Processed Meats Declared Too Dangerous For Human Consumption

Processed meats have been declared too dangerous for human consumption by pseudo-experts who are unable to differentiate between observational studies and clinical trials, thus posing tremendous risks to the collective IQ of the interwebz reading public [1].

The World Cancer Research Fund recently completed a detailed review of 7,000 studies covering links between diet and cancer. A grand total of 11 of these were actual clinical trials that tested two different dietary approaches or supplementation on cancer outcomes. Two of these 11 trials tested a dietary intervention, both using a low-fat diet versus a usual diet control. Researchers found that, “The low fat dietary pattern intervention did not reduce the risk of invasive colorectal cancer in any of its subsites” [2]. In other words, avoiding fat in foods like bacon, sausage, pork chops, and pepperoni will not reduce your risk of colon cancer; however, it may reduce your enjoyment of life considerably, and that, in itself, is a pain in the butt.

Upon conclusion, it is evident that reading research summaries written by people who don’t know the difference between an observational study and a clinical trial is dangerous for human intellect and the acquisition of accurate information. Consumers should stop reading processed articles full of information pollution and should instead watch re-runs of Gilligan’s Island. 

What are processed meats?
Processed meats include bacon, sausage, hot dogs, sandwich meat, packaged ham, pepperoni, salami and nearly all meat found in prepared frozen meals. Processed meats are usually manufactured with an ingredient known as sodium nitrate, which is often linked to cancer by pseudo-experts who don’t know how to look up stuff in PubMed. Sodium nitrate is primarily used as a colour fixer by meat companies to make the packaged meats look bright red and fresh. Monosodium glutamate is also added on a regular basis to enhance the savoury flavour. An extra letter “u” added to words can also enhance colour and savoury flavour.

Sodium Nitrate has been strongly linked to the formation of cancer-causing nitrasamines [sic] in the human body, leading to a sharp increase in the risk of cancer for those consuming them. This is especially frightening, since as far as actual science goes, there is no such thing as a nitrasamine. Scientists are very concerned, however, about nitrosamines, which do, in fact, actually exist. Their concern reflects a growing body of evidence that people writing about nutrition on the internet actually have no idea about which they are ostensibly talking:

“There has been widespread discussion about health risks related to the amount of nitrate in our diet. When dietary nitrate enters saliva it is rapidly reduced to nitrite in the mouth by mechanisms discussed above. Saliva containing large amounts of nitrite is acidified in the normal stomach to enhance generation of N-nitrosamines, which are powerful carcinogens in the experimental setting. More recently, it has been suggested that nitric oxide in the stomach could also be carcinogenic. A great number of studies have been performed examining the relationship between nitrate intake and gastric cancer in humans and animals. In general it has been found that there is either no relationship or an inverse relationship, such that a high nitrate intake is associated with a lower rate of cancer. Recently, studies have been performed suggesting that not only is nitrate harmless but in fact it may even be beneficial. Indeed, acidified nitrite may be an important part of gastric host defense against swallowed pathogens. The results presented here further support the interpretation that dietary nitrate is gastroprotective. They also suggest that the oral microflora, instead of being potentially harmful, is living in a true symbiotic relationship with its host. The host provides nitrate, which is an important nutrient for many anaerobic bacteria. In return, the bacteria help the host by generating the substrate (nitrite) necessary for generation of nitric oxide in the stomach” [3].

A 2005 Hawaii University study found that reading articles about processed meats written by ninnies who can’t spell “nitrosamine” increased the risk of a 5-point IQ reduction by 67%, whilst another study found that it increased the risk of twerking by 50%. These are scary numbers for those consuming articles about processed meats on a regular basis.

Monosodium glutamate (MSG) is a second dangerous-sounding chemical found in virtually all processed meat products. MSG is thought by people who are unable to navigate PubMed to be a dangerous excitotoxin linked to neurological disorders such as migraine headaches, Alzheimer’s disease, loss of appetite control, obesity and unrestrained blogging. Nutrition bloggers use MSG to add a deceptively scientifical-sounding level of paranoia to their articles about the addictive savory flavor of dead-tasting processed meat products. This will deflect unwary readers’ attention away from inane and poorly-worded concepts such as “addictive savory flavor of dead-tasting processed meat products.” On the other hand, the Joint FAO/WHO Expert Committee on Food Additives, the Scientific Committee for Food of the European Commission, the Federation of American Societies for Experimental Biology, and the Federal Drug Administration all concluded that, although there may be a subpopulation of people sensitive to its effect, no health risk have been found to be associated with MSG [4]. But what do they know?

