Author Archives: Paul Jaminet - Page 80

French Fried Potatoes and Sweet Potatoes

Posted by on July 17, 2011 38 comments

We had a reader request for “classic American dishes.” We decided to start with French fries.

Ingredients

The ingredients are simple:

  • We made three flavors using russet potatoes, Asian sweet potatoes, and American sweet potatoes.
  • For oil we used the Beef Tallow that we showed how to make last week.

Preparation

Start by cutting uncooked potatoes or sweet potatoes into appropriate shapes. We favor finger-sized slices or thin chips, and keeping the skin on. Here are russet potatoes, Asian sweet potatoes, and American sweet potatoes:

After slicing, soak them in a bowl of water as shown above. The purpose of this is to draw out starch. You can rub the potato with your fingers: it will feel slimy as long as there is starch there. You may need to rinse the potatoes 3-4 times to remove the starch. When you’re done, the slimy feel should be gone and the water should be clear.

Removing the starch will make the French fries crispy.

After the starch is removed, lay the fries out to dry:

It is important that they dry thoroughly. There must be no water when they are cooked. Drying takes at least 30 minutes.

Frying the potatoes occurs in two parts: once to cook the potatoes through, and a second time to make them crispy.

Put beef tallow (or whatever oil you are using) into a saucepan to a depth of a few inches, and heat it to a middling temperature about 275 F / 135 C. Add as many dried potato slices as will fit in the oil:

It doesn’t take long to cook: about 3 to 5 minutes. When they’re done, remove the fries; we used chopsticks.

At this stage the fries will look like this:

Set the fries aside for at least 10 minutes — 30 minutes is safer — to let them cool. They should be comfortable to the touch. If you want to freeze fries for future use, this would be a good stage to put them in the freezer.

But if you’re finishing the fries now, heat the oil to a high temperature — more like 350 F / 175 C, which is almost to the smoke point of most cooking oils — and return the cooled fries to the oil. Leave them in for just 2 to 3 minutes and remove. This will make the fries crispy, looking like this:

Sprinkle salt and any other spices you like on them, and they’re done!

Conclusion

French fries are really easy, if a bit time consuming, to make, and really hard to stop eating.

Our potatoes and Japanese sweet potatoes were superb, but the American sweet potato discs were only good — a little soft. Perhaps this species has extra water, or perhaps the disc shape needs more cooking time than we gave it.

We use our beef tallow for at most 3 batches — that is, 3 rounds at the low temperature and again at the high temperature — and then discard it. Because beef tallow solidifies at room temperature and can clog pipes, don’t pour it down a kitchen drain; let it solidify and discard it as solid trash in an appropriate container.

French fries have a tremendous taste to expense ratio — especially if you’ve been able to get beef fat for free from your butcher, like Paolo! Highly recommended.

Around the Web; Do You Know Where Your Neurotransmitters Were? Edition

Posted by on July 16, 2011 20 comments

We have guests this weekend and so I’ll be brief.

Just a reminder: Our meet-up at the beach is next Saturday, July 23, 4:30 to 6:30 pm, at the Massachusetts state park on the south end of Plum Island, which you access through the Parker River National Wildlife Refuge in Newburyport. I’ll have more detailed directions next week. We’ll picnic and will be delighted to chat, share food, play Frisbee, and just hang out with whoever cares to join us.

[1] Interesting posts this week: Emily Deans has been a rich source of information this week. She touched on an interesting topic – the ability of germs to produce human neurotransmitters:

Lactobacillus and Bifidobacterium species are known to produce GABA.  Escherichia, Bacillus, and Saccharomyces produce norepinephrine.  Candida, Streptococcus, Escherichia, and Enterococcus produce serotonin.  Bacillus and Serratia produce dopamine, and Lactobacillus species produce acetylcholine. That’s pretty much the entire hit parade of major neurotransmitters (there’s histamine and glutamate and a few others – and histamine is known to be produced by some bacteria that infect shellfish, for example, causing food poisoning).

It seems that many bugs may come pre-equipped with tools to modulate human moods and behaviors – if they can infect the central nervous system. No wonder the mechanisms of mental illness are so hard to understand.

Ned Kock explains why fasting might cause weight gain. Stan the Heretic thinks that statins and low-fat diets may cause osteoporosis.

The New York Times gave us evidence that maintaining immune function is the key to avoiding dementia (“Small Woes Increase Risk of Dementia”):

A runny nose, fallen arches and dentures aren’t risk factors typically associated with brain health. But new research suggests that small health problems can add up, and the combined effect can increase a person’s risk for dementia….

