Dr. Stephan Guyenet from Whole Health Source

StephanGuyenet

[Link to mp3]

Ladies and gentleman, the podcast is back!

…at least for now. And today’s guest is the brilliant Dr. Stephan Guyenet, who is an obesity researcher and runs WholeHealthSource.org. If you’ve never visited his site and you enjoy evidence-based discussions of nutrition science I recommend giving it a shot. He received his PhD in neurobiology from the University of Washington, which is that same place this author got his Master’s! However, we only just met for the first time a couple weeks ago at the Diamond Knot brewpub where this podcast was recorded.

Carrie Dennett was with me, and the last time you heard her she was a lowly grad student like me, but now she’s a registered and practicing dietitian. Carrie still blogs regularly in addition to writing her On Nutrition column for the Seattle Times. Where does she find the time??

Some technical notes: I stopped using Libsyn for my podhosting services. Not because I was unsatisfied with them, but because I was unemployed for a time last year and could not afford the monthly expense. Plus I wasn’t making new episodes anyway, so it was a no-brainer. Now I have uploaded all the episodes to the Internet Archive, and word on the street is that I can use the IA and WordPress for some free podhosting which is super kewl. The only problem is I haven’t had the time to set it up yet, so for the time being you won’t be able to get the shows on iTunes (or whatever podcatcher you might use). I’ll tweet about it when it’s up on iTunes or something if anyone cares.

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Nutrition, Pregnancy, and Omega-3s

 

[mp3]

FYI: My co-host Carrie Dennett has written a series of great posts on nutrition and pregnancy on NutritionByCarrie.com. You should definitely check them out. Now on to the post…

The thing about proper nutrition when you’re pregnant is the following: It’s DAMN IMPORTANT. For instance, not getting enough folate/folic acid during pregnancy can result in major neural tube defects.1–3 Think about it: You’re literally building a human from scratch. You’re going to need all the necessary components for doing that, plus some extra.

Really, the topic of nutrition and pregnancy is far too large to cover in one blog post, which is why Carrie had to break it up into several posts. So I am going to briefly touch on a few things that were discussed in the show.

Nutrition and Fertility

I mentioned Dr. Walter Willett appearing on The Diane Rehm Show some years ago to plug his book The Fertility Diet. I have not read The Fertility Diet, but Dr. Willett is chair of the department of nutrition at the Harvard School of Public Health. He is a bit of a rockstar in the field of nutrition because he has written many hard-hitting papers on the subject, and he’s a principal investigator on the Nurses’ Health Study.

I will let the science speak for itself, but one thing that struck me during the interview was that whole milk was associated with greater fertility than skim milk. So if you are a milk drinker, choose whole milk while trying to get pregnant or have a small dish of ice cream or full-fat yogurt every day.* For the other main takeaways from the fertility diet visit the HSPH website.

Prenatal Nutrition

I’m not going to go into a big long post on everything you need to know about nutrition and pregnancy. If you want something a bit more comprehensive visit Carrie’s posts linked above or check out the Mayo Clinic’s pages on what to eat and what not to eat during pregnancy. Or download this very informative review.4 Or buy a textbook on the subject.

What I would like to do is explore the topic of Omega-3 intake during pregnancy and IQ.

Omega-3s During Pregnancy and IQ

This is a very thorny issue indeed, but one that I think warrants further investigation. In that spirit I did some digging after we recorded our podcast and found the following…

A paper was published in 2005 in the American Journal of Preventive Medicine that you might call something of a meta-analysis.5 The author took all the relevant studies regarding n-3 fatty acids and cognitive development, aggregated them, and summarized their findings. This was the conclusion:

This analysis finds that an increase in maternal intake of DHA during pregnancy of 1 g/day will increase child IQ by 0.8 to 1.8 points (central estimate of 1.3 points). Because typical DHA intake associated with fish consumption is well under 1 g/day, changes in fish consumption will result in IQ effects amounting to a fraction of a point.

In other words, the evidence suggests that large amounts of DHA n-3 will have possibly the only the mildest effects on IQ. The analysis included 7 randomized controlled trials (RCTs) on formula feeding and one RCT on maternal supplementation during pregnancy. The author also points out that that there are large differences in the relevant studies so direct comparison is difficult, and that different tests were used to estimate IQ.

But what has been published since that analysis??

No Link

In 2008 a RCT published in the journal Pediatrics found nothing. From the conclusion:

Our study did not reveal any difference in overall IQ scores at 7 years of age between children whose mothers had taken n-3 very-long-chain PUFAs or n-6 long-chain PUFAs during pregnancy and lactation.

Positive Link

In 2007 an observational study was published in the Lancet where pregnant women completed a food frequency questionnaire (FFQ), and later their child was measured for pro-social behavior, fine motor skills, communication skills, and social development.6 From the paper:

[M]aternal consumption of more than 340 g seafood a week was beneficial for the child’s neurodevelopment.

American Journal of Epidemiology in 2008 published results of a cohort study that measured maternal fish intake and child cognition. Another mild association was found.

