Yearly Archives: 2011 - Page 28

Seafood Paella

Posted by on April 17, 2011 19 comments

Paella is the classic rice dish of Valencia on Spain’s Mediterranean coast.

It’s a great food for a dinner party: the ingredients take some time to gather, but paella can be made in bulk and provides a complete meal in one bowl. It also uses some wine, so you can drink while you cook and get in the party spirit before the guests arrive!

Ingredients

You’ll need a collection of meats, and seafoods are the usual choice. We chose shrimp, calamari, mussels, salmon, and spicy Italian sausage:

White wine and bone broth provide the necessary liquids. Our ox feet bone broth has plenty of collagen and fats as you can see:

Other ingredients we used are saffron (the threads are soaked in water overnight), red pepper, onion, uncooked white rice, a lemon, garlic, paprika, and parsley:

We also used olive oil and coconut oil (not shown).

Cooking

You can start by stir-frying the onion and garlic in olive oil for two minutes, then adding red pepper for a minute, then the saffron and paprika:

Immediately after the saffron and paprika, add the rice (this was 2/3 cup uncooked), stir to coat it in oil and spices, add the wine and broth, and cover:

Cover the pot and simmer the rice in the broth about 15 minutes at low heat. As it cooks it absorbs liquid; if the broth runs low, add more bone broth. After 15 minutes looks like this:

At this point add the meat, and cover again to steam-cook the meat:

When we made paella a second time, we cooked the shrimp in coconut oil separately and added it to the paella only after the other meats were cooked. This enhanced the flavor of the shrimp:

Once the meat is cooked, add the parsley, juice of a full lemon, salt, pepper, and any other spices. The first time we made it looked like this:

But it’s really better when it has more parsley. When we made the paella the second time, this was how much parsley we used:

You can see that the second time we used more broth. This is the proper amount of liquid to have; our first version was too dry.

Here was the finished product the first time:

Here it was the second time:

Conclusion

If you’re tired of Cambridge Fried Rice, this is a good alternative: it has similar macronutrient proportions but a totally different taste!

For a bonus, we asked Gordon Ramsay to do a paella video:

Around the Web; It’s Angst Week!

Posted by on April 16, 2011 35 comments

Here’s what caught my eye this week:

[1] Goodbye, Walter, and God bless: We’ve closely followed Walter Breuning’s career as the world’s oldest man, since he so well exemplifies our dietary practices. (See Happy Birthday, Walter Breuning!, Sep 21, 2010; What Makes a Supercentenarian?, Aug 18, 2010). Sadly, he passed away on Thursday. Hat tip, Chris Highcock.

[2] Interesting posts this week: Tom Naughton. Egyptian mummies. Enough said.

Jamie Scott considers the optimal training strategy in 10 hours per week – and whether Goldilocks training (not too hard, not too easy) has any merit. Emily Deans thinks doctors should be able to write prescriptions for grass-fed steak and wild-caught salmon. I’m all for that – we would actually get some value out of our health insurance! I can see it now: “I’m doing great on the Kobe beef and lobster, doc. What’s my co-pay?”

Prague Stepchild offers Staffan Lindeberg in a nutshell. (Note: human salt needs are higher on low-carb diets.) Life’s Little Mysteries reports that the leading cause of death after age 65 is falling down. Ned Kock reviews what the China Study shows about effect of foods on appetite.

Stephan critiqued the “drink less, pee more” theory for treating edema. Gary Taubes had a New York Times piece, “Is Sugar Toxic?” which starts slow (you won’t miss much if you start on page 4), but picks up. Bix at Fanatic Cook gave a high-carb dieter’s response. Chris Masterjohn reviewed an Experimental Biology conference. Some great photos there!

[3] I know what you’re thinking, Buttercup! You need a Robb Wolf spoof! Chris Highcock of Conditioning Research has you covered.

[4] I know what else you want! Penguin tickling!

[5] Long Fasts: Jimmy Moore is doing a 7-day total fast.

I would caution him to drink lots of water and take electrolytes (salt for sodium and chlorine, plus potassium and magnesium, maybe mineral water with calcium). Personally, I would ease any long fast a bit with coconut oil or MCTs. And if any troubles develop, cut the fast short.

