Category Archives: Disease - Page 16

Answer Day: What Causes High LDL on Low-Carb Paleo?

Posted by on March 3, 2011 383 comments

First, thank you to everyone who commented on the quiz. I enjoyed reading your thoughts.

Is High LDL Something to Worry About?

Perhaps this ought to be the first question. Jack Kronk says “I don’t believe that high LDL is necessarily a problem” and Poisonguy writes “Treat the symptoms, Larry, not the numbers.” Poisonguy’s comment assumes that the LDL number is not a symptom of trouble. Is it?

I think so. It helps to know a little about the biology of cholesterol and of blood vessels.

When cells in culture plates are separated from their neighbors and need to move, they make a lot of cholesterol and transport it to their membranes. When cells find good neighbors and settle down, they stop producing cholesterol.

The same thing happens in the body. Any time there is a wound or injury that needs to be healed, cholesterol production gets jacked up.

When people have widespread vascular injuries, cholesterol is produced in large quantities by cells lining blood vessels. Now, to repair injuries cells have to coordinate their functions. Endothelial cells are the coordinators of vascular repair: they direct other cell types, like smooth muscle cells and fibroblasts, in the healing of vascular injuries.

To heal vascular injuries, these cells not only need more cholesterol for movement; they also need to multiply. It turns out that LDL, which carries cholesterol, also causes vascular cells to reproduce (“mitogenesis”):

The best-characterized function of LDLs is to deliver cholesterol to cells. They may, however, have functions in addition to transporting cholesterol. For example, they seem to produce a mitogenic effect on endothelial cells, smooth muscle cells, and fibroblasts, and induce growth-factor production, chemotaxis, cell proliferation, and cytotoxicity (3). Moreover, an increase of LDL plasma concentration, which is observed during the development of atherosclerosis, can activate various mitogen-activated protein kinase (MAPK) pathways …

We also show … LDL-induced fibroblast spreading … [1]

If endothelial cells are the coordinators of vascular repair, and LDL particles their messengers to fibroblasts and smooth muscle cells, then ECs should be able to generate LDL particles locally. Guess what:  ECs make a lipase whose main effect is to decrease HDL levels but can also convert VLDL and IDL particles into LDL particles and remove fat from LDL particles to make them into small, dense LDL:

Endothelial lipase (EL) has recently been identified as a new member of the triglyceride lipase gene family. EL shares a relatively high degree of homology with lipoprotein lipase and hepatic lipase …

In vitro, EL has hydrolyzed phospholipids in chylomicrons, very low density lipoprotein (VLDL), intermediate density lipoprotein and LDL. [2]

Immune cells, of course, are essential for wound healing and they should be attracted to any site of vascular injury. It turns out that immune cells have LDL receptors and these receptors may help them congregate at sites of vascular injury. [3]

I don’t want to exaggerate the state of the literature here:  this is a surprisingly poorly investigated area. But I believe these things:

1.      Cholesterol and LDL particles are part of the vascular wound repair process.

2.      Very high LDL levels are a marker of widespread vascular injury.

Now this is not the “lipid hypothesis.” Compare the two views:

  • The lipid hypothesis:  LDL cholesterol causes vascular injury.
  • My view:  LDL cholesterol is the ambulance crew that arrives at the scene of the crime to help the victims. The lipid hypothesis is the view that ambulance drivers should be arrested for homicide because they are commonly found at murder scenes.

So, to Poisonguy, on my view high LDL numbers are a symptom of vascular injury and are a cause for concern.

Big-Picture View of the Cause of High LDL

So, on a micro-level, I think vascular damage causes high LDL. But what causes vascular damage?

Here I notice a striking difference in commenters’ perspectives and mine. I tend to take a big-picture, top-down view of biology. There are three basic causes of nearly all pathologies:

1.      Toxins, usually food toxins.

2.      Malnutrition.

3.      Pathogens.

The whole organization of our book is dictated by this view. It is organized in four Steps. Step One is about re-orienting people’s views of macronutrients away from high-grain, fat-phobic, vegetable-oil-rich diets toward diets rich in animal fats. The other steps are about removing the causes of disease:

1.      Step Two is “Eat Paleo, Not Toxic” – remove food toxins.

2.      Step Three is “Be Well Nourished” – eliminate malnutrition.

3.      Step Four is “Heal and Prevent Disease” – address pathogens by enhancing immunity and, where appropriate, taking advantage of antibiotic therapies.