Taken alone, none of these health conditions are related to a person’s dementia risk. But when investigators combined these relatively minor physical ailments into a single “frailty index,’’ they found a significant cumulative effect on dementia risk.

Some economists find that food deserts only correlate with obesity, they don’t cause it.

Brian St Pierre finds papers showing that brown rice isn’t more nutritious than white rice. Doug McGuff reports that exercise reduces inflammation in diabetics. Lucas Tafur reports that ketogenic diets help clear environmental toxins.

I was intrigued by the headline “Nutritionists salute First Lady’s burger binge.” It turns out what the nutritionists like is Michelle Obama’s “balance and moderation,” which is to say, her unwillingness to consistently follow her own health advice. I’m inclined to agree: the burgers may improve her health!

Via John Durant, photographic evidence that standing desks used to be widespread.

[2] Music: I believe the musical term for this is “a cupola”:

Via The Brothers Judd.

[3] Good hair day:

Via Yves Smith.

[4] It’s smart to eat rice: Emily Deans, with a hat tip to Jamie Scott, offers more evidence for the superiority of rice to wheat. Apparently kids who eat rice have more brain matter and 5 more IQ points than kids who eat wheat:

Japanese researchers (funded by a national Young Scientists’ grant) studied 290 healthy children ages 5-18 years.  In Japan, apparently boiled white rice or white bread make up a typical breakfast.  (I remember eating a lot of this cereal plus sugar in skim milk when I was a kid. Kapow!)  The scientists were able to split the children into groups of habitual rice-eaters, habitual white bread eaters, and those who consumed both regularly.  Then they tested the IQs (using standard measures for kids <16 and a separate standard test for 16 and older), scanned the kids in a MRI, and collected their data.  Questionnaires were filled out by the kids or their parents with respect to morning eating habits, health, wealth, etc.

Using varying statistical techniques and a couple varieties of imaging data collection, the researchers found that the gray matter ratios (gray matter volume divided by intracranial volume) were significantly higher among the rice eaters vs. the white bread eaters, even after adjusting for age, gender, wealth, average weekly frequency of eating breakfast, and number of breakfast side dishes.  The Verbal IQ in the rice group averaged 104.7, in the bread group 100.3.  The Performance IQ was 102.1 in the rice group and 97.9 in the bread group. This difference was non-significant.

As the kids became older, the differences in gray matter ratio increased between bread and rice groups.

If only I hadn’t wasted my youth eating Wonder bread.

[5] Sitting is bad for you: Obesity Panacea cites a review of prospective studies on the effects of being sedentary. It turns out that time spent sitting affects mortality much more than it affects weight:

Based on inconsistency in findings among the studies and lack of high-quality prospective studies, insufficient evidence was concluded for body weight–related measures, CVD risk, and endometrial cancer. Further, moderate evidence for a positive relationship between the time spent sitting and the risk for type 2 diabetes was concluded. Based on three high-quality studies, there was no evidence for a relationship between sedentary behavior and mortality from cancer, but strong evidence for all-cause and CVD mortality.

So a standing desk may not cut your weight, but it will reduce your chance of dying. That’s pretty good.

If you want to lose weight too, try eating some kimchi at your standing desk.

[6] Thomas Edison anticipates the Perfect Health Diet approach?: Every once in a while someone asks if I know of health care providers in their area who are familiar with our ideas and recommend our diet. Chris Kresser, who is located in the Bay Area but can do Internet consultations, is one. I know some other doctors recommend our book – for instance, a woman in the UK wrote to say that her doctor suggested our diet as a treatment for PCOS – but I don’t know their identities.

Well, I can offer another name, because Dr. Jay Wrigley of The Art of Living Center in Charlotte, North Carolina tells me that he is recommending our diet to his patients. That caused me to look up their site and it features this excellent quotation:

Doctors of the future will have less use for medicines of any kind. Instead, they will instruct patients in the proper care of the human mind and body through correct ways of eating, proper care of the human frame and the right attitude that facilitates healing of both the mind and body.

— Thomas Edison

I suppose that this was a failed prophecy: Doctors today must be more dependent on medicines than ever before. Perhaps Edison over-estimated the intelligence of the future. But as prescription, I have to agree. Diet and a healthy lifestyle are keys to good health.