I myself will soon be doing my longest fast of the year, from Holy Thursday evening to Easter Sunday, about 64 hours.

[6] Is It Like This Every Day?:

Victoria Falls on the Zambia/Zimbabwe border. Via Babel’s Dawn.

[7] Our national drug problem just keeps getting worse: The New York Times reports that the number of people hospitalized for medication side effects is up 50% in just 4 years, to 1.9 million.

I wonder how many people have been hospitalized for Paleo dieting?

[8] Females Rule!: Last week we had bear vs bison, and the bear was winning. This week, it’s bear vs milch cow:

Check out Richard Smith’s post for the full photo series, and the outcome that was happy – for the cows.

[9] Shhhhh, don’t tell anyone: John Durant has dandruff, and asks for tips.

I was the only one who suggested eating starch and supplementing minerals for anti-fungal immunity, since dandruff is usually caused by the fungal pathogen Malassezia whose growth is promoted on a zero-carb mineral-deficient diet. The consensus among his commenters: go more Paleo by giving up shampoo and hot water. Yes, John Durant is insufficiently Cro-Magnon.

[10] It is smart to drink: We’ve previously considered this question (Is It Smart to Drink?, Sep 9, 2010). Via Instapundit comes Repeated Ethanol Exposure Enhances Synaptic Plasticity in Key Brain Area, Study Finds. “Drinking alcohol primes certain areas of our brain to learn and remember better, says a new study …”

[11] Bill Murray Has a New Role as “Braco”: Via Seth Roberts we learned that looking at human faces is therapeutic for circadian rhythm disorders (Seth Roberts and Circadian Therapy, Mar 22, 2011). Now via Richard Fernandez, a Croatian man who heals by having people gaze at his face.

[12] Angst I: Richard Nikoley is getting bored.

[13] There Ought to be Angst: The Danish scientist who led a CDC-funded study that purported to disprove links between autism and vaccines has been indicted for stealing $1 million in research funds.

You’ll recall that Andrew Wakefield, the British scientist who first claimed to find an autism-vaccine link, was a fraud.

With frauds and thieves leading research on both sides of this issue, parents of autistic children must be frustrated.

As I’ve argued many times, we need patient-and-taxpayer-directed funding for biomedical research. Government-and-pharmaceutical-company-only funding stifles innovation, rewards established cliques, and directs research toward ineffective but patentable drugs over effective dietary, nutritional, and antimicrobial therapies.

[14] Angst II: Pål Jåbekk speaks a truth:

Most often when we find obvious contradictions in the same texts in scientific journals I think there are two main reasons: Lack of balls and lack of brains.

A third reason is that the scientist (often, correctly) believes that his career will be advanced by propounding error, and values his career above truth. I might call this lack of integrity.

He goes on to discuss his disappointment with Staffan Lindeberg’s “Food and Western Disease: Health and nutrition from an evolutionary perspective”:

[A]t closing the book after reading its last page I felt a strong sense of disappointment. Lean meat! LEAN MEAT! Come on, Staffan.

I have the same disappointment with all the “Paleo 1.0” writers. I’ve written before (Art de Vany’s New Book and Video, Dec 11, 2010; Old Diets, New Knowledge: For Auld Lang Syne, Dec 31, 2010) of how grateful I am to Art de Vany for introducing me to Paleo, but also that I became malnourished and my infections progressed eating what I considered to be a version of his diet. I’ve criticized Robb Wolf’s “lean meat and vegetables” meal plans. I was recently at a talk by Gary Taubes and afterward he said that he would eat a zero-carb diet if his wife would permit it. Gary has done the world a great service in helping defeat fat-phobia, but I can’t agree with this particular conclusion.

In our case, disappointment with others’ errors led us to write the book and start this blog. As Shou-Ching can attest, my attitude is rather like that of this cartoon character:

Alas, Pål’s disappointment is leading him to take a break from blogging. It’s a big loss for the blogosphere.

[15] Anti-Angst: Razib Khan writes:

[T]oo much focus on the “meta” aspects often get in the way of my main aim: learning as much interesting stuff as is possible before I die. Life is basically a race against the clock, I’m not a person who is much afflicted with the need to “kill time.”