So when someone offers a pathology, any pathology, my first question is: Which cause is behind this, and which step do they need to focus on?

In Larry’s case, he had been eating low-carb Paleo for years. So toxins were not a problem.

Pathogens might be a problem – after all, he’s 64, and everybody collects chronic infections which tend to grow increasingly severe with age – but Larry hadn’t reported any other symptoms. More to the point, low-carb Paleo diets typically enhance immunity, yet Larry had fine LDL numbers before adopting low-carb Paleo and then his LDL got worse. So it wouldn’t be infectious in origin unless his diet had suppressed immunity through malnutrition – in which case the first step would be to address the malnutrition.

Step Three, malnutrition, was the only logical answer. The conversion to Paleo removes a lot of foods from the diet and could easily have removed the primary sources of some micronutrients.

So I was immediately convinced, just from the time-course of the pathology, that the cause was malnutrition.

Micronutrient Deficiencies are Very Common

In the book (Step Three) we explain why nearly everyone is deficient in micronutrients. The problems are most severe for minerals:  water treatment removes minerals from water, and mineral depletion of soil by industrial agriculture leads to mineral deficiencies in farmed plants and grain-fed animals.

This is why our “essential supplements” include a multimineral supplement plus additional quantities of five minerals – magnesium, copper, chromium, iodine, and selenium. Vitamins get a lot of attention, but minerals are where the big health gains are.

Copper Deficiency and LDL

Some micronutrient deficiencies are known to cause elevated LDL.

Readers of our book know that copper causes vascular disease; blog readers may be more familiar with an excellent post by Stephan, “Copper and Cardiovascular Disease”, discussing evidence that copper deficiency causes cardiovascular disease. As I’ve just argued that cardiovascular disease causes high LDL, it shouldn’t be a surprise that copper deficiency also causes hypercholesterolemia:

Copper and iron are essential nutrients in human physiology as their importance is linked to their role as cofactors of many redox enzymes involved in a wide range of biological processes, as well as in oxygen and electron transport. Mild dietary deficiencies of both metals … may cause long-term deleterious effects in cardiovascular system and alterations in lipid metabolism (3)….

Several studies showed a clear correlation among copper deficiency and dyslipidemia. The main alterations concern higher plasma CL and triglyceride (TG) concentrations, increased VLDL-LDL to HDL lipoproteins ratio, and the shape alteration of HDL lipoproteins.  [4]

The essentiality of copper (Cu) in humans is demonstrated by various clinical features associated with deficiency, such as anaemia, hypercholesterolaemia and bone malformations. [5]

Over the last couple of decades, dietary copper deficiency has been shown to cause a variety of metabolic changes, including hypercholesterolemia, hypertriglyceridemia, hypertension, and glucose intolerance. [6]

Copper deficiency is, I believe, the single most likely cause of elevated LDL on low-carb Paleo diets. The solution is to eat beef liver or supplement.

So, was my advice to Larry to supplement copper?  Yes, but that was not my only advice.

Other Micronutrient Deficiencies and Elevated LDL

Another common micronutrient deficiency that causes elevated LDL cholesterol is choline deficiency that is NOT accompanied by methionine deficiency. That is discussed in my post “Choline Deficiency and Plant Oil Induced Diabetes”:

Choline deficiency (CD) by itself induces metabolic syndrome (indicated by insulin resistance and elevated serum triglycerides and cholesterol) and obesity.

A combined methionine and choline deficiency (MCD) actually causes weight loss and reduces serum triglycerides and cholesterol …

I quote both these effects because it illustrates the complexity of nutrition. A deficiency of a micronutrient can present with totally different symptoms depending on the status of other micronutrients.

Julianne had a really nice comment, unfortunately caught in the spam filter for a while, with a number of links. She mentions vitamin C deficiency and, with other commenters, noted the link between hypothyroidism and elevated LDL. As one cause of hypothyroidism is iodine or selenium deficiency, this is another pathway by which mineral deficiencies can elevate LDL.

UPDATE: Mike Gruber reduced his LDL by 200 mg/dl by supplementing iodine. Clearly iodine can have big effects!