Food items to check carefully for aliveness before piling them into your cart:

  • Beef jerky
  • Bacon
  • Sausage
  • Pepperoni
  • Hot dogs
  • Sandwich meat
  • Deli slices
  • Ham

…and many more meat products

If it’s so dangerous to consume such stupidity, why are they allowed to write it?

Unfortunately nowadays, access to operational brain cells is not a prerequisite for access to a keyboard and a WordPress account. That and First Amendment concerns have allowed unsuspecting readers curious about the real health effects of some food components to be misled, confused, and frightened by the insidious repetition of poorly-researched half-truths written by bloggers with a frail grasp on reality and an affinity for really big words that they don’t quite know the meaning of, like nitrso , um, nitarsa, um, nirstirammidngieaygyieg.

Unfortunately, these bloggers seem to hold tremendous influence over the blogosphere, and as a result consumers have little protection from dangerous propaganda intentionally added to internet, even in places that aren’t Reddit.

To avoid the dangers of idiot bloggers writing about processed meats:

  • Always read primary sources for yourself. If there are no primary sources, leave a pleasantly snarky comment to that effect on the blog site and never go there again.
  • Don’t read any articles about sodium nitrate or MSG from bloggers who don’t know how to spell “nitrosamine.”
  • Avoid eating red meats served by restaurants, schools, hospitals, hotels or other institutions without asking for it to be served thick and juicy, just the way you like it. This will give you the courage and moral fortitude to look up stuff yourself on PubMed, without having to rely on bloggers who don’t know how to spell “nitrosamine.”
  • If you are fixated on fresh something, be fixated on Fresh Prince.
  • Avoid processed blog material as much as possible
  • Spread the word and tell others about the dangers of reading idiot blogs about the dangers of sodium nitrate and MSG

Vitamin C naturally found in lime juice that has been gently squeezed into a tumbler of tequila has been shown to help prevent the formation of permanent facepalms after accidently ingesting an idiot nutrition blog and can help protect you from the devastating IQ-lowering effects of blobbers who cant spll. The best defense of course is to avoid the interwebz all together and go dancewalking.


Sources:

  1. http://hollyleehealth.com/2013/04/02/processed-meats-declared-too-dangerous-for-human-consumption/
  2. http://www.wcrf.org/PDFs/Colorectal-cancer-CUP-report-2010.pdf
  3. http://www.jci.org/articles/view/19019

The NaCl Debacle Part 2: We don’t need no stinkin’ science!

Sodium-Slashing Superheroes Low-Sodium Larry and his bodacious side-kick Linda “The Less Salt the Better” Van Horn team up to protect Americans from the evils lurking in a teaspoon of salt!
(Drawings courtesy of Butcher Billy)

Yesterday, we found our Sodium-Slashing Superheroes Larry and Linda determined to make sure that no American endangered his/her health by ingesting more than ¾ of a teaspoon of salt a day. But recently, an Institute of Medicine report determined that recommendations to reduce sodium intake to such low levels provided no health benefits and could be detrimental to the health of some people. [In case you missed it and your job is really boring, you can read Part 1 of the NaCl Debacle here.]

Our story picks up as the 2010 USDA/HHS Dietary Guidelines Advisory Committee, fearlessly led by Linda and Larry, arrives at the foregone conclusion that most, if not all, US adults would (somehow) benefit from reducing their sodium intake to 1500 mg/day.  The American Heart Association, in a report written by—surprise!—Larry and Linda, goes on to state that “The health benefits [of reducing sodium intake to 1500 mg/day] apply to Americans in all groups, and there is no compelling evidence to exempt special populations from this public health recommendation.”

Does that mean there is “compelling evidence” to include special populations, or for that matter ordinary populations, in this 1500 mg/day recommendation? No, but who cares?

Does that mean there is science to prove that “excess” sodium intake (i.e. more than ¾ of a teaspoon of salt a day) leads to high blood pressure and thus cardiovascular disease, or that salt makes you fat, or that sodium consumption will eventually lead to the zombie apocalypse? No, no, and no—but who cares?

Larry and Linda KNOW that salt is BAD. Science? They don’t need no stinkin’ science.

Because the one thing everyone seems to be able to agree on is that the science on salt does indeed stink. The IOM report has had to use many of the same methodologically-flawed studies available to the 2010 Dietary Guidelines Advisory Committee, full of the same confounding, measurement error, reverse causation and lame-ass dietary assessment that we know and love about all nutrition epidemiology studies.  But the 2010 Dietary Guidelines Advisory Committee didn’t actually bother to look at these studies.

Why not?  (And let me remind you that the Dietary Guidelines folks usually <heart> methodologically-flawed study designs, full of confounding, measurement error, reverse causation and lame-ass dietary assessment.)

First, a little lesson in how the USDA/HHS folks create dietary guidance meant to improve the health and well-being of the American people:

  1. Take a clinical marker, whose health implications are unclear, but whose levels we can measure cheaply and easily (like blood pressure, cholesterol, weight).
  2. Suggest that this marker—like Karnac the Magnificent—can somehow predict risk of a chronic disease whose origins are multiple and murky (like obesity, heart disease, cancer).
  3. Use this suggestion to establish some arbitrary clinical cut offs for when this marker is “good” and “bad.” (Note to public health advocacy organizations: Be sure to frequently move those goalposts in whichever direction requires more pharmaceuticals to be purchased from the companies that sponsor you.)
  4. Find some dietary factor that can easily and profitably be removed from our food supply, but whose intake is difficult to track (like saturated fat, sodium, calories).
  5. Implicate the chosen food factor in the regulation of the arbitrary marker, the details of which we don’t quite understand. (How? Use observational data—see methodological flaws above—but hunches and wild guesses will also work.)
  6. Create policy that insists that the entire population—including people who, by the way, are not (at least at this point) fat, sick or dead—attempt to prevent this chronic disease by avoiding this particular dietary factor. (Note to public health advocacy organizations: Be sure to offer food manufacturers the opportunity to have the food products from which they have removed the offensive component labeled with a special logo from your organization—for a “small administrative fee,” of course.)
  7. Commence collecting weak, inconclusive, and inconsistent data to prove that yes indeedy this dietary factor we can’t accurately measure does in fact have some relationship to this arbitrary clinical marker, whose regulation and health implications we don’t fully understand.
  8. Finally—here’s the kicker—measure the success of your intervention by whether or not people are willing to eat expensive, tasteless, chemical-filled food devoid of the chosen food factor in order to attempt to regulate the arbitrary clinical marker.
  9. Whatever you do, DO NOT EVER measure the success of your intervention by looking at whether or not attempts to follow your intervention has made people fat, sick, or dead in the process.
  10. Ooops. I think I just described the entire history of nutrition epidemiology of chronic disease.

Blood pressure is easy to measure, but we don’t always know what causes it to go up (or down). There is no real physiological difference between having a blood pressure reading of 120/80, which will get you a diagnosis of “pre-hypertension” and a fistful of prescriptions, and a reading of 119/79, which won’t.  Blood pressure is not considered to be a “distinct underlying cause of death,” which means that, technically, no one ever dies of blood pressure (high or low). We certainly don’t know how to disentangle the effects of lowering dietary sodium on blood pressure from other effects (like weight loss) that may be related to dietary changes that are a part of an attempt to lower sodium (and we have an embarrassingly hard time collecting accurate dietary intake information from Food Fantasy Questionnaires anyway). We also know that individual response to sodium varies widely.

So doesn’t it make perfect sense that the folks at the USDA/HHS should ignore science that investigates the relationship between sodium intake and whether or not a person stayed out of the hospital, had a heart attack, or up and died? Well, it doesn’t to me, but nevertheless the USDA/HHS has remained obsessively fixated on one thing and one thing only, what effects reducing sodium has on blood pressure,  and they pay not one whit of attention to what effects reducing sodium has on, say, aliveness.

So let’s just get this out there and agree to agree: reducing sodium in most cases will reduce blood pressure.  But then, just to be clear, so will dismemberment, dysentery, and death.  We can’t just assume that lowering sodium will only affect blood pressure or will only positively affect health (I mean, we can’t unless we are Larry or Linda). Recent research, which prompted the IOM review, indicates that reducing sodium will also increase triglyceride levels, insulin resistance, and sympathetic nervous system activity. For the record, clinicians generally don’t consider these to be good things.

This may sound radical but in their review of the evidence, the IOM committee decided to do a few things differently.

First, they gave more weight to studies that determined sodium intake levels through multiple high-quality 24-hour urine collections. Remember, this is Low-Sodium Larry’s favorite way of estimating intake.

Also, they did not approach the data with a predetermined “healthy” range already established in their brains. Because of the extreme variability in intake levels among population groups, they decided to—this is crazy, I know—let the outcomes speak for themselves.

Finally, and most importantly, in the new IOM report, the authors, unlike Larry and Linda, focused on—hold on to your hats, folks!—actual health outcomes, something the Dietary Guidelines Have. Never. Done. Ever.

The IOM committee found, in a nutshell:

“that evidence from studies on direct health outcomes is inconsistent and insufficient to conclude that lowering sodium intakes below 2,300 mg per day either increases or decreases risk of CVD outcomes (including stroke and CVD mortality) or all-cause mortality in the general U.S. population.”

In other words, there is no science to indicate that we all need to be consuming less than ¾ of a teaspoon of salt a day. Furthermore, while there may be some subpopulations that may benefit from sodium reduction, reducing sodium intake to 1500 mg/day may increase risk of adverse health outcomes for people with congestive heart failure, diabetes, chronic kidney disease, or heart disease. (If you’d like to wallow in some of the studies reviewed by the IOM, I’ve provided the Reader’s Digest Condensed Version at the bottom of the page.)

Of course, the American Heart Association, eager to provide the public with the most up-to-date recommendations about heart health as long as they don’t contradict outdated recommendations of which the AHA is fond, responded to the IOM report by saying, ”The American Heart Association is not changing its position. The association rejects the Institute of Medicine’s conclusions because the studies on which they were based had methodological flaws.”

Um, hello AHA? Exactly what completely non-existent, massive, highly-controlled and yet highly-generalizable randomized controlled trials about sodium intake and health effects were you planning on using to make your case? I believe it was the AHA that mentioned that “It is well-known, however, that such trials are not feasible because of logistic, financial, and often ethical considerations.” Besides, I don’t know what the AHA is whining about. The quality of the science hardly matters if you are not going to pay any attention to it in the first place.

No, folks that giant smacking sound you hear is not my head on my keyboard. That was the sound of science crashing into a giant wall of Consistent Public Health Message. Apparently, those public health advocates at the AHA seem to think that changing public health messages—even when they are wrong—confuses widdle ol’ Americans. The AHA—and the USDA/HHS team—doesn’t want us to have to worry our pretty little heads about all that crazy scientifical stuff with big scary words and no funny pictures or halftime shows.

Frankly, I appreciate that. I hate to have my pretty little head worried. But there’s one other problem with this particular Consistent Public Health Message. Not only is there no science to back it up; not only is it likely to be downright detrimental to the health of certain groups of people; not only is it likely to introduce an arsenal of synthetic chemical salt-replacements that will be consumed at unprecedented levels without testing for negative interactions or toxicities (remember how well that worked out when we replaced saturated fat with partially-hydrogenated vegetable oils?)—it is, apparently, incompatible with eating food.

Researchers set out to find what would really happen if Americans were muddle-headed and sheep-like enough to actually try to reduce their sodium intake to 1500 mg/day. They discovered that, “the 2010 Dietary Guidelines for sodium were incompatible with potassium guidelines and with nutritionally adequate diets, even after reducing the sodium content of all US foods by 10%.”  Way to go, Guidelines

While these researchers suggested that a feasibility study (this is a scientifical term for “reality check”) should precede the issuing of dietary guidelines to the public, I have a different suggestion.

How about we just stop with the whole 30-year-long dietary experiment to prevent chronic disease by telling Americans what not to eat? I hate to be the one to point this out, but it doesn’t seem to be working out all that well.  It’s hard to keep assuming that the AHA and the USDA/HHS mean well when, if you look at it for what it is, they are willing to continue to jeopardize the health of Americans just so they don’t have to admit that they might have been wrong about a few things.  I suppose if a Consistent Public Health Message means anything, it means never having to say you’re sorry for 30 years-worth of lousy dietary advice.