That’s how I feel too. It’s why I spend little time on this blog, and none in our book, refuting error. The pursuit of truth can fill more than one lifetime. Getting distracted by error would take time away from interesting truths.

[16] Song of the week: Emily Deans often puts music in her posts, and she’s a rising star of the blogosphere, with a great gig at Psychology Today.

Now, I’m not saying correlation implies causation, but I’m thinking that if we show off our musical taste, maybe we’ll get picked up by My Weekly Reader:

[17] Not the weekly video: UPDATED! (was this, via Richard Nikoley’s comment section) This is for cat lovers:

[18] Weekly video: Gross! If you have to teach your 8-year-old about biology, you may be able to learn from Julia Sweeney’s experience:

(Via Craig Newmark)

HDL: Higher is Good, But is Highest Best?

Posted by on April 14, 2011 79 comments

(I was going to give a how-to guide for raising HDL today, but I’ll do that Tuesday; today I want to address some interesting preliminary matters.)

On Tuesday I raised the possibility that the primary function of HDL particles is immune: HDL gathers anti-pathogenic immune molecules and acts as a “Trojan horse” to attach those molecules to pathogens, helping white blood cells find and kill them.

Another Function of HDL: Toxin Clearance

I probably should have mentioned that HDL has another function: toxin clearance. The primary lipoprotein in HDL, apolipoprotein A-I, not only binds to immune proteins, it also can pick up an assortment of toxins, including oxidized LDL.

The liver is the body’s toxin-destruction organ, and I would propose that its toxin transport function is why HDL tends to return to the liver. As this hypothesis would predict, when HDL has picked up oxidative toxins, its reverse efflux back to the liver is enhanced. [1]

Since toxins cause inflammation, removal of these toxins from the vasculature is anti-inflammatory. This is why HDL is said to be anti-inflammatory.

What are the sources of toxins that HDL clears? One review says reverse efflux, i.e. HDL toxin clearance, is triggered by “genetic mutations, smoking, stress, and high-fat diets.” [2] By high-fat diets they mean high-omega-6 diets which create lots of toxic peroxidized lipids. So if you want your HDL to be devoted to toxin clearance, rather than immune defense, eat a lot of soybean or corn oil.

Interestingly, as aging proceeds and health becomes impaired, HDL becomes less effective at picking up toxins and carrying them back to the liver. [2]

My interpretation of this observation would be that as we age, our burden of chronic infections increases. This causes more of our HDL to pick up immune proteins, converting them into pathogen-fighting HDL rather than toxin-clearing HDL.

These pathogen-fighting HDL particles do not go back to the liver. [3] So when HDL gets converted to pathogen-fighting particles, it can no longer clear toxins. Toxins linger in vascular cells and macrophages for lack of HDL transport.

Conventional Wisdom: “Dysfunctional” HDL

I often criticize mainstream scientists and doctors for an anti-natural view of human biology. Mainstream research paradigms neglect pathogens and toxins as the cause of disease, and presume instead that disease results from some malfunctioning of the human body – from genetic mutations, from autoimmune self-attacks, from kamikaze poisoning by evolved entities like LDL particles.

Last September I mocked this attitude in a parable. This week, I was amused to see this attitude at work in the scientists who study HDL.

When HDL particles pick up immune protein complexes and take on their anti-pathogen functions, some scientists call the resulting particles “dysfunctional” or “pro-inflammatory” HDL. [3, 4, 5] This is contrasted to the “anti-inflammatory” HDL that is light, fluffy, fatty and available to carry toxins back to the liver.

The reasoning seems to be that since inflammation is bad, HDL that participates in the inflammatory response must be “dysfunctional.” To me, this is rather like calling white blood cells “dysfunctional blood cells.” After all, white blood cells are pro-inflammatory.

Aside: Why I Don’t Often Use the Word “Inflammation”

This is why I rarely use the word inflammation:  it has a bad connotation, even though it is a natural process involved in healing and immune defense. Like LDL, it has been demonized for its association with disease. Like firefighters who associate with fires, and ambulance drivers that associate with heart attack victims, inflammation should not be blamed for the dysfunction it attends.