Other commenters brought up fish oil. They may be interested to know that fish oil not only balances omega-6 to modulate inflammatory pathways, it also suppresses endothelial lipase and thus moderates the LDL-raising and HDL-lowering effect of vascular damage:

On the other hand, physical exercise and fish oil (a rich source of eicosapentaenoic acid and docosahexaenoic acid) suppress the activity of EL and this, in turn, enhances the plasma concentrations of HDL cholesterol. [7]

Whether this effect is always desirable is a topic for another day.

My December Advice to Larry

So what was my December advice to Larry?

It was simple. In adopting a low-carb Paleo diet, he had implemented Steps One and Two of our book. My advice was to implement Step Three (“Be well nourished”) by taking our recommended supplements. Eating egg yolks and beef liver for copper and choline is a good idea too.

Just to cover all bases, I advised to include most of our “therapeutic supplements” as well as all the “essential supplements.”

Since December, Larry has been taking all the recommended supplements and eating 5 ounces per week of beef liver. As I noted yesterday, Larry’s LDL decreased from 295 mg/dl to 213 mg/dl, HDL rose from 74 mg/dl to 92 mg/dl, and triglycerides fell from 102 to 76 mg/dl since he started Step Three. This is all consistent with a healthier vasculature and reduced production of endothelial lipase.

Conclusion

Some people think there is something wrong with a diet if supplements are recommended. They believe that a well-designed diet should provide sufficient nutrition from food alone, and that if supplements are advised then the diet must be flawed.

I think this is quite mistaken. The reality is that Paleolithic man was often mildly malnourished, and modern man – due to the absence of minerals from treated water and agriculturally produced food, and the reduced diversity and higher caloric density of our foods – is severely malnourished compared to Paleolithic man.

We recommend eating a micronutrient-rich diet, including nourishing foods like egg yolks, liver, bone broth soups, seaweed, fermented vegetables, and so forth. But I think it’s only prudent to acknowledge and compensate for the widespread nutrient depletion that is so prevalent today. Even when nutrient-rich food is regularly eaten, micronutrient deficiencies are still possible.

Eating Paleo-style is not enough to guarantee perfect health. Luckily, supplementation of the key nutrients that we need for health and that are often missing from foods will often get us the rest of the way.

References

[1] Dobreva I et al. LDLs induce fibroblast spreading independently of the LDL receptor via activation of the p38 MAPK pathway. J Lipid Res. 2003 Dec;44(12):2382-90. http://pmid.us/12951358.

[2] Paradis ME, Lamarche B. Endothelial lipase: its role in cardiovascular disease. Can J Cardiol. 2006 Feb;22 Suppl B:31B-34B. http://pmid.us/16498510.

[3] Giulian D et al. The role of mononuclear phagocytes in wound healing after traumatic injury to adult mammalian brain. J Neurosci. 1989 Dec;9(12):4416-29. http://pmid.us/2480402.

[4] Tosco A et al. Molecular bases of copper and iron deficiency-associated dyslipidemia: a microarray analysis of the rat intestinal transcriptome. Genes Nutr. 2010 Mar;5(1):1-8. http://pmid.us/19821111.

[5] Harvey LJ, McArdle HJ. Biomarkers of copper status: a brief update. Br J Nutr. 2008 Jun;99 Suppl 3:S10-3. http://pmid.us/18598583.

[6] Aliabadi H. A deleterious interaction between copper deficiency and sugar ingestion may be the missing link in heart disease. Med Hypotheses. 2008;70(6):1163-6. http://pmid.us/18178013.

[7] Das UN. Long-chain polyunsaturated fatty acids, endothelial lipase and atherosclerosis. Prostaglandins Leukot Essent Fatty Acids. 2005 Mar;72(3):173-9. http://pmid.us/15664301.

Low Carb Paleo, and LDL is Soaring – Help!

Posted by on March 2, 2011 59 comments

To Kindy, Zach’s parents, and the NBIA/PKAN kids: I’ve been reading papers on the disease and trying to figure out the best diet for the disease. But the biochemistry is a bit complex, more complex than I realized last week, and I want to make sure my advice is sound. So I’m delaying my NBIA/PKAN/ketogenic diet posts until next week.

My sincere apologies for the delay!

I’m a little busy this week – busy with work, busy with learning about NBIA/PKAN, and eager to spend time with my brother who is visiting from Germany – and so I thought I’d do a “You be the doctor” quiz.

Here’s the puzzle. Someone adopts a low-carb Paleo diet. Very healthy diet, right? But their LDL cholesterol level starts to rise. And rise. And rise.

