur have not yet been determined, nor has the relative importance of each mechanism been teased out. Undoubtedly different mechanisms are of varying importance in different conditions and circumstances.  Indeed, relatively early studies of alcohol-induced liver disease showed that, depending on experimental conditions such as method and length of exposure, hepatic lipids could be derived from dietary, adipose, or de novo hepatic sources [5]. Teasing out what we already know (or think we know), and how each of these mechanisms interact to lead to fatty liver disease is beyond the scope of this blog post (it’s beyond the scope of most medical texts, really), but the role of dietary fats deserves some airtime in this discussion, and is what I wish to talk about here.

 

The research into the pathogenesis of alcoholic fatty liver is long and tortuous (or is that torturous, if you’re a graduate student trying to get a handle on past research?). Without going into too much depth, there has been controversy over the years as to whether alcohol itself causes fatty liver, or whether fatty liver occurs with alcohol consumption as a result of simultaneous nutrient deficiencies. Because chronic alcohol consumption is frequently accompanied by a very poor diet, it was postulated that liver disease occurred primarily as a result of nutrient deficiency, not alcohol consumption. This proved to be partially true in animal models, where a diet deficient in nutrients such as choline and methionine exacerbates the development of alcoholic liver disease.  Alas, nutritional supplementation only diminishes or slows, but does not prevent, alcoholic liver disease development and progression [6, 7]. Steatosis still occurs in the presence of an adequate diet, showing that nutritional deficiencies alone cannot account for the development of fatty liver.

 

Before I delve into the research, here is a quick primer on lipids (skip it if you’re already a pro). For the purpose of this post, there are two important ways to classify fatty acids. The first is length. Here I will discuss both medium chain fatty acids (MCFA), which are 6-12 carbons long, and long chain fatty acids (LCFA), which are greater than 12 carbons in length (usually 14-22; most have 18). Secondly, fatty acids can have varying amounts of saturation (how many hydrogens are bound to the carbons). A fatty acid that has the maximal number of hydrogens is a saturated fatty acid (SAFA), while one which has one double bond is monounsaturated (MUFA) and a fatty acid with more than one double bond is called a polyunsaturated fatty acid (PUFA)*.

 

Most alcohol researchers rely on an isocaloric liquid diet containing 35% of the calories from alcohol in the treatment group with the alcohol replaced by a carbohydrate in the control group. It was discovered pretty early on (in the 1960s) that eliminating dietary fatty acids significantly reduced the amount of fat accumulated in the liver and that you needed at least 25% of calories from fat, and ideally around 40%, to get a good model of alcoholic fatty liver (granted this is in rats, not humans). It didn’t take long for researchers to realize that different types of fatty acids were better (or perhaps more interestingly, worse) at creating fatty liver than others. The first notable realization (at least as far as I’m aware) is that medium chain fatty acids (MCFA) caused much less steatosis than long chain fatty acids (LCFA). Indeed, as early as 1972 researchers were showing that alcoholic fatty liver in rats could be reversed by replacing corn oil (an excellent source of LCFA, especially polyunsaturated fatty acids (PUFAs)) with MCFA. Stunningly (to me at least), there was a more rapid regression of fatty liver when the corn oil was replaced with MCFA than when the alcohol was replaced with sucrose [8]!

 

Another fascinating and interesting piece to this puzzle came in the mid 80s when it was shown that beef fat prevents alcoholic liver disease in rats. This research was conducted after epidemiological studies showed that a high intake of saturated fat was relatively protective against ALD disease while a high intake of polyunsaturated fats promoted ALD.  Researchers took this epidemiological finding to the lab, and showed that rats that were fed an alcohol-containing diet with tallow (beef fat) developed none of the symptoms of alcoholic fatty liver disease, while those fed alcohol with corn oil developed severe pathology [9]. More recent research (which I will explore in an upcoming post) delves into the protective mechanisms of SAFAs.

 

Alas, a high fat model of ALD that doesn’t actually give you liver pathology is not particularly useful for studying fatty liver, so most ALD research uses a diet that combines olive oil, corn oil, and/or soy oil and produces significant fat accumulation in the liver (indeed, this is what my PhD research was based on).  But what can research that has used other sources of fats tell us about alcoholic liver disease, and perhaps more interestingly (as the NAFLD epidemic continues to sweep the nation and the world) what can this research tell us about fatty liver disease that has nothing to do with alcohol consumption?