Not all anti-inflammatory therapies are good for you. Clearing your body of “dysfunctional HDL” would temporarily reduce inflammation – but it would let pathogens run wild, potentially leading to the fate of Emily’s great uncle.

Can There Be Too Much HDL?

In biology, it’s a general rule that you can get too much of a good thing. The benefits from something usually follow an upside-down U: they increase for a while, reach an optimum, then they fall. Many nutrients are like this: beneficial in small doses, toxic in large doses.

Indeed, our diet is predicated on the idea that we should try to get all good things into their optimal “plateau range.”

It’s also a good rule of thumb that evolution selects for the optimum. Evolution prefers that we be healthy, so the natural evolutionarily selected levels of biomarkers are usually best for us. In general we should eat a healthy diet, and trust that our body will regulate components, like HDL, to their optimal amount.

So that raises the question:  Is it bad to manipulate the body to raise HDL to unusually high levels? Might HDL, like other good things, have a U-shaped benefits curve – so that there is an optimum and raising HDL above that is damaging? Shouldn’t we just live naturally and let our body adjust HDL to whatever level it wants, trusting evolution to have chosen the optimal HDL level for us?

In concrete terms: Is Richard Nikoley’s coconut oil-induced HDL of 133 mg/dl too high?

It’s a fair question!

What Evolutionary Milieu is Our HDL Particle Number Optimized For?

Evolution did select for an optimal level of HDL – that’s why our HDL level is not infinite.

So why did evolution limit HDL? If higher HDL clears toxins and kills pathogens, what would cause evolution to give us too little of it?

A likely answer is that it is costly to produce HDL, and there are diminishing returns to immunity at high HDL levels.

Let’s imagine the Paleolithic environment. Pathogens then were less dangerous. Because the entire global human population was in the hundreds of thousands, human-human transmission was more rare. Without domesticated animals, zoonotic transmission was rare.

Also, food was less available. Today supermarkets are everywhere and people rarely go hungry; but in the Paleolithic the body had to be careful about preserving resources.

So the evolutionary impulse was to conserve resources: the body wouldn’t make more HDL than necessary, since sources for HDL could be better used to scrimp on food.

If this correct, then the optimum HDL level in the Paleolithic was low.

Then the Neolithic came: animals were domesticated and lived near and with humans. People settled in towns, and population density rose. Feces polluted the local water, facilitating pathogen transmission. Pathogens evolved for greater virulence.

In the medieval period, the world’s great civilizations became densely populated. China, especially, became home to hundreds of millions of people living in close contact. These civilizations were subject to the greatest pathogen loads and must have been under strong selective pressure for enhanced immunity, and thus higher HDL levels.

But evolution doesn’t work overnight. Our natural HDL levels may not yet have evolved to their optimum. They may still be undershooting optimal levels.

HDL Epidemiology

If I’m right, then HDL must be undergoing current evolutionary selection for higher levels.

Historically, HDL levels should have been rising since the Neolithic, and rising the fastest in the most densely populated civilizations.

There are other factors too: geography plays a big role. Pathogens flourish in Africa, and in tropical climes generally. Northerly latitudes with their cold winters are low in pathogens.

So let’s consider what the geographic distribution of HDL levels should be, ignoring contributions from diet.

If my argument is correct, populations who until recently lived as isolated, low-density hunter-gatherers – like Australian aborigines, Melanesians and Polynesians – will have the lowest HDL levels, levels similar to those of our Paleolithic ancestors.

Meanwhile, people who have lived for the last few millennia with the highest population densities – East Asians – or the highest disease burdens – Africans – will have the highest HDL.

Europeans, with a favorable geography and middling historical population density, should be intermediate in HDL levels.

What does the data show?

HDL in Kitava averaged 44.5 mg/dl. [6]

For American populations in NHANES III, African-Americans averaged 53 mg/dl and white Americans averaged 49 mg/dl. This is a good comparison because Americans of different races eat similar diets.