Larry Eshelman emailed me last December with this problem. His LDL history:

  • 103 mg/dl (1990-2002, eating a low fat diet)
  • 115 mg/dl (2002-2007, eating a low carb diet)
  • 195 mg/dl (2007-2009, after reading Gary Taubes and adding saturated fat)
  • 254 mg/dl (Dec 2009, very low-carb Paleo for 5 weeks)
  • 295 mg/dl (Jun 2010, very low-carb Paleo for 7 months)

(SI system readers, convert to mmol/l by dividing by 38.67.)

A common problem

This is not a terribly uncommon problem in the Paleo community; it afflicts famous and brilliant bloggers as well as ordinary folks. It’s been discussed by Richard Nikoley in several posts:

Some examples of high LDL on a Paleo diet, with links – most of these provided to me by Larry (thanks Larry!):

OK, that’s enough: this is a minority phenomenon, but it’s definitely not an exceptional n=1 phenomenon.

Larry’s Progress

Larry wrote me at the beginning of December asking for advice. He implemented everything I suggested. I just heard back from him this week with new data.

His LDL decreased from 295 mg/dl to 213 mg/dl in a recent test. His HDL rose from 74 mg/dl to 92 mg/dl. His triglycerides fell from 102 to 76 mg/dl.

LDL is still high, but improving; the others are excellent and improving.

So, quiz questions:

  • Can you guess what my December advice to Larry was?
  • What causes these cases of soaring LDL on Paleo? (Of course, there are multiple possible causes of high LDL, but I think among Paleo dieters one explanation is more likely than others, and that’s what I’m looking for.)

My answers tomorrow night.

UPDATE: Answers here: Answer Day: What Causes High LDL on Low-Carb Paleo?

Ketogenic Diet for NBIA (Neurodegeneration with Brain Iron Accumulation)

Posted by on February 22, 2011 63 comments

It’s always a pleasure to hear from readers who report improved health.

Some of these emails are poignant: distressing because of the pain of their diseases, yet heartening because of the improvements a good diet brings.

It can’t get more poignant than to hear that children with a painful, deadly, and untreatable disease have, thanks to diet, begun smiling, laughing, and getting better.

Last week Kindy Flyvholm, who bought our pre-publication e-book, wrote with just such a report. I’m delighted to be able to pass it on, and hopeful that this report will help other children escape unnecessary suffering and enjoy life more abundantly. Thank you, Kindy, for sharing your story!

Ketogenic diets as therapy for neurological dysfunction

In our book and on this blog, we advise everyone with a neurological or brain disorder to try a ketogenic (“ketone generating”) diet. The book spells out how to tweak the Perfect Health Diet to make it ketogenic: basically, reduce carbs and add copious amounts of coconut oil.

Ketogenic diets can be surprisingly helpful with brain and nerve dysfunctions. The reason is that neurons have very limited metabolic options: they can burn only glucose or ketones. Glucose metabolism is complex and prone to failure; ketone metabolism is simple and robust. Especially in disease states, a neuron on glucose can be a totally different creature from a neuron on ketones. Neurological diseases that are disastrous on a glucose-rich diet can become mild when neurons are fed ketones.

It doesn’t work for every brain disease, in part because ketones don’t diffuse through the brain all that well. Ketones reach the subcortical and inner cortical layers of the brain easily, but don’t readily reach superficial layers. [1] However, in some diseases the places reached by ketones are the ones in trouble. The evolutionarily oldest parts of the brain, such as the brain stem, are the most likely to benefit from a ketogenic diet. Thus, neurodegenerative diseases that cripple the body may be top candidates for a therapeutic ketogenic diet.

NBIA (Neurodegeneration with Brain Iron Accumulation)

One such disease is NBIA, short for Neurodegeneration with Brain Iron Accumulation. NBIA is most commonly caused by a mutation in the gene PANK2, which codes for the mitochondrial enzyme that converts vitamin B5 (pantothenic acid) into CoenzymeA (a crucial metabolic substrate). This version of NBIA is called PKAN, for pantothenate kinase-associated neurodegeneration.

NBIA/PKAN is characterized by an accumulation of iron in the basal ganglia of the brain. The iron is readily visible in brain MRIs, producing an “eye of the tiger” brightness pattern. [2] It produces symptoms that overlap with those of Parkinson’s disease. [3] About 1 in 500 people carries a PANK2 mutation, so some form of the disease strikes 1 in 250,000 people.