[7] Shou-Ching’s photo art:

[8] Weekly video: As a former physicist with artists in the family, I like to see the two subjects married:

Low Serum Cholesterol in Newborn Babies

Posted by on July 14, 2011 59 comments

Don Matesz, who has embraced low-fat and low-cholesterol dieting, recently stated that “I now consider anything over ~160 mg/dl [to be] excess serum cholesterol” and cited in his support the Cordain-Eaton claims that healthy hunter-gatherers had low serum cholesterol. Of course, we looked at that and found that healthy hunter-gatherers generally had serum cholesterol over 200 mg/dl and that hunter-gatherers with low serum cholesterol generally had high infectious burdens and short lifespans. See:

When Erik referenced our series and asked, “What do you think of the argument that low cholesterol in hunter gatherer populations stems from infections and parasites?”, Don replied:

Mean total blood cholesterol of healthy human neonates is about 72 mg/dl.

Is this due to infections and parasites?

In case this question was not merely rhetorical, let me answer: No.

But it’s an interesting biology question. Why do neonates have low serum cholesterol?

Neonates and Infants

The study that Don cited [1] looked at cord blood from neonates. Cord blood is blood that circulates on the fetal side of the placenta in utero. As soon as the baby is delivered, the cord is cut and blood ceases to circulate.

So the cord blood serum cholesterol of 70.3 mg/dl is really sampling fetal cholesterol – the blood of babies who have never eaten and never breathed.

The not eating part is relevant, because HDL is generated from the metabolism of chylomicrons created in the intestine when fat is eaten, and LDL is generated from VLDL particles that carry excess calories as triglycerides from the liver. So eating generates LDL and HDL. We might expect that LDL and HDL, and thus TC, levels will rise as soon as the neonate starts feeding.

We can check this out by looking at cholesterol levels in infants. The following data is from Japan [2], but any healthy population would give similar results:

Serum total cholesterol in infants, mg/dl, by feeding method

Infant Age Formula-fed Partially breastfed Breastfed
One month 117 142 163
Six months 140 162 194

Source: Tables 2 and 3, Isomura et al 2011.

The key data is in the rightmost column, the breastfed babies. By one month postpartum, TC is 163 mg/dl (“excess serum cholesterol” on Don’s view). By six months, it is 194 mg/dl.

Formula fed babies had a much smaller rise in TC.

To understand the pattern of this data, let’s look at three issues:

  • Why do formula-fed babies have lower TC than breastfed babies?
  • Why do neonates have low TC?
  • Why do breastfed babies end up with TC near 200 mg/dl?

Formula is a lipid-deficient food

Why do formula fed babies have lower serum cholesterol? One contributing factor may be a dietary lipid deficiency.

Human breast milk is rich in cholesterol. One study found that the cholesterol content of human breast milk follows a diurnal rhythm with a low of 140 mg/L during sleeping hours and early morning, and a high of 220 mg/L in the afternoon and evening. Other studies agree that human breast milk always has more than 100 mg/L cholesterol. Babies typically drink 750 mL/day, so a breastfed baby’s daily cholesterol intake is 100 to 200 mg.

Scaled by body weight, this would be the equivalent of 1.5 to 3 grams cholesterol per day for adults – approximately ten times the typical cholesterol intake of American adults.

Clearly, evolution thinks babies should get plenty of cholesterol.

But cholesterol levels in formula are much lower:

Since … infant formulas contain very little cholesterol (10 to 30 mg/L) (Huisman et al., 1996; Wong et al., 1993), it is not surprising that plasma cholesterol concentrations are higher in infants fed human milk than in formula-fed infants.

I guess the formula makers don’t consider cholesterol to be a desirable nutrient. This may be an extremely consequential mistake.

Low TC in Neonates May Have Evolved to Suppress Immunity

So why do neonates have a very low TC?

In addition to fat and cholesterol transport, LDL and HDL both have immune functions. Low serum cholesterol signifies a loss of these immune functions. Normal immune function is associated with TC around 200 mg/dl or higher.

But infants are well known to have suppressed immunity. This is important: if the fetus had an ability to generate antibodies and mount an immune response, it might generate immune attacks against the mother leading to miscarriage.

After birth, a baby’s immune system gradually matures:

A baby’s immune system is not fully developed until he/she is about six months-old. In the meantime, pregnant mothers pass immunoglobulin antibodies from their bloodstream, through the placenta, and to the fetus. These antibodies are an essential part of the fetus’s immune system. They identify and bind to harmful substances, such as bacteria, viruses, and fungi that enter the body. This triggers other immune cells to destroy the foreign substance….