In the Beijing Eye Study, Chinese were found to average 62.3 mg/dl, with one Beijing resident having an HDL over 270 mg/dl! [7] In the InterASIA study, however, Chinese averaged only 51.7 mg/dl. [8]

It’s difficult to infer much from this data, since diet and infectious burden affect HDL levels. The lower HDL in Kitava could be due to their higher carbohydrate intake. But overall, it is consistent with my evolutionary hypothesis. Kitavans have the lowest HDL levels, Americans of European descent are intermediate, and African-Americans and Chinese have the highest HDL levels.

What About Within Populations?

If our optimal HDL levels are higher than our “natural” evolved HDL levels, then the rare people with highly elevated HDL – those blessed with genetic variants that increase HDL, or that live the lifestyles that most elevate HDL – should live longest and be healthiest.

Indeed, that seems to be what is observed. As noted on Tuesday, in the VA Normative Aging Study, “Each 10-mg/dl increment in HDL cholesterol was associated with a 14% [decrease] in risk of mortality before 85 years of age.” [9]

Conclusion

There’s little data to evaluate the healthfulness of very high HDL levels, but what data we have suggests that more is better.

There’s also a plausible (to me) evolutionary story for why our optimal HDL levels may be far higher than the ones selected by evolution.

For most biomarkers I would trust evolutionary selection and let my body do whatever it wants; but for HDL I will make an exception. I think we will benefit from dietary tactics that raise HDL levels above the evolutionary norm. And this is especially true for those with infectious diseases.

So my judgment is: let’s be like Richard Nikoley and aim for high HDL. I’ll discuss how on Tuesday.

References

[1] Pirillo A et al. Modification of HDL3 by mild oxidative stress increases ATP-binding cassette transporter 1-mediated cholesterol efflux. Cardiovasc Res. 2007 Aug 1;75(3):566-74. http://pmid.us/17524375.

[2] Berrougui H, Khalil A. Age-associated decrease of high-density lipoprotein-mediated reverse cholesterol transport activity. Rejuvenation Res. 2009 Apr;12(2):117-26. http://pmid.us/19405812.

[3] Feingold KR, Grunfeld C. The acute phase response inhibits reverse cholesterol transport. J Lipid Res. 2010 Apr;51(4):682-4. http://pmid.us/20071695.

[4] Undurti A et al. Modification of high density lipoprotein by myeloperoxidase generates a pro-inflammatory particle. J Biol Chem. 2009 Nov 6;284(45):30825-35. http://pmid.us/19726691.

[5] Smith JD. Myeloperoxidase, inflammation, and dysfunctional high-density lipoprotein. J Clin Lipidol. 2010 Sep-Oct;4(5):382-8. http://pmid.us/21076633.

[6] Lindeberg S et al. Determinants of serum triglycerides and high-density lipoprotein cholesterol in traditional Trobriand Islanders: the Kitava Study. Scand J Clin Lab Invest. 2003;63(3):175-80. http://pmid.us/12817903.

[7] Wang S et al. Prevalence and associated factors of dyslipidemia in the adult chinese population. PLoS One. 2011 Mar 10;6(3):e17326. http://pmid.us/21423741.

[8] He J et al. Serum total and lipoprotein cholesterol levels and awareness, treatment, and control of hypercholesterolemia in China. Circulation. 2004 Jul 27;110(4):405-11. http://pmid.us/15238453.

[9] Rahilly-Tierney CR et al. Relation Between High-Density Lipoprotein Cholesterol and Survival to Age 85 Years in Men (from the VA Normative Aging Study). Am J Cardiol. 2011 Apr 15;107(8):1173-7. http://pmid.us/21296318.

HDL and Immunity

Posted by on April 12, 2011 42 comments

HDL – high-density lipoprotein – particles are good for you: High HDL levels are associated with lower mortality overall and lower mortality from many diseases – not only cardiovascular disease but also cancer and infection.

People with high HDL are only one-sixth as likely to develop pneumonia [1], and in the Leiden 85-Plus study, those with high HDL experienced 35% lower mortality from infection [2].