The disease typically first presents itself about age 3, when leg dystonia and spasticity causes an impaired gait, sometimes including toe-walking. The disease progresses and children lose the ability to walk. Dystonia extends to the hands and the face; the head cannot be held upright, and swallowing becomes difficult. Blindness from retinopathy and hearing loss often develop. Premature death occurs usually in the teens, often by age 10 or younger. The last years are excruciatingly painful.

Here is a picture of Zach, age 12:

You can see his inability to hold his head upright, and the hand position characteristic of dystonia. Zach cannot swallow naturally and has to be tube-fed.

The bumps in his chest are from the battery packs used to drive a deep brain stimulation device. The idea is to introduce signals that counter the excruciatingly painful dystonic spasms. Like other therapies for NBIA, deep brain stimulation is often ineffective. In Zach’s case, the device worked for less than one month. It is now turned off but is not removed because the operation would be too traumatic.

Ketogenic Diet Therapy

Kindy writes:

It was in desperation that we began researching options (ANY OPTION) to prevent the horrible pain that precedes death especially in the case of children with early-onset NBIA.

Many research paths led to the ketogenic diet being an option.  A lot of discouraging information was presented as well (like how impossible it is to follow or how disruptive it is to family life, etc).

It’s remarkable, but doctors are so divorced from dietary science that they do not know how simple and natural a ketogenic diet can be, and assume that only absurdly onerous formulations are needed. As we point out in the book, a large fraction of mammals eat ketogenic diets as their natural diet; and all mammals including humans subsist on ketones during starvation.

Doctors were pessimistic about its chances, but a ketogenic diet produced amazing results:

My son, who is 6, … has been on the diet for less than one month and his hands have relaxed enough for him to regain his pointing ability (which had been lost).

Zach, the 12 year old on the diet, is much further progressed in the disease.  Zach has been on the diet since late October, 2010, reaching 80% fat levels towards mid-December.  The following are the improvements that have been noted by Zach’s family and therapists:  Zach has begun holding up his head even though his neck has been hyper extended backwards since he was 9, he has begun pointing with his finger again instead of the palm of his hand, he is moving his right arm again some, and the latest thing is that he is now able to go from a laying position to a sitting position on his own by hanging on to something or someone.  He has not done this since he was 9 years old.

Both boys have begun smiling and laughing all the time.

I know just how they feel!

The previous picture was Zach before starting the ketogenic diet. Here he is on the diet:

Kindy continues:

Zach has gotten off all pain medicine and only has a small amount of 3 [anti-spasmodic] medicines left which hopefully he can get off of over the next year.

Going in and out of ketosis has immediate effects, as this anecdote shows:

Zach had a recent day where his muscle spasms returned severely.   Bad enough he needed to go to the hospital for morphine.  At the last minute (before going to the hospital), the parent looked at her recipe for that day and realized she had used a lot of white chicken meat.  She added in some more coconut oil into his next few tube feedings and the spasms went away immediately.  This is extremely powerful.

Kindy concludes:

We are not under any delusions.  Our children may be taken from us at any time.  If they are taken pain free, then we are blessed compared to the alternative.  The situation thus far with our ‘experiment’ has proven much more than we could have hoped.

Conclusion

Kindy, it’s wonderful that your research and perseverance has bought hope to your son, and that you’re spreading the word to help others find the same hope. I’m so grateful that you’ve shared your story with us. Hopefully your experiences will reach the NBIA community, save children from unnecessary pain, and maybe extend their lives significantly!

We salute every parent who has to deal with neurological and genetic diseases in their children. As this disease illustrates, anyone with a neurological disorder should experiment with a ketogenic diet. Ketogenic diets have been tested in very few diseases, and there is no telling how many neurological diseases may prove amenable to this therapy. But there is already considerable evidence that neurological diseases of the elderly, such as Alzheimer’s and Parkinson’s, are treatable with a ketogenic diet.

Last Thursday, I defended the idea of a healthy diet as the best therapy for disease (“Therapy AND Life”). The NBIA kids illustrate just how powerful dietary therapies can be.

Medical doctors seem to have great misapprehensions and fear of experimenting with this diet. They do not understand it, don’t know how it should be implemented, and have never tried it themselves. Many of the medical ketogenic diets are malnourishing and generate terrible side effects. Not surprisingly, many patients quit the diets.