[M]aternal fish intake more than twice a week was associated with improved performance on tests of language and visual motor skills.

But what about n-3s? Some fish are sources of a ton of n-3s while others not so much. The authors accounted for n-3s. For each 100 mg of maternal daily DHA & EPA intake from fish, children had Peabody Picture Vocabulary Test (PPVT) scores that were 0.5 points higher and Wide Range Assessment of Visual Motor Abilities (WRAVMA) total scores that were 1.1 points higher – another mild endorsement of the link between n-3s and cognition. However, the authors noted that higher prenatal mercury exposure was associated with lower developmental test scores. Unfortunately, often times fish and mercury go hand in hand. Ugh… what now?

Fish and Mercury

Pregnant women are often cautioned to avoid eating too much fish because of the mercury levels. This is important, and like alluded to earlier can have impacts on the child’s cognitive development. The thing is that mercury levels can vary greatly by the type of fish, whether it was farmed or wild-caught, and where it was sourced. For more information visit the NRDC website or check out this handy chart from the University of Maine.

Nutrition and the Epigenome

We touched on nutrition, epigenetics, and the pop science book Survival of the Sickest (If you’ve read it, tell me what you think in the comments section). I’d like to discuss that area of research, but it’s so meaty7 that it requires its own post.

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* However, to be clear most of the evidence presented in the book comes from the Nurses’ Health Study, which is an epidemiological study. An important fact about epidemiological studies is that they measure associations (or links) not necessarily causes. So it may be true that there is something about whole milk that produces greater fertility over skim milk, but it is also possible that more fertile women prefer whole milk over skim milk and that the milk really doesn’t affect fertility. It’s difficult to determine, and won’t be determined unless/until some sort of randomized controlled trial takes place. This is important to clarify, especially since I made the mistake of saying in the podcast that milk influences fertility. It would be more accurate to say that skim milk is associated with infertility or whole milk is linked to fertility or something like that.

Refs

  1. Honein MA, Paulozzi LJ, Mathews TJ, Erickson JD, Wong LY. Impact of folic acid fortification of the US food supply on the occurrence of neural tube defects. JAMA 2001; 285: 2981–6.
  2. Berry RJ, Li Z, Erickson JD, et al. Prevention of neural-tube defects with folic acid in China. China-U.S. Collaborative Project for Neural Tube Defect Prevention. N Engl J Med 1999; 341: 1485–90.
  3. Laurence KM, James N, Miller MH, Tennant GB, Campbell H. Double-blind randomised controlled trial of folate treatment before conception to prevent recurrence of neural-tube defects. Br Med J 1981; 282: 1509–11.
  4. Williamson CS. Nutrition in pregnancy. BNF Nutr Bull 2006; 31: 28–59.
  5. Cohen JT, Bellinger DC, Connor WE, Shaywitz BA. A quantitative analysis of prenatal intake of n-3 polyunsaturated fatty acids and cognitive development. Am J Prev Med 2005; 29: 366–74.
  6. Hibbeln JR, Davis JM, Steer C, et al. Maternal seafood consumption in pregnancy and neurodevelopmental outcomes in childhood (ALSPAC study): an observational cohort study. Lancet 2007; 369: 578–85.
  7. Pardon the pun.

Trans Fat Alternatives

[Trans-Fat Alternatives and Organics mp3]

Today’s episode is a discussion about the types of fat currently being used in food manufacturing and the restaurant industry to replace trans-fatty acids. We also discuss a recent meta-analysis published in the Annals of Internal Medicine about organic foods.

Carrie has written a great piece outlining the issue in Nutrition Nuts and Bolts, a blog run by another fellow UW Nutrition Science student.

I’d like to expound a bit on the chemical structure of fatty acids and why that is important.

The Basics

Fats are essentially chains of carbon. All carbon atoms must have four bonds; no more and no less. This means that when carbon is organized in a long chain two of the available bonds are attached to other carbons, and the remaining two bonds are attached to the most abundant atom in the universe: hydrogen. This type of fat, when all the available bonds are saturated with hydrogen, is known as a saturated fat.

The picture below is a representation of a saturated fat called palmitic acid. The black balls represent carbon, the white balls represent hydrogen, and the red balls at the end represent oxygen.

When fats are saturated they naturally take the shape of a kind of flat zig-zag structure because this is the most stable form.  This can allow for the fatty acids to neatly stack against each other, making them nearly always solid at room temperature.

By contrast, unsaturated fatty acids have one or more double bonds in the carbon chain. This produces kinks that prevent the fatty acids from forming a solid.


The main difference then, chemically speaking, between butter and oil is that the fatty acids in oil are chock-full of double bonds.

Where do trans-fats come in?

In the latter half of the 20th century saturated fats began to acquire a bad reputation. Various kinds of studies began to show that saturated fat was associated with heart diseases and cancers.1 Unsaturated fats, on the other hand, were largely considered to be healthier. Two problems though: when making biscuits or cookies or any number of other baked goods you really cannot substitute oil for butter.2 The second problem was that unsaturated fats are prone to oxidation and rancidity.

What do we do about this? Well, there was a process called hydrogenation that developed in the early 20th century to try and increase the shelf life of vegetable oils and fish oils. The resulting fats were actually more shelf-stable (because they were resistant to oxidation), cheaper to produce, were delicious, and could easily replace butter or lard in a recipe. This made them desirable to the food industry. Moreover, the fatty acids, although structurally similar to saturated fatty acids, were in fact unsaturated.

From Wikipedia:

In most naturally occurring unsaturated fatty acids, the hydrogen atoms are on the same side of the double bonds of the carbon chain (cis configuration — from the Latin, meaning “on the same side”). However, partial hydrogenation reconfigures most of the double bonds that do not become chemically saturated, twisting them so that the hydrogen atoms end up on different sides of the chain. This type of configuration is called trans, from the Latin, meaning “across.” The trans configuration is the lower energy form, and is favored when catalytically equilibrated as a side reaction in hydrogenation.

The fact that these fats were technically unsaturated led some health advocates to push for saturated fat to be replaced with trans-fat in common food products. Unfortunately, as we all know now trans fats are far worse than saturated fats in almost every way, at least in terms of human health.

Recently we’ve all been privy to the slow removal of trans fats from the food industry. Carrie and I discuss how it’s being done and what the implications might be.

Like I mentioned earlier, we also discussed organic foods and their latest controversy, but that portion will have its own forthcoming blog post.

  1. I’m not going to discuss the reasons for it in this blog post, but suffice it to say when saturated fats (as opposed to unsaturated fats) become incorporated into the lipid membranes of cells it starts to disrupt cell function. Membranes need to have a certain amount of fluidity and flexibility, but if they made up of mainly saturated fats then the cell membrane becomes rigid and it’s more difficult to do housekeeping chores like importing nutrients, exporting waste, cell signaling, etc. This is not the only reason for saturated fats negative health effects, but it’s a major one.
  2. Actually you can, but you won’t like the results.

Eggs and Heart Disease

[Eggs and Heart Disease mp3]

What’s the deal with eggs?

It seems that some foods like eggs and margarine are on a perpetual pendulum with the media and, by extension, public opinion. Some days the egg is vilified as a harbinger of heart disease, while other days everything is coming up roses for the little guy. Case in point: Here is a recent article from a local Charleston news station stating

A new study suggests just three egg yolks per week can accelerate heart disease almost as much as smoking.

This article is based off a recent study from Canada published in the journal Atherosclerosis.1 Contrast this with the Harvard School of Public Health’s official position on eggs:

Recent research has shown that moderate egg consumption—up to one a day—does not increase heart disease risk in healthy individuals and can be part of a healthy diet.

So which is it? Three eggs a week is as bad as smoking or one egg per day is perfectly healthy? It cannot be both. So what should we believe?

As of now the link between serum cholesterol2 and heart disease is about as near to a capital-F Fact as you get in nutrition science.  So when you hear that eggs are really high in cholesterol compared with most other foods commonly consumed in the United States, one logical conclusion you could draw from this (if you eat a fair amount of eggs) is the following: If I stop eating eggs I will reduce my risk of heart disease. However, the waters of truth become muddier when you try to examine the actual science behind this bit of conventional wisdom.

Lucky for us my colleague Carrie Dennett did most of the leg work and found the best research available on the subject. What follows is adapted from her research.

Epidemiological Studies

  • An analysis of data from the Framingham Heart Study in 1982 was one of the first epidemiological studies to suggest that there was no significant association between egg consumption and coronary heart disease (CHD), myocardial infarction, or all-cause mortality.3
  • The “Harvard Egg Study” looked at the association between egg consumption and the risk of CHD in two prospective cohorts, the Health Professionals Follow-up Study and the Nurses’ Health Study. After adjustment for age, smoking and other CHD risk factors, there was no significant association between recent or long-term consumption of up to 1 egg per day and risk of CHD or stroke. However, subjects with existing hypercholesterolemia, cardiovascular disease, diabetes, or cancer were excluded from analysis.4
  • Djousse and Gaziano examined the association between egg consumption and CVD and total mortality among 21,327 participants from the Physicians’ Health Study I. The authors concluded that consumption of up to 6 eggs per week does not influence the risk of myocardial infarction, stroke, or total mortality in healthy U.S. male physicians.5 Individuals who ate beyond six eggs per week, however, did see an increase in CVD risk.
  • Data from the First National Health and Nutrition Examination Survey (NHANES-1) and the NHANES-1 Epidemiological Follow-up Study (NHEFS) was examined and a multivariate analysis found no significant difference in the relative risk of incident stroke, ischemic stroke, coronary artery disease (CAD) and mortality between low (1 egg/week or less), moderate (1-6 eggs/week), and high egg consumers (greater than 6 eggs/week).6 One important exception were high-egg-consuming diabetics who had twice the normal risk of CAD.
  • The Japan Public Health Center-based prospective study on cancer and CVD, which involved 90,735 men and women (ages 40-69), found no association between almost daily egg consumption and CHD incidence.7
  • Researchers in Spain looked at egg consumption among 14,185 subjects from the prospective cohort participating in the SUN (Seguimiento Universidad de Navarra) Project and found no association between the highest level of egg consumption (greater than 4 eggs/week) and the lowest (less than 1 egg/week).8

All of the above studies suggest that eggs are relatively benign and have little effect on one’s risk of cardiovascular disease. However, there would have to be at least a few that show some detrimental associations of eggs. After all, the well-ingrained idea that eggs are risky business has to be more than just a hunch, right? And indeed there are a handful of such studies.

  • Australian Aborigines were followed from 1988-89 to 2002 and it was found that consumption of 2+ eggs per week was associated with a 2.6-fold increased risk of CHD.9
  • A prospective study of 10,802 men and women in the United Kingdom found a 2.7-fold increased risk of death among subjects who consumed 6 or more eggs per week.10

However, Carrie notes in the podcast that the authors of the first paper did not collect information on fruit and vegetable intake and thus were unable to determine if there was an inverse association between high fat consumption and low intake of fruits and vegetables. Furthermore, the authors of the second paper used a food frequency questionnaire (FFQ) that was validated only for fiber intake. This means it has been shown that the FFQ they used measures fiber intake fairly accurately, but it has not been proven that it can do the same for other nutrients.

Controlled Trials

It was noted in the podcast that hyperlipidemic individuals are usually excluded from major studies like these. An exception that we discussed was a randomized, placebo-controlled crossover trial of 40 hyperlipidemic adults by Njike et al.11 Study subjects were randomly assigned to daily consumption of two hardboiled eggs or egg substitute for six weeks, separated by a 4-week washout. They found that egg consumption did not have a detrimental effect on endothelial function or plasma lipids. What was interesting, though, was that the egg substitute group showed a significant improvement in endothelial function, total cholesterol, and LDL cholesterol. Similar results were seen in an identically structured study by Katz et al that used treatment with daily consumption of either two eggs or oats for 6 weeks by 50 healthy men and women (mean age 56 years).12

Carrie also mentioned a study involving hyper- and hyporesponders13 of dietary cholesterol. A randomized crossover trial in Mexico examined the effect of dietary cholesterol from eggs.14 The subjects (30 boys and 30 girls aged 8-12 years) were randomly assigned to eat either two whole eggs or egg substitute for 30 days, with a three-week washout period. Each child was then classified as a hyperresponder or hyporesponder based on their degree of plasma cholesterol response. The hyperresponders had an increase in LDL and HDL cholesterol during the period of whole egg consumption, with the LDL:HDL ratio remaining the same. Hyporesponders had no significant alterations to LDL or HDL.

Of course now we get into even more complicated waters when we include discussions of not just total cholesterol but also LDL:HDL ratios. The previous study even mentions differentiating the small, dense LDL particles from larger, more buoyant LDL particles. There is actually a big difference between the two types, with the former more strongly linked to the heart diseases that we all want to try and avoid. But that is perhaps a topic for another day.

Choline

Carrie also brought up the fact that eggs were a major dietary source of choline. However, we were both having some trouble trying to remember what good non-animal sources of choline were available to vegetarians and vegans. Luckily Wikipedia never disappoints.15 Vegans should have no trouble incorporating some of those foods into their diet. Although, on a gram-for-gram basis eggs seem to be a good way to go, otherwise you’ll have to eat an entire pound of spinach to get a similar amount of choline that one egg’ll give ya.

Bottom Line

Eating a few eggs a week is not likely to increase your risk of heart disease, especially if you’re already healthy. On the other hand, if you have diabetes or some other metabolic disorder such as hyperlipidemia or hypercholesterolemia you should be mindful of how many eggs you are eating in a given week. You may need to limit your egg consumption to only 1 or 2 per week. In any case, discuss it with your primary physician.

  1. which is not a fringe journal
  2. the cholesterol circulating in your blood vessels
  3. Dawber TR, Nickerson RJ, Brand FN, et al. Eggs, serum cholesterol, and coronary heart disease. The American Journal of Clinical Nutrition 1982;36(4):617-25.
  4. Hu FB, Stampfer MJ, Rimm EB, et al. A Prospective Study of Egg Consumption and Risk of Cardiovascular Disease in Men and Women. JAMA: The Journal of the American Medical Association 1999;281(15):1387-94.
  5. Djoussé L, Gaziano JM. Egg consumption in relation to cardiovascular disease and mortality: the Physicians’ Health Study. The American Journal of Clinical Nutrition 2008;87(4):964-9.
  6. Qureshi A, Suri M, Ahmed S, et al. Regular egg consumption does not increase the risk of stroke and cardiovascular diseases. Med Sci Monitor 2007;13(1):CR1-8.
  7. Nakamura Y, Iso H, Kita Y, et al. Egg consumption, serum total cholesterol concentrations and coronary heart disease incidence: Japan Public Health Center-based prospective study. British Journal of Nutrition 2006;96(05):921-8.
  8. Zazpe I, Beunza JJ, Bes-Rastrollo M, et al. Egg consumption and risk of cardiovascular disease in the SUN Project. European Journal of Clinical Nutrition 2011;65(6):676-82.
  9. Burke V, Zhao Y, Lee AH, et al. Health-related behaviours as predictors of mortality and morbidity in Australian Aborigines. Preventive Medicine 2007;44(2):135-42.
  10. Mann JI, Appleby PN, Key TJ, et al. Dietary determinants of ischaemic heart disease in health conscious individuals. Heart 1997;78(5):450-5.
  11. Njike V, Faridi Z, Dutta S, et al. Daily egg consumption in hyperlipidemic adults: Effects on endothelial function and cardiovascular risk. Nutrition Journal 2010;9(28).
  12. Katz DL, Evans MA, Nawaz H, et al. Egg consumption and endothelial function: a randomized controlled crossover trial. International Journal of Cardiology 2005;99(1):65-70.
  13. Hyperresonders in this context means those individuals who have an increase in serum cholesterol in proportion to increased dietary cholesterol. Hyporesonders are those individuals that do not see such an increase in serum cholesterol.
  14. Ballesteros MN, Cabrera RM, del Socorro Saucedo M, et al. Dietary cholesterol does not increase biomarkers for chronic disease in a pediatric population from northern Mexico. The American Journal of Clinical Nutrition 2004;80(4):855-61.
  15. That’s not true. I’ve been disappointed by Wikipedia a few times.

Lipids, Inflammation, and Atherosclerosis

[Lipids, Inflammation, and Atherosclerosis mp3]

Today’s guest is the venerable Dr. Michael Rosenfeld, cardiovascular disease researcher and college professor extraordinaire. Most of his studies focus on atherosclerosis and the myriad factors that influence it.

Aside from being a pain-in-the-ass to pronounce, what exactly is atherosclerosis?

Before discussing the etiology of the disease it is important to have an understanding of how lipids are transported by the body. This is actually a more complex issue than one might suppose. Think about it: the human body is essentially an aquatic environment, and we all know that lipids are insoluble in water and will aggregate with other lipids in polar environments. So how would you be able to reliably and consistently transport dietary fat from your intestines to your liver and other organs and tissues as needed? You also need to consider that while some blood vessels are large in diameter others are quite small. Organisms like us have evolved a system to transport fats using what are called lipoproteins. They are basically tiny balls of triglycerides and cholesterol with a surface coat of various proteins and phospholipids that allow them to move about and interact in the polar environment of human plasma. There are essentially four kinds of lipoproteins: chylomicrons, very-low density lipoproteins (VLDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL). I won’t go into great detail about all of them right now, but each contains varying amounts of triglycerides and cholesterol and have slightly different proteins on their surfaces.

What do lipoproteins have to do with atherosclerosis? I’ll tell you. LDL particles are like the hot dog vendors at baseball games. They swim around the blood saying “Hiyoooo! Who needs cholesterol?? Get your cholesterol here! Use it for all kinds of things: bile salts, vitamin D, lipids rafts, testosterone… you name it! I got some fresh hot cholesterol just for you.” If a cell needs some cholesterol then it manufactures an LDL receptor, sticks it onto the cell membrane, and grabs any available circulating LDL. The LDL particle gets endocytosed and the cell can then use the delicious, gooey cholesterol for whatever it needs.

So what’s the problem? The problem is that LDL has a tendency to migrate through the endothelial cell layer of blood vessel walls and become trapped in the intima where it becomes oxidized or modified in some way. The oxidized/modified LDL particles trigger an immune response which ultimately leads to macrophages – informally known as scavengers or sometimes even garbage collectors – coming in and engulfing the oxidized/modified LDL. Now one of two things can happen here: 1) The cholesterol from macrophages can be handed off to HDL particles. The HDL can then take up this cholesterol and transport the it back to the liver to be recycled. The HDL could also give it to other lipoproteins in the blood. This process is known as reverse cholesterol transport. Or 2) The macrophage can hang out in the intima and continue to gobble-up incoming modified/oxidized LDL particles. This will lead to the formation of foam cells.1, 2


To make a long story short one or two or five foam cells within the vessel wall is no big deal, but over time, if the conditions are right, foam cells can accumulate within the vessel walls leading to a host of things you don’t want to happen with your arteries such as: narrowing of the blood vessel, chronic inflammation, recruitment of more macrophages, rupturing foam cells leading to all the oxidized LDL spilling out all over the place, migrating smooth muscle cells into the intima to wall-off the lesion, formation of a necrotic core filled with dead cells and cholesterol, and eventually rupture of the vessel wall (called a thrombosis) when all the contents spill out and can slow or stop the flow of blood. Platelets are then mobilized to repair the damage, but this probably only exacerbates the problem. If the thrombosis occurs in a coronary artery this can be deadly.


Inside an artery with advanced atherosclerosis

So what does this have to do with nutrition? There are several risk factors for atherosclerosis that can be manipulated via the diet. The following are risk factors that are considered to be “definitely modifiable” in the scientific and medical literature:

  • Cholesterol
  • HDL
  • Triglycerides
  • Blood Pressure
  • Cigarettes
  • Diabetes
  • Obesity
  • Sedentary Lifestyle
  • Alcohol

The following risk factors are classified as “potentially modifiable”

  • Lipoprotein(a)
  • Oxidized Lipids
  • Glucose Intolerance
  • Homocysteine

And there are some factors you just can’t do anything about

  • Age
  • Sex
  • Genetics

Now one might think that levels of cholesterol in the blood are directly related to the amount of cholesterol ingested in the diet. It appears to make logical sense, right? As it turns out dietary cholesterol doesn’t have a huge effect on circulating cholesterol. Most of us only absorb roughly 50% of dietary cholesterol. Even if you do ingest quite a bit of cholesterol from your diet your cells can compensate somewhat by down-regulating things like endogenous cholesterol synthesis. There is even a remarkable case study about a farmer that ate approximately 25 eggs a day (which adds up to an enormous amount of dietary cholesterol) and still had more or less normal serum cholesterol levels. The author claims that farmer was able to maintain cholesterol homeostasis by producing a ton of bile acids (made from cholesterol) and probably excreting most of it in the stool. Bear in mind, however, that this guy was probably an outlier as many case-studies are.

 

Okay, if dietary cholesterol doesn’t have a huge influence on serum cholesterol, then just what the hell does? Surprisingly saturated fat intake has a much larger effect on LDL than actual cholesterol intake. What do I mean by this? Well many studies have shown that if you subsist on a diet where your main source of fat is of the saturated kind, then it is likely that your LDL levels are high, but if you switched to fats consisting of mainly mono- and polyunsaturated fatty acids then your LDL levels are likely to drop significantly. Good news, right? Sure, olive oil all around! Oh, and with the caveat that your HDL levels could also decrease. Bummer. The good news is that LDL levels will decrease much more than the HDL. And just to further complicate matters the short and medium-chain saturated fatty acids commonly found in plant-based fats like coconut oil and palm oil don’t have the effect that other saturated fatty acids do when it comes to increasing serum cholesterol. This is because short-chain fatty acids (SCFA) and medium-chain fatty acids (MCFA) are processed differently by the body; they are not packaged into lipoproteins like other fats are but instead hitch a ride on serum albumin to get to their destinations. Think of the long-chain fatty acids (LCFA) as having to get on an enormous and crowded bus to get anywhere, whereas the SCFAs and the MCFAs are small and fit and can get on a bike to go where they need. That’s kinda where the metaphor stops, though.3

What else can you do to reduce your risk of atherosclerosis? They are all in the list.

  • If you’re obese you should lose weight, not just because of the reduced risk of atherosclerosis but also the substantial decreased risk in a legion of diseases, cancers, and what-have-you.
  • If you’re still smoking then I assume you are well aware of the above risks but choose to ignore them.
  • Get your blood pressure under control if you’re hypertensive.
  • Exercise regularly or at least semi-regularly.
  • Try not to get old. If you figure out how to do this let me know.
  • If you have Type 2 diabetes and you can’t shake it then at least learn to manage your glucose levels.
  • If you have hyperhomocysteinemia then you may have a B vitamin deficiency. Potentially an easy fix.
  • There are some gene therapies being studied right now if you have a genetic disorder that causes hypercholesterolemia.
  • There is also a large and growing body of evidence on phytochemicals and their antioxidant and protective effects.
  • There is also a substantial amount of evidence regarding omega-3 fatty acids and their role in modulating inflammation. Take this into account please.
  • If all else fails or you just want to keep eating steak and ice cream then talk to your doctor about statins.

This is all boilerplate stuff, of course. If you are reading this blog then I assume you are at least marginally interested in nutrition and already heed most of these recommendations. I didn’t get too much into inflammation in this post, but Dr. Rosenfeld and I talk about it more in the podcast. Inflammation truly deserves one or more posts on its own.

  1. Word on the street is that when the blokes that were first researching atherosclerosis were dissecting and examining diseased blood vessels they came upon a type of cell that looked like beer foam, and that’s how the foam cells got their name.
  2. It’s actually more complicated than that as you can probably imagine. It seems that if a macrophage ingests unmodified LDL then it can maintain normal cholesterol homeostasis, and get rid of the excess via reverse cholesterol transport. If the macrophage ingests a lot of oxidized LDL then it will become a foam cell.
  3. Wait… lemme try to extend it… So these buses sometimes get stuck on the highway and then the macrophage troll that hides underground comes and gobbles up the bus. If there are a bunch of buses then the troll will gobble those up as well and if he eats enough LDL buses then he morphs into the foam troll. Then foam troll can use his new powers of chemotaxis to silently call other trolls like a dog whistle and if enough buses and trolls show up then you have a traffic jam and everybody dies. Got it?

Astrup A, et al. (2011) The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010? Am J Clin Nutr. 93:684-688.

Breslow JN. (2006) n-3 Fatty acids and cardiovascular disease. Am J Clin Nutr. 83:1477S-1482S.

Fernandez ML and West KL. (2005) Mechanisms by which Dietary Fatty Acids Modulate Plasma Lipids. J Nutr. 135:2075–2078.

Genest J. (2003) Lipoprotein disorders and cardiovascular risk. J Inherit Metab Dis. 26:267-287.

Glass CK and Witztum JL. (2001) Atherosclerosis: The Road Ahead. Cell. 104:503–516.

Grundy, SM. (1990) Cholesterol and Atherosclerosis: Diagnosis and Treatment. New York, NY: Gower Medical Publishing.

Grundy SM. (1991) Multifactorial Etiology of Hypercholesterolemia Implications for Prevention of Coronary Heart Disease. Arterioscler Thromb Vasc Biol. 11:1619-1635.

Kern F. (1991) Normal Plasma Cholesterol in an 88-Year Old Man Who Eats 25 Eggs a Day: Mechanisms of Adaptation. NEJM. 324:896-899.

Loscalzo J (Ed.) (2005) Molecular Mechanisms of Atherosclerosis. Abingdon, Oxon: Taylor & Francis.

Nicolosi RJ, et al. (2001) Dietary Effects on Cardiovascular Disease Risk Factors: Beyond Saturated Fatty Acids and Cholesterol. J Am Coll Nutr. 20:421S-427S.

Ross R. (1999) Atherosclerosis – An Inflammatory Disease. NEJM. 340:115-126.

Siri-Tarino SW, et al. (2010) Saturated fat, carbohydrate, and cardiovascular disease. Am J Clin Nutr. 91:502-509.

The Philosophy of Nutrition: Animal Ethics

[Animal Ethics mp3]

[BONUS EPISODE: Puppies, Pigs, and People featuring Alastair Norcross mp3]

This episode is more about philosophy than science, so there will not be many references to scientific literature in this blog post. However, I do think areas of neuroscience can greatly inform us about topics like animal welfare and the ethics of eating animals because neuroscience can give us insights into sentience, pain, suffering, etc., but alas I am no neuroscientist so I cannot comment too intelligently on the matter. But what I can do is yammer-on about myself for a couple of paragraphs and link to some things that were discussed.

Last year I attended an animal ethics conference at Colorado State University. I didn’t even want to go. Mainly because it started at 8am on a weekend, but also because I didn’t really care too much for the topic. It’s not that I thought issues of animal welfare to be unimportant, but I guessed that the bulk of the conference was going to detail the conditions of animals in factory-farming conditions and explaining why you shouldn’t be eating animals raised in this way.1 Both of which I was already well-aware. I rarely eat red meat or poultry, but I do enjoy the taste of scrambled eggs in the morning and intensive egg-production conditions are among the worst in all of industrial animal agriculture.2 So needless to say I did not really want to get up early and schlep my audio equipment to campus only to be shamed and disgusted at my own behavior. But on the plus side there would be free breakfast at the conference and I knew that some of my friends were going to be there. Another motivating factor for me was that I was producing another podcast at the time and desperately needed some content to publish—hence the schlepping of the audio epquipment.3

I actually enjoyed the majority of the conference. The speakers that were chosen made for a diversity of opinion on several matters, so it was not any kind of pro-vegan indoctrination session that I had feared. One person, Dr. Norcross, stood out to me as being quite interesting, informed, and articulate about bioethical issues so after the conference I cornered him and asked for an interview. To my joy he accepted, and we conducted the interview at a nearby bar.

One thing that was mentioned was an article by the late David Foster Wallace titled Consider the Lobster that was originally published in the now-defunct Gourmet magazine.4 It’s very long for a magazine article, but typical length for a DFW article. I really enjoyed reading it, and I would encourage anyone else to do the same.

In the bonus episode Norcross discusses the fictional case of a man named Fred who has a problem enjoying the taste of chocolate. Here is Norcross’s paper where that story originally appeared5 if you want a more in-depth analysis of the metaphor with argument and refutation. I’ll warn you that it contains formal logic6 and Latin terms like modus ponens that you may not understand if you don’t have a basic background in philosophy.

  1. or even eating any animals in general
  2. Factory-farming is largely based on economies of scale. In other words, cram as many animals as possible into the smallest area possible to achieve the highest profit margins. When it comes to egg production hens are usually housed in what are called battery cages. It’s not a pretty picture. They are also subject to debeaking and other distasteful things.
  3. Yes, I re-purposed some of the content from that podcast. Here is the original episode it came from, although I used the Norcross interview in full. The second half of the original episode has some discussion with a philosophy PhD student about sentience, though, if you are so inclined. The bonus episode on the other hand is all new stuff.
  4. although the Gourmet website still seems to be churning out regular posts
  5. Norcross A. (2004) Puppies, Pigs, and People: Eating Meat and Marginal Cases. Philosophical Perspectives. 18:229-245
  6. Hell, I don’t even know what “formal logic” is! It may not contain any formal logic.

Nutrition 101: Carbohydrates

[Nutrition 101: Carbohydrates mp3]

I need a co-host!! As you can no doubt tell I don’t have the dulcet baritone voice I might want on the podcast. I also don’t have special ribbon or condenser mics normally used for radio personalities. I can do some EQ-ing in post to try and maximize the bass that’s picked up, but I usually don’t do that. It’s not just my voice, though; it’s also about how strange it feels to talk into a mic alone. In any case, if you know me personally and would like to contribute let me know. I could use a different perspective and dual dynamic.

So with that out of the way today’s podcast is about carbohydrates. I don’t know how many of you know what they truly are. I certainly didn’t a few years ago; I just knew that there was a lot of ‘em in pasta, bread, potatoes, and sugary stuff. Of course that didn’t stop me from telling people to stay away from them because they were “bad for you” and made you fat, even though I had essentially zero knowledge of nutrition or food science. I bet I was really annoying back then.

I will abbreviate carbohydrate sometimes as “CHO” for typing ease and because it refers to Carbon, Hydrogen, and Oxygen which are the constitutive elements of carbohydrates. Also if you take any higher education course that might deal with CHO the instructor(s) will likely abbreviate them this way as well.

As I mentioned in the podcast there are primarily three types of CHO: monosaccharides, disaccharides, and polysaccharides.1  Below are examples of the first two.

 

The main monosaccharides are glucose, fructose, and galactose. These are not the only monosaccharides that exist in nature; others include ribose, xylose, deoxyribose, arabinose, mannose, glucosamine, and on and on. However, glucose, fructose, and galactose are going to be the most nutritionally relevant because you will be eating far more of them than any other monosaccharides. Below is a diagram comparing the three sugars and, as you can see, they are quite similar. In fact, their chemical formulas are all exactly the same (C6H12O6), but each of their structures differs slightly.


There is nothing fancy about disaccharides either except that they are two monosaccharides bound together that will eventually be pulled apart by the enzymes in your gut. There are also a few more disaccharides in existence than pictured2, but they are not commonly found in the diet.

Lastly we have polysaccharides which are classified as either starch or dietary fiber.3 I also mentioned glycogen in the podcast. Glycogen is physiologically significant and plays an important role in muscle tissue, but as far as nutrition goes it’s pretty inconsequential. That said, here’s a pretty picture of glycogen that I took from Wikipedia.

 

Your muscles will just break off some carbon whenever it needs a little energy.4

Regarding starch, there are two main types: amylose and amylopectin. I have provided another picture for you. You are welcome.

 

As you can see they are both composed of long glucose chains and have a fairly similar structure, although the amylopectin is highly-branched. I have been looking through the literature to see if there is any meaningful difference between the two in terms of health benefits. The evidence is mixed, but it seems that amylose is considered by more researchers to confer health benefits over amylopectin because it is more slowly digested, thus giving amylose a lower glycemic index. Again, the evidence is not so clear-cut so avoiding amylopectin like the plague is probably unnecessary.

And lastly we have dietary fiber which also comes in two major forms: soluble and insoluble. Soluble fiber has a wide range of benefits that include lowering total cholesterol, regulating blood glucose, delaying gastric emptying which increases satiety, and providing tasty goodies for the bacteria in your gut. That last part is actually a relatively new field in nutrition science, and one I happen to be intimately involved in at the FHCRC5 at the moment. The bacteria can take soluble fiber or other compounds that you might not otherwise digest and use them for energy. As a by-product of this fermentation in your gut you can receive short-chain fatty acids or other bioactive compounds. This is not a bad thing. In fact these fatty acids and other bioactive compounds can be quite beneficial to you. As for the insoluble fiber, well… it helps you poop. And for this it deserves its own special place in heaven.

Why can’t we digest fiber and harness the energy contained it its chemical bonds like we can with other carbohydrates? Like I mentioned in the podcast dietary fibers such as cellulose are achingly similar to other CHOs like starch, but the reason we can’t mess with it all boils down to chemistry and the physical bonds that link them. Take a look at this simple picture:

 

We just don’t possess the enzymes capable of breaking the bonds on cellulose.

What about digestion and absorption? Here are a couple diagrams on how starch molecules are broken down to monosaccharides.

 

And here’s a very brief and simplistic overview of how those monosaccharides are absorbed.

 

(click to embiggen)

I did not get into carbohydrate metabolism or blood-glucose homeostasis because I wanted to start with the very basics. CHO metabolism is certainly an important topic and one I’m sure I will cover in the future but not today. However, if you’re interested here is a nice overview of how the body maintains blood-glucose levels in the fed and fasted state.

  1. You can make the argument that there are also “oligosaccharides,” but the difference between an oligosaccharide and a polysaccharide is relative – much like the difference between a “group” and a “crowd.” In this instance I am lumping oligosaccharides in with polysaccharides.
  2. like trehalose or cellobiose
  3. At least as far as the diet of primates like you and me are concerned
  4. Much like a Kit-Kat bar. Well…. Not really.
  5. Fred Hutchinson Cancer Research Center