 

During my time in the lab (and even more so while writing my dissertation), I came to recognize that there are many similarities between fatty liver diseases of apparently very different etiologies. From a cell signaling perspective (my specialty), I was surprised by the parallels of our ALD fatty liver model and the fatty liver caused by protein malnutrition (yes- protein malnutrition leads to fatty liver- bizarre, no?). I have had less time to focus on the parallels between ALD and NAFLD (not caused by protein-malnutrition), however most of the medical information on this topic suggests life-style modification that focuses on the importance of reducing fat, especially (*eye roll*) saturated fat. I have yet to see the smoking gun for saturated fats in the pathogenesis of NAFLD, and if the process is anything like that of alcoholic liver disease (as I much suspect to be the case), minimizing saturated fats for those with NAFLD will likely do more harm than good.

 

I will expound on this statement in an upcoming post.

 

 

*For the lipid lovers in the crowd… Yes- there are significant differences in the effects of various types of PUFAs when it comes to alcoholic liver disease, though there are some interesting complications with the Omega3s depending on what research you look at. For the sake of this post (and most research), when I say PUFA I am generally referring to linoleic acid, the main PUFA in the dietary models of ALD and the modern diet.

 

 

1.            Kondili, L.A., G. Taliani, G. Cerga, M.E. Tosti, A. Babameto, and B. Resuli, Correlation of alcohol consumption with liver histological features in non-cirrhotic patients. Eur J Gastroenterol Hepatol, 2005. 17(2): p. 155-9.

2.            Kim, C.H. and Z.M. Younossi, Nonalcoholic fatty liver disease: a manifestation of the metabolic syndrome. Cleve Clin J Med, 2008. 75(10): p. 721-8.

3.            Jin, R., N.A. Le, S. Liu, M. Farkas Epperson, T.R. Ziegler, J.A. Welsh, D.P. Jones, C.J. McClain, and M.B. Vos, Children with NAFLD Are More Sensitive to the Adverse Metabolic Effects of Fructose Beverages than Children without NAFLD. J Clin Endocrinol Metab, 2012. 97(7): p. E1088-98.

4.            Lim, J.S., M. Mietus-Snyder, A. Valente, J.M. Schwarz, and R.H. Lustig, The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome. Nat Rev Gastroenterol Hepatol, 2010. 7(5): p. 251-64.

5.            Lieber, C.S., N. Spritz, and L.M. DeCarli, Role of dietary, adipose, and endogenously synthesized fatty acids in the pathogenesis of the alcoholic fatty liver. J Clin Invest, 1966. 45(1): p. 51-62.

6.            Nieto, N. and M. Rojkind, Repeated whiskey binges promote liver injury in rats fed a choline-deficient diet. J Hepatol, 2007. 46(2): p. 330-9.

7.            Kajikawa, S., K. Imada, T. Takeuchi, Y. Shimizu, A. Kawashima, T. Harada, and K. Mizuguchi, Eicosapentaenoic acid attenuates progression of hepatic fibrosis with inhibition of reactive oxygen species production in rats fed methionine- and choline-deficient diet. Dig Dis Sci, 2011. 56(4): p. 1065-74.

8.            Theuer, R.C., W.H. Martin, T.J. Friday, B.L. Zoumas, and H.P. Sarett, Regression of alcoholic fatty liver in the rat by medium-chain triglycerides. Am J Clin Nutr, 1972. 25(2): p. 175-81.

9.            Nanji, A.A., C.L. Mendenhall, and S.W. French, Beef fat prevents alcoholic liver disease in the rat. Alcohol Clin Exp Res, 1989. 13(1): p. 15-9.

 

 

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Season’s Greetings!

Posted in Food, Life, tagged , , on May 12, 2012| 1 Comment »

The hours of my surgery clerkship have my internal clock a little out of whack, but don’t worry, I’m not 7 months out of step.  Actually, I’m all-abuzz about the arrival of spring, and all the great things that this season brings! (I’m also all-abuzz because I have a full weekend off for the first time in 3 weeks… Hazzah!).

I don’t think there’s a place I’ve been where spring doesn’t bring a certain sense of joy and optimism- there’s something about the change in temperature, the awakening of plants, and the enthusiasm of spring mating games (human and otherwise) that makes this a very special time of year. While I haven’t been able to enjoy as much of the spring weather, spring sun, and spring scenery as I would like (not to mention the spring mating games), I am enjoying taking advantage of one of the benefits of spring- the food!