This coming Thursday, I’ll discuss how to implement a safe, healthy, and pleasurable-to-eat ketogenic diet. There’s no reason for an unpalatable or malnourishing diet to stop patients from enjoying the benefits that Zach has seen!

References

[1] Hawkins RA, Biebuyck JF. Ketone bodies are selectively used by individual brain regions. Science. 1979 Jul 20;205(4403):325-7. http://pmid.us/451608.

[2] Gregory AM, Hayflick SJ. Neurodegeneration with brain Iron Accumulation. Orphanet Encyclopedia, September 2004. http://www.orpha.net/data/patho/GB/uk-NBIA.pdf.

[3] Klein C et al. Hereditary parkinsonism: Parkinson disease look-alikes–an algorithm for clinicians to “PARK” genes and beyond. Mov Disord. 2009 Oct 30;24(14):2042-58. http://pmid.us/19735092. Paisán-Ruiz C et al. Early-onset L-dopa-responsive parkinsonism with pyramidal signs due to ATP13A2, PLA2G6, FBXO7 and spatacsin mutations. Mov Disord. 2010 Sep 15;25(12):1791-800. http://pmid.us/20669327.

Around the Web; Eating Disorders and Hypothyroidism

Posted by on February 19, 2011 37 comments

Items that caught my eye this week:

(1) Would You Be My Meatheart?: I wasn’t clever enough to give this to Shou-Ching for Valentine’s Day, but would have known to use genuine hearts from the Asian market. Wait till next year honey!

(2) By the way: Who knew Manolo has a food blog?

(3) Ronaldo Forced Out of Soccer for Lack of Thyroid Hormone. Famed soccer star Ronaldo is retiring because he has hypothyroidism and he says soccer authorities consider treatment to be doping – so he has to retire to fix his health.

Absurd! Mary Shomon agrees.

(4) Ronaldo may play the “beautiful game,” but we Americans play the crazy game. This running back plays football like I used to:

(5) Startling if True: Paleo Pepper abridges a talk by Dr. Flechas at iodine4health.com claiming that thyroid hormone replacement may actually increase risk of breast cancer among hypothyroid women – what is needed is high-dose iodine:

A women with hypothyroidism has a 6% chance of developing breast cancer. Once she starts taking thyroid hormone, it doubles her chances. Once she’s been on thyroid hormone replacement for 15 years, it more than triples it – she now has a 19.6% chance of developing breast cancer.

I have not seen such statistics before and would have to check these claims. We recommend iodine and selenium as the first steps in dealing with hypothyroidism, but generally support thyroid hormone replacement.

(6) Burying the Lede: Is “strengthens pelvic floor muscles” really the number one benefit?

(7) Another Perfect Health breakfast idea: Emily suggests cream of rice with cream, butter, and apricot applesauce.

(8) Paleolithic Dairy?: Ravi at Daia Sol Gaia argues that dogs may have been domesticated and goats tamed and used for milk as early as 35,000 years ago – the start of the Upper Paleolithic. Is goat milk a Paleo food?

(9) The authentic way to drink Paleo goat milk: Paleolithic settlers at Gough Cave in England, c. 13,000 to 10,000 BC, ate human bone marrow and brain and used the skulls as drinking chalices:

Via Dienekes. Apparently drinking from human skulls is a widely attested practice, both in Paleolithic and historical times – see e.g. the Krum and Herodotus’s Scythians.

Reference: Bello SM et al. Earliest Directly-Dated Human Skull-Cups. PLoS ONE 6(2): e17026. doi:10.1371/journal.pone.0017026. Link.

(10) Avoid vegetable oils if you want a baby: Chris Highcock found a paper showing that infertile women eat 23% more polyunsaturated fat, and 17% less saturated fat, than fertile women. Infertile men eat 20% more polyunsaturated fat than fertile men.

Reference: Revonta M et al. Health and life style among infertile men and women. Sex Reprod Healthc. 2010 Aug;1(3):91-8. http://pmid.us/21122604.

(11) Never give up:

“I had the head doctor of surgical I.C.U. say, ‘Miracles happen.’“

(Via Craig Newmark)

(12) Which Machine for the Hippo? I thought this was a cool picture:

(From NPR via John Durant)

(13) Finally, our video: We’ve had a bit of discussion of eating disorders this week, in the comments to the “Therapy AND Life” post. That reminded me of this CBS News interview of a “Biggest Loser” contestant who said she developed an eating disorder during the show: