In offense of food

I'm an avid reader of those who push the boundaries of the way we think about food, writers like Michael Pollan and Eric Schlosser (see the recent flick Food, Inc. for an overarching if brief overview of their positions). And as much merit as there is in eating healthy and being conscious of our food choices, every now and then you can use a good cheat meal - both to satisfy those occasional urges and to remind you of what you're choosing to not choose.

Tonight M, JD, and I prepared a veritable low-rent feast of a cheat meal, based entirely on manufactured foodstuffs from our childhoods: Steakums with Cheese Whiz, frozen meat? lasagna, and Reddi Wip (straight from the nozzle for dessert, of course):



To provide at least a little bit of usable food knowledge, here's a link to an interesting piece about carbohydrate composition and dietary health. We all know that many people espouse the idea, in various guises, of restricting or even avoiding carbohydrate intake. This author discusses evidence that some populations with carbohydrate-rich diets, and ample caloric intake, can maintain healthy lifestyles, with low incidences of the diseases of affluence that afflict Western cultures: cardiovascular disease, obseity, diabetes, etc. The proposed idea is that the carbohydrates in these diets are primarily plant-sourced, and rich in starch broken down into glucose, as opposed to Western diets high in sucrose which metabolizes into glucose and fructose. Note that in the cited populations - Kitavans, Okinawans, Zulus - there are often confounding factors, such as the high intake of fish in island cultures or perhaps instances of caloric restriction; either way, something tasty to chew over with a mouth full of Cheese Whiz...
Some of the original sources:
Lindeberg et al., 1997
Wilcox et al., 2007

Calorie restriction delays disease onset and mortality in monkeys

New study (Colman et al, 2009) in this week's issue of Science on the effect of calorie restriction over a 20 year period in rhesus macaques. Researchers at the Wisconsin National Primate Research Center examined monkeys under 30% CR and controls matched for baseline intake, age, and weight. According to the abstract:

Caloric restriction (CR), without malnutrition, delays aging and extends life span in diverse species; however, its effect on resistance to illness and mortality in primates has not been clearly established. We report findings of a 20-year longitudinal adult-onset CR study in rhesus monkeys aimed at filling this critical gap in aging research. In a population of rhesus macaques maintained at the Wisconsin National Primate Research Center, moderate CR lowered the incidence of aging-related deaths. At the time point reported, 50% of control fed animals survived as compared with 80% of the CR animals. Furthermore, CR delayed the onset of age-associated pathologies. Specifically, CR reduced the incidence of diabetes, cancer, cardiovascular disease, and brain atrophy. These data demonstrate that CR slows aging in a primate species.

Their general findings indicate a clear quantifiable effect of CR in reducing both mortality and age-related morbidities (cancer, cardiovascular disease, metabolic derangements) as well as age-associated loss of gray matter:

Food for thought, though confounding issues such as frequency of eating rather than total amount of caloric intake are not directly addressed.

Chuck the Nalgenes?

So there's been a lot of fuss lately about bisphenol A (BPA) in polycarbonate bottles. Just to add to the confusion, the FDA deemed that an adequate margin of safety existed for exposure to BPA from food contact uses. Here's the executive summary from the draft assessment released on the 14th:

This document describes the Food and Drug Administration’s (FDA) safety assessment of Bisphenol A (BPA) as it relates to exposure through use in food contact materials. This assessment is particularly focused on the concerns for developmental toxicity identified in recent assessments of BPA, including those of the National Toxicology Program and their expert panel. BPA is an impurity in FDA-regulated food additives, including epoxy-based food can liners and polycarbonate baby bottles. FDA estimates that BPA exposure from use in food contact materials in infants and adults is 2.42 μg/kg bw/day and 0.185 μg/kg bw/day, respectively. FDA has determined the appropriate no observed adverse effect level (NOAEL) for its assessment of BPA to be the NOAEL for systemic toxicity of 5 mg/kg bw/day (5000 μg/kg bw/day) derived from two multigenerational rodent studies. This NOAEL results in adequate margins of safety of approximately 2,000 and 27,000 for infants and adults, respectively. The data reviewed on highlighted endpoints, such as the prostate gland and developmental neural and behavioral toxicity, were insufficient to provide a basis to alter the NOAEL used to calculate the margins of safety. FDA has concluded that an adequate margin of safety exists for BPA at current levels of exposure from food contact uses. At a later date, FDA will publish a separate document that provides a safety assessment of BPA exposure from other FDA-regulated products.