Each rise of 16.6 mg/dl in HDL reduced the risk of bowel cancer by 22% in the EPIC study. [3]

In terms of overall mortality, in the VA Normative Aging Study, “Each 10-mg/dl increment in HDL cholesterol was associated with a 14% [decrease] in risk of mortality before 85 years of age.” [4]

This must be surprising to those who think HDL is only a carrier of cholesterol. The lipid hypothesis presumed that the function of HDL is to clear toxic cholesterol from arteries, cholesterol having evolved for the purpose of giving us heart attacks. HDL then brings cholesterol to the liver which disposes of it returns it to the blood via LDL (which evolved for the purpose of poisoning arteries with cholesterol, and giving HDL something to do). (Hat tip to Peter for this formulation of the lipid hypothesis.)

But there is an alternative hypothesis: that infections cause disease, and that HDL has an immune function. This hypothesis would explain why HDL protects against infections and against all diseases of aging.

Immune Functions of HDL

I got interested in immune functions of HDL upon reading an article in ScienceDaily last year (“How Disease-Causing Parasite Gets Around Human Innate Immunity,” Sept 13, 2010). The article states:

Several species of African trypanosomes infect non-primate mammals and cause important veterinary disease yet are unable to infect humans. The trypanosomes that cause human disease, Trypanosoma brucei gambiense and T. b. rhodensiense, have evolved mechanisms to avoid the native human defense molecules in the circulatory system that kill the parasites that cause animal disease….

Human innate immunity against most African trypanosomes is mediated by a subclass of HDL (high density lipoprotein, which people know from blood tests as “good cholesterol”) called trypanosome lytic factor-1, or TLF-1….

The parasite that causes fast-onset, acute sleeping sickness in humans, T. b. rhodensiense, is able to cause disease because it has evolved an inhibitor of TLF-1 called Serum Resistance Associated (SRA) protein…. T. b. gambiense resistance to TLF-1 is caused by a marked reduction of TLF-1 uptake by the parasite….

To survive in the bloodstream of humans, these parasites have apparently evolved mutations in the gene encoding a surface protein receptor. These mutations result in a receptor with decreased TLF-1 binding, leading to reduced uptake and thus allow the parasites to avoid the toxicity of TLF-1.

“Humans have evolved TLF-1 as a highly specific toxin against African trypanosomes by tricking the parasite into taking up this HDL because it resembles a nutrient the parasite needs for survival,” said Hajduk, “but T. b. gambiense has evolved a counter measure to these human ‘Trojan horses’ simply by barring the door and not allowing TLF-1 to enter the cell, effectively blocking human innate immunity and leading to infection and ultimately disease.”

So HDL is actually an immune particle carrying proteins that poison pathogens. The TLF-1 HDL subclass consists of those HDL particles carrying two anti-trypanosome proteins, apolipoprotein L-1 and haptoglobin-related protein. [5]

Any HDL particle can become an anti-trypanosome defender simply by acquiring and carrying these proteins.

It turns out that HDL can carry a great assortment of immune proteins. The orchestrator of HDL’s immune functions seems to be a circulating plasma protein called phospholipid transfer protein (PLTP), which forms complexes with immune molecules and then associates with apolipoprotein A-I (the primary HDL protein). PLTP brings 24 different immune molecules into HDL particles, including apolipoproteins such as clusterin (apoJ), coagulation factors, and complement factors. [6] These immune protein complexes add protein but not fat to HDL particles:

Unexpectedly, lipids accounted for only 3% of the mass of the PLTP complexes. Collectively, our observations indicate that PLTP in human plasma resides on lipid-poor complexes dominated by clusterin and proteins implicated in host defense and inflammation. [6]

It looks like HDL may not be primarily a carrier of cholesterol, but rather a carrier of antimicrobial proteins. Its cholesterol and lipids may serve, as the ScienceDaily article suggests, to make the HDL particle attractive to pathogens so that it may enter as a “Trojan Horse.”

HDL-associated immune proteins under strong selection

As pathogens evolve, immune proteins have to evolve. It turns out that apolipoprotein L-1, the immune protein that protects against trypanosomes, is under strong selection in both Africa and Europe.

The version selected in Europe does not protect against Trypanosoma brucei rhodesiense, cause of one of the African sleeping sickness diseases, but the version selected in Africa does. Unfortunately, the African version also increases risk of kidney disease – which may explain why African-Americans have higher rates of kidney disease than white Americans. [7]

So Africans have sacrificed kidney health for greater immunity against sleeping sickness. This suggests that African sleeping sickness may be a relatively recently evolved human disease.