To me, the start of spring is signified by the start of the asparagus season.  While I’ve had limited success growing it myself (probably a combined issue of a poor planting location and an inability to let the first couple years of spears grow unmolested (you shouldn’t pick the spears for the first few years so the crowns can grow to be big and strong… I suppose patience (at least for asparagus) is not one of my redeeming characteristics)), there is a farm ½ a mile down the road that produces it by the bucket load.  As soon as the roadside stand comes out, you can be guaranteed to find asparagus in my fridge.  This asparagus is fresh, with no need to *snap* the bottoms off and with excellent texture and flavor. For a month or so, asparagus is a staple of my diet, and there are days when I’ll have it at every meal of the day (honestly- asparagus, poached eggs, and Hollandaise sauce- it works for breakfast, lunch, or dinner!).  Outside of this brief season, I’ll never buy asparagus (you’re just setting yourself up for disappointment), and if I happen to be served asparagus at other times of the year I’m puzzled by the physical resemblance but gustatory dissimilarity between the tender and tasty spring spears I’m accustomed to and the tasteless stringy curiosities I’ve been served mid-winter.

My mention of poached eggs, asparagus, and Hollandaise sauce was no accident. Not only is this one of my favorite meals, but it’s also (at least to me) an excellent seasonal meal. While my hens produce eggs year-round, they outdo themselves in the spring. Production is up, and as they feast on new grass and fresh bugs, the quality (and flavor!) of their yolks increases. Similarly, butter from cows grazing on spring grass is brilliantly yellow with a decadent taste. Combined (with a squeeze of a not-so-local lemon) these ingredients come together to form a culinary delight that complements asparagus and poached eggs perfectly (as well as a number of other delicious things).

In my book, asparagus is the ultimate ‘spring-tiding’, yet there are other signs of spring (along with the orange yolks of my chickens’ eggs) that I look forward to every year. Spring brings the first fresh greens (arugula being my favorite), and fresh fruit-like-substance to the table. Rhubarb, a stem that is transformed by stewing and sweetening into a dessert, is another tiding of spring. My father reasons (and he might well be right), that the only reason anyone ever ate rhubarb is that it is one of the earliest spring products. If this curious, tart, stem came to maturity during the summer, between waves of berries and stone fruit, it seems unlikely that it would be paid much attention, but as one of the earliest edibles of the year, it finds it’s way to our table.

There are a number of great books that explore the difficulties and pleasures of seasonal and local eating. I read “The Dirty Life” last year, and recently enjoyed “Animal, Vegetable, Miracle”.  “The Dirty Life” documents the life of a young couple that work a farm that provides a complete pantry (from maple syrup and flour to vegetables and meat) CSA style, while “Animal, Vegetable, Mineral” follows the year long adventure of a family that aims to ‘eat local’ for a year. The task in both books is daunting and the process is time consuming (and at times limiting) yet the benefits, and the connection such a commitment brings to the environment and your food are vast.  I highly recommend both books, especially to those that enjoy reading about the trials and tribulations of farming and eating local. (By no means are either book “Paleo”, as both authors embrace grains, yet the tenets of ‘eat local, eat seasonal’ are ones that I think all should embrace.)

I am not a puritan. I enjoy non-local, non-seasonal fruits and vegetables, and some of my dietary staples are things that never have been and never will be local or seasonal to my environment (Oh, to live in a place where avocados, cacao, coffee or coconuts are local or seasonal!). Yet every winter I await the coming of spring and the bounties that the ensuing seasons will bring. The pungent reminder of asparagus recently consumed harkens the arrival of a bounty of crops that the following months will bring!

Seasonal bounty: Spring greens, Spring eggs, rhubarb, asparagus, and (teensy) radishes

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Odd Bits

Posted in Food, General, tagged , , on May 6, 2012| 14 Comments »

Earlier this week I received a newsletter from PaleolithicDiet.com that included the challenge to write a blog post about what you would cook if you were selected to receive a copy of Jennifer McLagan’s book Odd Bits: How to Cook the Rest of the Animal. In all fairness, I don’t need a copy of McLagan’s book (I already own one), but I like having a topic that I’m enthusiastic about and that doesn’t require I pull any scholarly papers and reference my sources! I like to write, but I haven’t had time to really research some of the more academic topics I’m interested in recently. I accept Patrik’s challenge, and if he wants to send me another copy, I’ll make sure to share it with someone that will love, appreciate, and use it!

Perhaps more important that what I would (or do) cook from Odd Bits, is why I cook offal. To me there are three main reasons (in no specific order).

1: It’s the right thing to do, in respect for the animal you are eating.

As I mentioned in my post on the ethics of eating meat, I have raised (and slaughtered) my own chickens for a number of years.  When I learned to “process” chickens, I was taught to save the heart and liver, both organs that I knew I should eat, but ones I’d never eaten before. My parents are British, and while it may have deeply pained them, I’d never been one for steak and kidney pie, nor had I been one to eat other ‘odd’ bits of animal. I, like so many, fell victim to the ‘eww’ factor of eating odd bits and stuck to the traditional muscle meats. This changed when I started killing my own chickens. First- I knew how much time and effort went into raising and butchering these animals, and throwing away edible bits just seemed wrong. Second- and more importantly, I was taking an animals life, and while I had done my best to make their life (and death) as pleasant as possible, it only seemed right that when I killed them, I used all the bits I could. Third- at that point I was well on the slippery slope to “evolutionary wellness”, and had been reading up on the nutritional benefits of eating organs.

I’ll admit that the first time I cooked chicken livers and hearts I needed a bit of Dutch courage. After imbibing a couple glasses of a delicious Marlborough region Sauvignon Blanc (my weakness when it comes to white wine), I briefly sautéed fresh livers (cut into bite sized pieces) and hearts (halved) in a generous portion of butter and then topped them with salt and fresh pepper. With my Dutch (or perhaps I should say Kiwi?) courage, I took my first bites and was hooked. While I rarely eat chicken these days, if I spot hearts and livers from pastured chickens for sale at the farmers market I usually nab a couple pounds. Not only are they delicious, but it seems only right that if we kill an animal, we should make the most of that sacrifice.

The same concept applies to the cattle that my family raises. I think the old guy that runs the slaughter house we go to gets a kick out of me and my enthusiasm for odd bits (or at least he’s good natured about humoring me- I can imagine him telling his friends about some ‘young woman with a hankering for weird cow parts’), and it seems like each year my list of ‘bits to save’ gets longer. Along with the cut sheets for our animals I include a cover sheet that includes all the extra bits I want to make sure he saves for us. Usually this butcher will return the heart, liver, tail, and tongue, but I’ve added sweet breads, kidneys, marrow bones, and fat to the list. This generally adds a couple extra boxes to my pickup run, and he had a funny smile last time he handed over a 40+ lb box of suet, but he complies (and I think I might need to start making soap- I probably already have a lifetime supply of tallow!). Much like with the chickens, I feel it is important to get the most out of the animals that my family has cared for that have died to feed us.

2: Offal is darn nutritious!

Not only do I think it is morally appropriate to eat ‘nose to tail’, it’s also an excellent nutritional choice. Organ meats are rich in compounds that are lacking (or low) in other parts of the animal. Liver, for example, is very rich in vitamin A (although you should never eat Polar Bear liver- it is so rich in Vitamin A it is toxic!), many of the B vitamins, and iron (to only list a few). Heart, kidney, marrow, and sweet breads all offer different nutritional profiles. I’m generally not joking (nor am I alone) when I refer to liver as “Nature’s multivitamin”.

3- Odd bits are tasty!

Once you get over the ‘weird’ factor of eating different bits of animals, you’ll start to realize they’re really not so odd and that they can be VERY tasty. Tongue tacos, grilled heart, sautéed liver (+/- bacon), steak and kidney… these are all very cookable dishes that can be very delicious. Just like anything else in the kitchen, you can mess them up, but cooked right, these dishes are a delicacy! There’s a reason that some of the fanciest restaurants serve offal, and it’s not just the ‘wow’ factor of serving something unique- offal is delicious!

In conclusion…

It’s only in our modern society that ‘nose to tail’ eating is not the norm. I’d wager that for most of our evolutionary past, humans have taken advantage of all the edible bits an animal had to offer. While many still find ‘odd bits’ off-putting, the interest in them is growing. That’s not only obvious by the publication of books such as Odd Bits, but also by observing changes in the people around me.  When my family sold our first beef cattle, few (if any) customers wanted ‘odd bits’.  As I find customers that are interested in evolutionary eating, my stash of unclaimed offal diminishes (I think I miss the extra tongues the most!). I’m happy, however, if others start to embrace offal, in it’s many forms. Eating offal is delicious, nutritious, and shows respect to the animal you’re eating.  If you’re intimidated by the idea of cooking offal at home, order out (Korean BBQ is a great way to have tongue (and if you’re brave, intestines-yum!)) or you can go the route I travelled and obtain a bit of liquid courage*!

*attempt at your own risk!

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