Immediately after birth, the newborn has high levels of the mother’s antibodies in the bloodstream. Babies who are breastfed continue to receive antibodies via breast milk…. This is called passive immunity because the mother is “passing” her antibodies to her child. This helps prevent the baby from developing diseases and infections.

During the next several months, the antibodies passed from the mother to the infant steadily decrease. When healthy babies are about two to three months old, the immune system will start producing its own antibodies. During this time, the baby will experience the body’s natural low point of antibodies in the bloodstream. This is because the maternal antibodies have decreased, and young children, who are making antibodies for the first time, produce them at a much slower rate than adults.

Once healthy babies reach six months of age, their antibodies are produced at a normal rate.

LDL particles, by presenting pathogen toxins to macrophages which can then present them on MHC molecules, play an important role in the generation of antibodies. (See Blood Lipids and Infectious Disease, Part II, July 12, 2011.) Low LDL signifies a reduced ability to generate antibodies.

Low LDL is therefore highly desirable as long as the baby remains in the womb, and in fact LDL levels are very low in utero.

But persistent low LDL after birth is dangerous: it makes the infant vulnerable to infections. Likewise, HDL has important immune functions (see HDL and Immunity, April 12, 2011). So LDL and HDL gradually rise to normal physiological levels, finally reaching a TC of 200 mg/dl after 6 months in breastfed babies – precisely when the babies attain normal immune function.

If TC of 190 mg/dl or higher signifies normal immune function, then formula fed babies are still immune suppressed at 6 months. Extrapolating the rise in TC, partially breast fed babies might achieve normal immune function at 12 months and formula fed babies might not achieve normal immunity until age 24 months!

Immunity Matters for Infant Health

I don’t want to delve too deeply into this, but infants are vulnerable to infections – this is why infant mortality has always been high. It still is today, and 6 months of age is still the canonical age when the danger lessens:

Globally, approximately 4,000,000 children less than 6 months of age die each year at a rate of 450 deaths per hour. In addition, high hospitalization costs for infected infants are incurred in the United States with an annual estimated cost of $690,000,000.

Formula feeding definitely escalates the risk:

In the United States, more than 40% of all infant hospitalizations are attributable to infectious disease … Diarrhoeal diseases and digestive tract infections are the most common infectious diseases in infants….

Breast feeding has been shown to have a number of beneficial effects in infants, including protection against infectious and allergic diseases. [3]

In this study, 41% of formula-fed infants developed infections between ages 5 and 8 months. [3]

A study from Brazil [4] shows that breastfeeding makes a huge difference in infant mortality:

In a population-based case-control study of infant mortality in two urban areas of southern Brazil, the type of milk in an infant’s diet was found to be an important risk factor for deaths from diarrhoeal and respiratory infections. Compared with infants who were breast-fed with no milk supplements, and after adjusting for confounding variables, those completely weaned had 14.2 and 3.6 times the risk of death from diarrhoea and respiratory infections, respectively. Part-weaning was associated with corresponding relative risks (RR) of 4.2 and 1.6. [4]

Now, deficient serum cholesterol is not the sole factor accounting for higher mortality in formula fed babies. But it is a contributing factor.

Conclusion

If serum cholesterol is healthiest below 160 mg/dl, then formula fed babies have excellent blood lipids despite a high disease and mortality rate, but breastfed babies are already in trouble at age one month and are suffering a shocking dyslipidemia at age six months, despite excellent health.

I think that’s absurd. A more logical interpretation of the evidence is this.

Healthy babies achieve serum cholesterol levels around the adult norm of 200 mg/dl by age six months.

Serum cholesterol levels below 190 mg/dl or so indicate immune suppression and increased risk of infectious disease – whatever the age of the human in question. Formula fed babies are immune suppressed for an extended period – well beyond the six month period of a healthy breastfed baby.

There are multiple causes of low serum cholesterol. A high infectious burden is one; never having eaten is another; a lipid-deficient diet is a third. But there is no evidence I am aware of suggesting that low serum cholesterol is a desirable condition.

References

[1] Mishkel MA. Neonatal plasma lipids as measured in cord blood. Can Med Assoc J. 1974 Oct 19; 111(8):775-80. http://pmid.us/4370703.

[2] Isomura H et al. Type of milk feeding affects hematological parameters and serum lipid profile in Japanese infants. Pediatr Int. 2011 Mar 21. http://pmid.us/21418403.