HDL neutralizes toxins

HDL binds bacterial endotoxins, especially lipopolysaccharide (LPS), and neutralizes their toxicity. As a result, people with high HDL have substantially less release of tumor necrosis factor-alpha (TNF-α) during infection. [8]

TNF-α is an inflammatory molecule that stimulates the acute phase response to infections. Levels of C-reactive protein are a good index of TNF-α levels, so generally speaking high HDL will lead to low TNF-α and low CRP.

What’s the best HDL profile?

It should be desirable to have more HDL particles. Since each HDL particle is capable of poisoning a pathogen, the more you have, the stronger your immune defenses.

However, the weight of each HDL particle is likely to be an indicator of infection severity. An infection-free person will have few immune proteins to pick up; the HDL particles will be fat-rich and buoyant. But a person with extensive infections will have heavier HDL particles freighted with immune proteins.

Conventional tests in the doctor’s office measure the weight of HDL in mg per deciliter of blood. Since having more HDL particles (which raises the weight) is good, but having heavy HDL particles indicates infection which is bad, mass is not the best measure of HDL status. We would expect the number or concentration of HDL particles to provide a better indicator of health.

Indeed, this appears to be what is observed. The most important determinant of HDL status is the number of HDL particles:

The association between HDL size and CAD risk was abolished on adjustment for apolipoprotein B and triglyceride levels (adjusted odds ratio, 1.00 [95% CI, 0.71 to 1.39] for top vs. bottom quartile), whereas HDL particle concentration remained independently associated with CAD risk (adjusted odds ratio, 0.50 [CI, 0.37 to 0.66]). [9]

Conclusion

HDL particles are “Trojan Horses” that attack pathogens and neutralize their toxins.

If you want to remain free from infectious diseases – which is to say, all diseases – to a ripe old age, it’s important to make your HDL particles numerous.

On Thursday, I’ll discuss ways to do that.

References

[1] Gruber M et al. Prognostic impact of plasma lipids in patients with lower respiratory tract infections – an observational study. Swiss Med Wkly. 2009 Mar 21;139(11-12):166-72. http://pmid.us/19330560.

[2] Berbée JF et al. Plasma apolipoprotein CI protects against mortality from infection in old age. J Gerontol A Biol Sci Med Sci. 2008 Feb;63(2):122-6. http://pmid.us/18314445

[3] van Duijnhoven FJ et al. Blood lipid and lipoprotein concentrations and colorectal cancer risk in the European Prospective Investigation into Cancer and Nutrition. Gut. 2011 Mar 7. [Epub ahead of print] http://pmid.us/21383385.

[4] Rahilly-Tierney CR et al. Relation Between High-Density Lipoprotein Cholesterol and Survival to Age 85 Years in Men (from the VA Normative Aging Study). Am J Cardiol. 2011 Apr 15;107(8):1173-7. http://pmid.us/21296318.

[5] Kieft R et al. Mechanism of Trypanosoma brucei gambiense (group 1) resistance to human trypanosome lytic factor. Proc Natl Acad Sci U S A. 2010 Sep 14;107(37):16137-16141. http://pmid.us/20805508.

[6] Cheung MC et al. Phospholipid transfer protein in human plasma associates with proteins linked to immunity and inflammation. Biochemistry. 2010 Aug 31;49(34):7314-22. http://pmid.us/20666409.

[7] Genovese G et al. Association of trypanolytic ApoL1 variants with kidney disease in African Americans. Science. 2010 Aug 13;329(5993):841-5. http://pmid.us/20647424.

[8] Henning MF et al. Contribution of the C-terminal end of apolipoprotein AI to neutralization of lipopolysaccharide endotoxic effect. Innate Immun. 2010 May 25. [Epub ahead of print] http://pmid.us/20501516.

[9] El Harchaoui K et al. High-density lipoprotein particle size and concentration and coronary risk. Ann Intern Med. 2009 Jan 20;150(2):84-93. http://pmid.us/19153411.