More interesting information from the National Toxicology Program's (NTP) draft report on BPA (a major scientific review underlying the FDA report) can be found here.

Sugar kills

In case you hadn't heard it enough from me, here are some reminders:

Via BoingBoing

Amount of sugar in a Coke (39 g), via MacRumors thread

Carbohydrates and heart disease

Atherogenic dyslipidemia is a lipoprotein profile that predisposes one to cardiovascular disease. Grundy (1997) characterizes it by four markers: 1) a borderline high-risk LDL cholesterol (130 to 159 mg/dL), 2) moderately raised (often high normal) triglycerides (greater than 150 mg/dL), 3) small LDL particles, and 4) low HDL cholesterol (less than 40 mg/dL for men and 50 mg/dL for women). The third marker is due to data indicating that not all LDL particles are atherogenic; a preponderance of small, dense LDL particles (known as a pattern B phenotype) is associated with increased coronary artery disease (Austin et al., 1988). The presence of atherogenic dyslipidemia itself is a marker for metabolic syndrome.

Source:

Ronald Krauss and colleagues have convincingly shown that changes in carbohydrate intake profoundly affects LDL phenotypes (reviewed in Krauss, 2001). The figure below is a nice summary of the basic observation that restricting carbohydrates reduces the incidence of the atherogenic LDL particle pattern. Note especially the apparent continuity of the effect, and the fact that the carbohydrates are not even severely restricted (certainly nowhere near the levels required to induce ketosis). If you have a half hour to spare, you can catch a recent webcast talk by Krauss summarizing the Pathophysiology of Atherogenic Dyslipidemia.

Source: Krauss, 2001

If you want to full scoop on recent research on the relationship between carbohydrates and dyslipidemia and metabolic syndrome, definitely take the time to check out this review article from Jeff Volek and colleagues (it's technically still in press, but you can grab the galley proofs online). It covers a lot of ground, and is well worth the effort.

Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome.

Volek JS, Fernandez ML, Feinman RD, Phinney SD.

Department of Kinesiology, University of Connecticut

Abstract: Abnormal fatty acid metabolism and dyslipidemia play an intimate role in the pathogenesis of metabolic syndrome and cardiovascular diseases. The availability of glucose and insulin predominate as upstream regulatory elements that operate through a collection of transcription factors to partition lipids toward anabolic pathways. The unraveling of the details of these cellular events has proceeded rapidly, but their physiologic relevance to lifestyle modification has been largely ignored. Here we highlight the role of dietary input, specifically carbohydrate intake, in the mechanism of metabolic regulation germane to metabolic syndrome. The key principle is that carbohydrate, directly or indirectly through the effect of insulin, controls the disposition of excess dietary nutrients. Dietary carbohydrate modulates lipolysis, lipoprotein assembly and processing and affects the relation between dietary intake of saturated fat intake and circulating levels. Several of these processes are the subject of intense investigation at the cellular level. We see the need to integrate these cellular mechanisms with results from low-carbohydrate diet trials that have shown reduced cardiovascular risk through improvement in hepatic, intravascular, and peripheral processing of lipoproteins, alterations in fatty acid composition, and reductions in other cardiovascular risk factors, notably inflammation. From the current state of the literature, however, low-carbohydrate diets are grounded in basic metabolic principles and the data suggest that some form of carbohydrate restriction is a candidate to be the preferred dietary strategy for cardiovascular health beyond weight regulation.

PMID: 18396172

Is the omega-6:omega-3 ratio of beef relevant?

Although it's still debatable what the optimal dietary ratio of omega-6 to omega-3 fatty acids is, there's good evidence that the contemporary dietary intake of polyunsaturated fatty acids has over time become heavily skewed towards a higher intake of omega-6 than omega-3 fatty acids (Cordain et al., 2005; Simopoulos, 2002). The current US diet is estimated to have a omega-6:omega-3 ratio between 10:1 to 12:1, while Cordain and colleagues estimate a ratio of between 2:1 and 3:1 for a traditional hunter-gatherer diet. There is growing consensus that reducing the omega-6:omega-3 dietary ratio may reduce the morbidity and mortality associated with a wide range of metabolic disorders.

This is all well and good, but ratios can be misleading and it's important to keep in mind the absolute mass of fatty acids consumed (Mozaffarian & Rimm, 2006; Wijendran & Hayes 2004). Case in point: one of the purported benefits of grass-fed beef is that grass-fed beef has a better omega-6:omega-3 ratio than grain-fed beef. This is also one of the reasons that wild-caught salmon is recommended over farm-raised salmon. What do the actual data look like? The table below shows the fatty acid profiles of the aforementioned meats.


A few things to note. First, the total PUFA content of grass and grain-fed beef is pretty low. Second, grass-fed beef only contains marginally more omega-3 fatty acids than grain-fed beef. This, together with a marginally lower omega-6 content results in a slightly lower omega-6:omega-3 ratio for grass-fed beef. In addition, the two samples of grain-fed beef are very similar in most respects, but one sample has an omega-6:omega-3 ratio of >17 while the other is <5. Does that mean one is healthier to eat than the other? Not in any meaningful way, looking at the ratio alone is misleading since it conceals the fact that this difference is due to a mere 30 mg of omega-3 fatty acids. To get a sense of how small that is, recall that current recommendations for daily omega-3 intake are over 2000 mg (ALA+EPA+DHA). The absolute amount of omega-3 fatty acids derived from beef is just too small, regardless of whether it is grass or grain-fed. A one pound steak only has between 70-225 mg of omega-3 fatty acids (most of which isn't the more beneficial marine omega-3s, EPA and DHA). Compare this to the amount of omega-3s you get from either wild-caught or farmed salmon. So while it's true that the omega-6:omega-3 ratios are lower for grass-fed beef, a look at the absolute masses of the separate fatty acid classes suggests that this isn't really practically relevant.

Now don't get me wrong, there are many other benefits of grass-fed beef. If money weren't a constraint, I would eat it all the time. However, I don't think that the omega-3 content of beef should be a factor when deciding whether to buy grass-fed over grain-fed. If you want to improve your omega-6:omega-3 dietary ratio, you would do better to eat more seafood and reduce your intake of vegetable oils.

Intermittent fasting or caloric restriction?

Intermittent fasting and caloric restriction are associated with many of the same benefits (Mattson, 2005). In trying to sort out the differences between these protocols, people will often treat IF and CR as if they are completely different things. It's not clear to me that they are entirely dissociable. I've previously mentioned that it is common for intermittently fasted rodents to eat slightly less than ad libitum controls. This varies from study to study and with the duration of dietary restriction (as does the degree of bodyweight difference between IF and control animals). The data in the figure below are from rats (Leveille, 1972) and mice (Anson et al., 2003), respectively.

It's worth noting that the C57BL/6 strain of mice (right panel) are intermediate (relative to other mouse strains) in terms of how much less IF mice eat than controls (Goodrick et al., 1990). And while Anson et al. (2003) claim a dissociation between IF and CR, the truth is that their animals were calorically restricted for much of the study. The question in my mind is whether both dietary protocols tap into the same underlying mechanism? Or can IF and CR interact to produce better than predicted results? The problem is that IF involves some CR and CR involves some IF. The following quote is from Leveille's paper, and is worth reproducing. Note that the term "meal-fed" refers to an intermittent diet where access to food is provided for only 2 hours each day and "nibbling" refers to ad libitum food access.

The results of the longevity study (experiment A) are difficult to interpret. Although the meal-fed animals had a significantly longer life-span than the nibbling rats the difference cannot be ascribed to meal-eating, per se. In addition to the metabolic differences between the meal-fed and nibbling rats there existed a significant difference in body weight and presumably in body fat. Thus these results can be interpreted as supportive of the classic experiments of McCay et al. (21, 22) showing that rats whose food intake was restricted had a significantly longer life-span. However, it is important to note that in McCay's studies as well as other similar studies (23,24) the restricted animals were very likely "meal-fed." It has recently been noted that restricting rats to 80% of ad libitum intake quickly results in a shift in eating pattern in which the animals ingest their daily food allowance within a 2-hour period (25). Thus one cannot determine unequivocally whether the increase in life span is due to the reduced food intake or to the meal pattern.

Masoro (2004) makes a similar point, and while his earlier study (Masoro et al., 1995) attempts to tease apart IF and CR, even he admits that the evidence does not conclusively eliminate the role of meal patterning. It seems that studying the meal patterning of individual animals within days may help to clarify this issue. This may also bear on the confusing results from human studies, since meal patterning is often not reported and maybe not even recorded.

Good ideas for simple food

Links to some blogs with great (mostly Paleo) recipes:

Naomi's Paleo Kitchen
George Mounce's Paleo Recipe Corner
Nikki Young's Blog spot
Tracy Reifkind's Training blog (with posts about the food she's eating)
Robb Wolf's Intermittent fasting blog (occasional recipes)
Scott Kuste's Modern Forager
Marc's Feel Good Eating
Scott Hagnas' blog

Also worth checking out:
Paleofood.com

Intermittent fasting facilitates learning

Several very interesting papers on the physiological changes that may underlie the benefits of intermittent fasting have been published recently. In rodents, intermittent fasting (typically implemented as alternate day fasting) results in numerous physiological changes that are correlated with disease reduction, increased stress resistance, improved insulin sensitivity and upregulation of neuroprotective trophic factors (reviewed by Mattson, 2005; Varady & Hellerstein, 2007). While many IF studies have used relatively short dietary interventions, a recent study by Fontán-Lozano and colleagues (2007) highlights the intriguing possibility that long-term intermittent fasting can lead to improved cognitive function. In a nice series of experiments, these authors demonstrate that fasted mice exhibit improved learning and memory compared to controls (fed ad libitum), and they go on to provide evidence for the underlying mechanism for this cognitive improvement.

Fontán-Lozano et al. mice placed on an alternate day fasting (ADF) regimen for 6-8 months (starting post-natal week 9, the average lifespan of a mouse is about 2 years). Mice on an ADF diet will typically eat more food on their feed days to compensate for the fasting day, and after some adjustment period will eat a bit less than twice as much food on their feed day as a normal mouse would on an typical diet. So in addition to fasting every other day, there is usually some mild caloric restriction involved. It's well-documented that ADF mice live longer than controls.



Survival distributions (n=40) of male C57BL/6J mice fed ad libitum (left curve) or every other day (ADF, right shifted curve). Souce: Talan & Ingram, 1985




ADF mice will also typically weigh less than control mice (Anson et al., 2003), although the ADF mice in Fontán-Lozano et al.'s experiments weighed the same as control mice. This might be due to the longer time spent on the ADF diet, although there are mouse strain differences in addition to diet duration differences (Goodrick et al., 1990). Fontán-Lozano et al. used a simple battery of behavioral tests to assess the learning and memory capacities of ADF mice. They found that compared to control mice, ADF mice learned faster (in a motor learning task, operant food reward task, and Pavlovian eyeblink conditioning task) and were better able to discriminate novel from familiar objects from briefer presentations.

Subsequent physiological experiments revealed that ADF mice exhibited increased theta-band activity in the hippocampus. Explorations of synaptic plasticity revealed that ADF mice exhibited enhanced paired-pulse facilitation at the CA3-CA1 synapse. Moreover, LTP could be elicited at the Schaffer's collateral–CA1 synapse using fewer high-frequency stimulations. These results are interesting since it is a well-accepted hypothesis that learning and memory are based on modifications of synaptic strength among neurons, an idea that goes at least back to Donald Hebb (1949).

A possible mechanism for the observed potentiation of synaptic plasticity is suggested by the observation that ADF mice also show changes in NMDA receptor subunit composition; this glutamate receptor is critical for many types of synaptic plasticity, and various isoforms exist which are composed of different protein subunits. It's known that the relative expression of NR2B subunits change over the course of a rodent's life; the fraction of NR2B subunits declines (and NR2A increases) in adulthood (Moyner et al., 1994). Fontán-Lozano et al. noted increased expression of NR2B NDMAR subunits in the hippocampus and perirhinal cortex of ADF mice.

Photomicrographs and immunohistochemical analyses of the NR2B expression pattern in the hippocampus of IFD (ADF) and control (ad libitum, AL) mice. The graphs represent the densitometric analysis of NR2B expression in the different areas of hippocampus (n = 5 animals per group in all tests). s luc, Stratum lucidum; mol, molecular layer; l mol, lacunosum moleculare layer; Molec, molecular layer; Lac mol, lacunosum moleculare layer; O.D., optical density. ***p ≤ 0.001. Source: Fontán-Lozano et al., 2007

Remarkably, the behavioral improvements as well as the synaptic enhancements seen in ADF mice are returned to control levels when these mice are administered a NR2B antagonist, which strongly suggests that the relative increase in NR2B subunit expression is responsible for arresting the cognitive decline that accompanies natural aging. This is reminiscent of the genetically-engineered smart mice created by Joe Tsien's group (Tang et al., 1999).

The causal mechanisms underlying the changes in NR2B expression are still unknown. Interestingly, exercise increases NR2B subunit expression in the hippocampus (Farmer et al., 2004), and there is some evidence that ADF can increase basal levels of activity (Carlson & Hoelzel, 1946). Whether there is a link between fasting-induced increases in activity and NR2B subunit expression is an important question for future research.

One thing to keep in mind is that enhanced synaptic plasticity may not necessarily be a good thing. Presumably, there was some selective pressure that led to downregulating NR2B subunit expression with age. It's not clear what this might be, but it may turn out that increased NR2B subunit expression is actually maladaptive once we figure out what the selective pressure was (is, it may still be acting?).

Watch that tuna intake

You may be surprised by the mercury levels found in tuna in NYC. Seem to be a bit higher than I expected. Gotta start shopping at Fairway!

Junk food monkeys

A humorous anecdote by Robert Sapolsky (the embedded viewer is not great, see a better version here):

Read this doc on Scribd: Junk food monkeys by Robert Sapolsky

Merry Christmas!

We've been working out pretty hard here in Iowa. We got in on Monday and pretty much just used that as a warmup day. Tuesday Scott managed to do the following in record time.

"Sugar"

As many rounds as possible in 30 min of:

5 Peanut Brittle
10 Sugared Walnuts
3 Cookies
1 glass Egg Nog

SS: 14 + some chile and chocolate
AS: 8 + some crackers

We were on pace to do a bit better, but Adrienne crashed near round 6 and Scott got distracted at round 12 by a card game, or a TV on. Nicely surprised that the egg nog was a little diluted and managed to help the rest slide down until about round 5, after which the nog was getting pretty heavy. Pushups were the weak link.