[3] Picaud JC et al. Incidence of infectious diseases in infants fed follow-on formula containing synbiotics: an observational study. Acta Paediatr. 2010 Nov;99(11):1695-700. http://pmid.us/20560895.

[4] Victora CG et al. Evidence for protection by breast-feeding against infant deaths from infectious diseases in Brazil. Lancet. 1987 Aug 8;2(8554):319-22. http://pmid.us/2886775.

Blood Lipids and Infectious Disease, Part II

Posted by on July 12, 2011 95 comments

OK, after a diversion into hunter-gatherer lipid profiles I’m back on the original goal of this series: trying to understand why serum cholesterol is protective against infections — and considering whether or under what circumstances that knowledge should affect how we eat.

In part I (Blood Lipids and Infectious Disease, Part I, Jun 21, 2011), we learned that mortality from infectious disease is essentially zero as long as serum cholesterol remains in the physiologically normal range of 200 to 240 mg/dl, and rises precipitously as serum cholesterol falls below 180 mg/dl.

Why is that? In a previous post we found that HDL has important immune functions (HDL and Immunity, April 12, 2011). Today, we’ll look at the immune functions of lipoproteins more generally.

The Logic of Evolution and the Multiple Functions of Lipoproteins

In understanding why these particles have immune functions, it may be helpful to understand the thrust of evolution.

By the time of the Cambrian explosion 530 million years ago, organisms had similar numbers of genes to organisms today, and most of these genes must have been similar in sequence to their modern descendants. We know this because their descendant genes in nearly all modern species are “homologous” and share nucleotide sequences.

So for the last 500 million years, evolution has not been adding genes or even changing genes dramatically. It’s been tweaking a fairly stable genome. And the direction of the tweaking has been toward making the genes interact in a wider and more complex number of ways with the other genes.

The effect is to give every molecule in the body a diversity of functions. Possibly serum lipoprotein particles started out merely as transporters. But they developed new functions. The most important additional functions were roles in immunity.

Because these particles circulate in the blood, and pathogens have to transit the blood in order to cause tissue infections, blood is the natural location for the strongest defenses against pathogens. For hundreds of millions of years, every blood component will have been under selective pressure to develop immune functions.

It’s commonly said that the primary function of LDL and HDL is lipid transport. But this is too narrow a view. Since pathogens are the primary cause of disease, it may be the immune functions of LDL and HDL which account for their significance as biomarkers of health and disease.

The Immune Functions of Lipoproteins

Most of the following discussion will draw from a recent review, “Plasma lipoproteins are important components of the immune system” [1]. References from this paper will be listed in parentheses, eg (1).

Lipoproteins have been shown to:

  1. Prevent bacterial, viral, and parasitic infections.
  2. Detoxify pathogen “die-off” toxins and protect against pathogen toxin-induced tissue damage.
  3. Present pathogen “die-off” toxins to the immune system to trigger antibody formation.

Detoxification and Toxin Defense

When a pathogen dies, it typically fragments and releases compounds which are toxic to humans. Such “die-off” toxins include lipopolysaccharides (LPS) and lipooligosaccharides (LOS) from Gram-negative bacteria, lipoteichoic acid (LTA) from Gram-positive bacteria, fungal cell wall components, and so on.

During infection, the number of such circulating toxins can be vastly larger than the number of pathogens. Such toxins can do a great deal of harm, and often account for most of the ill effects of disease. Medical researchers studying the often-fatal condition of sepsis commonly induce nearly all the characteristics of sepsis in animals merely by injecting LPS.

VLDL, LDL, lipoprotein(a) and HDL can all detoxify LPS and LTA; HDL is the most potent (2, 4, 5). Injecting reconstituted HDL (rHDL) into humans relieves endotoxemia (6) and LPS-induced inflammation in cirrhosis patients (7). Both LDL and HDL detoxify E. coli LPS (35).

LDL binds and inactivates some toxins, including Staphylococcus aureus ?-toxin (8), Yersinia pestis topH6-Ag (30). (Methicillin-resistant S. aureus, or MRSA, is an increasing cause of death in hospitals, and last year claimed my next-door neighbor. See The FDA Is On The Side of the Microbes, Aug 11, 2010).

LDL probably works against many other toxins too, since rats with low LDL have higher mortality when infected, but the mortality can be lessened with injections of human LDL (9). Injections of LDL prevent lethality in Vibrio vulnificus infections of mice (34).

In mice with the LDL receptor knocked out, LDL concentrations in blood are higher and there is enhanced immunity to Klebsiella pneumoniae (27) and Salmonella typhimurium (29). If the gene for apoE, a protein found in IDL which upregulates VLDL levels, is knocked out, mice become more susceptible to infection, so it appears that apoE also has immune functions (28). Mice lacking apoE are susceptible to Listeria monocytogenes (32) and Mycobacterium tuberculosis (33).

Lipoproteins may be even more important against viruses. HDL has a broad antiviral activity (18-20), and can prevent many virus species including influenza and hepatitis C from entering cells. VLDL and LDL have specific activity against certain types of virus including togaviruses and rhabdoviruses (3). Trypanosoma brucei, the parasite that causes sleeping sickness, does not always cause disease in humans because a subspecies can be destroyed by a subfraction of HDL particles which include haptoglobin-related protein and apolipoprotein L-I (10).

The role of oxLDL

Evolution has a way of turning lemons into lemonade, and fragile molecules into sensors. In the book we discuss how the body uses fragile polyunsaturated fats as signaling molecules, exploiting their proclivity to oxidize. Something similar happens with LDL.

LDL particles are fragile and easily oxidized. The body uses them as a sensor of infections, and as signaling molecules that control the response to infections.

For instance, LPS (an endotoxin) induces neutrophils to adhere to endothelial cells, promoting vascular inflammation. LPS also oxidizes LDL, creating a compound called oxPAPC which inhibits neutrophil adhesion to endothelial cells, thereby limiting the inflammatory response (12). Minimally oxidized LDL detoxifies LPS (13).

OxLDL is taken in not by the LDL receptor, but by receptors on immune cells called macrophages. When macrophages take up oxLDL they upregulate their scavenger receptors (classes A and E) by which they phagocytose (eat) bacteria and clear endotoxins (39). It has been shown that infection causes an increase in oxidation of LDL and that the resulting oxLDL promotes phagocytosis by macrophages of the specific pathogens which oxidized the LDL (42).

This may explain why atherosclerotic lesions contain large amounts of bacterial and viral DNA. Macrophages in these lesions have been stimulated by oxLDL to scavenge bacteria and viruses from the blood.

OxLDL stimulates antibody formation, including antibodies against phosphorylcholine (PC), a compound found on a wide range of pathogens including bacteria, parasites, and fungi (45-49). Anti-PC antibodies help to prevent upper airway infections (50-53).

It is thought that oxidation of LDL is an important part of the host defense to infections. OxLDL inhibits cell entry of hepatitis C (59) and Plasmodium sporozite (60).

The role of Lp(a)

Lp(a) is essentially an LDL particle with an extra apo(a) molecule bound to the apoB100 molecule by a disulfide bridge.

Some insight into the immune functions of Lp(a) developed after considering the role of plasminogen. Many pathogens recruit human plasminogen and use it to penetrate tissue barriers, enabling them to invade tissue (70, 71, 72). For instance, group A streptococcus releases an enzyme called streptokinase that activates human plasminogen and promotes invasion (73). Lp(a) has anti-fibrinolytic activity and recruits plasminogen itself, reducing availability for pathogens. For instance, Lp(a) blocks streptokinase activity (75), inhibits Staphylococcus aureus activation of plasminogen.

Moreover, Lp(a) inhibits the inflammatory response to LPS. As there is great variation in Lp(a) levels among individuals (76), this may account for variability in inflammatory response to infections.

The Exception: Candida

HDL may promote fungal infections. A recent study found that infusion of reconstituted HDL enhances the growth of Candida (25).

LDL also seems to promote fungal infections. In LDL receptor knockout mice, which have high levels of LDL, there is decreased resistance to Candida (37, 38).

OxLDL also loses its normal anti-infective role against Candida. Worse, it inhibits production of antibodies against Candida albicans (63), thus actually hurting anti-fungal immunity.

Candida is an unusual pathogen that is unusually well-adapted to living in the human body. It has learned to turn an important part of human immune defense to its own advantage.

Conclusion

High serum cholesterol protects against a host of bacterial and viral infections and some parasites, but increases risk for Candida fungal infections.

Related Posts

Other posts in this series include:

References

[1] Han R. Plasma lipoproteins are important components of the immune system. Microbiol Immunol. 2010 Apr;54(4):246-53. http://pmid.us/20377753.