Marion Nestle has noted that, up until now, ”every single committee that has dealt with this question [of sodium-reduction] says, ‘We really need to lower the sodium in the food supply.’ Now either every single committee that has ever dealt with this issue is delusional, which I find hard to believe—I mean they can’t all be making this up—[or] there must be a clinical or rational basis for the unanimity of these decisions.”

Weeeell, I got some bad news for you, Marion. Believe it. They have been delusional. They are making this up. And no, apparently there is no clinical or rational basis for the unanimity of these decisions.

But, thanks to the IOM report, perhaps we can no longer consider these decisions to be unanimous.

Praise the lard and pass the salt.

Read ‘em and weep:  The Reader’s Digest Condensed Version of the science from the IOM report.  Studies marked with an asterix (*) are studies that were available to the 2010 Dietary Guidelines Advisory Committee.  

Studies that looked at Cardiovascular Disease, Stroke, and Mortality

*Cohen et al. (2006)

When intakes of sodium less than 2300 mg per day were compared to intakes greater than 2300 mg per day, the “lower sodium intake was statistically significantly associated with increased risk of all-cause mortality.”

*Cohen et al. (2008)

When a fully-adjusted (for confounders) model was used, “there was a statistically significant higher risk of CVD mortality with the lowest vs. the highest quartile of sodium intake.”

Gardener et al. (2012)

Risk of stroke was positively related to sodium intake when comparing the highest levels of intake to the lowest levels of intake. There was no statistically significant increase in risk for those consuming between 1500 and 4000 mg of sodium per day.

*Larsson et al. (2008)

“The analyses found no significant association between dietary sodium intake and risk of any stroke subtype.”

*Nagata et al. (2004)

“Among men, a 2.3-fold increased risk of stroke mortality was associated with the highest tertile of sodium intake.” That sounds bad, but the average sodium intake in the high-risk group was 6613 mg per day. The lowest risk group had an average intake of 4070 mg per day. “Thus, the average sodium intake in the US would be within the lowest tertile of this study.”

Stolarz-Skrzypek at al. (2011)

“Overall, the authors found that lower sodium intake was associated with higher CVD mortality.”

Takachi et al. (2010)

The authors found “a significant positive association between sodium consumption at the highest compared to the lowest quintile and risk of stroke.” As with the Nagata (2004) study, this sounds bad, but the average sodium intake in the high-risk group was 6844 mg per day. The lowest risk group had an average intake of 3084 mg per day. “Thus, the average sodium intake in the US would be close to the lowest quintile of this study.”

*Umesawa et al. (2008)

“The authors found an association between greater dietary sodium intake and greater mortality from total stroke, ischemic stroke, and total CVD.” However, as with the Nagata and the Takchi studies (above), lower quintiles—in this case, quintiles one and two—would be comparable to average US intake.

Yang et al. (2011)

Higher usual sodium intake was found to be associated with all-cause mortality, but not cardiovascular disease mortality or ischemic heart disease mortality. “However, the finding that correction for regression dilution increased the effect on all-cause mortality, but not on CVD mortality, is inconsistent with the theoretical causal pathway.”  In other words, high sodium intake might be bad for health, but not because it raises blood pressure and leads to heart disease.

Studies in Populations 51 Years of Age or Older

*Geleijnse et al. (2007)

“This study found no significant difference between urinary sodium level and risk of CVD mortality or all-cause mortality.” Relative risk was lowest in the medium intake group, with an average estimated intake of 2, 415 mg/day.

Other

“Five of the nine reported studies in the general population listed above also analyzed the data on health outcomes by age and found no interaction (Cohen et al., 2006, 2008; Cook et al., 2007; Gardener et al., 2012; Yang et al., 2011).”

Studies in Populations with Chronic Kidney Disease

Dong et al. (2010)

“The authors found that the lowest sodium intake was associated with increased mortality risk.”

Heerspink et al. (2012)

“Results from this study suggest that ARBs were more effective at decreasing CKD progression and CVD when sodium intake was in the lowest tertile” which had an estimated average sodium intake of about 2783 mg/day.

Studies on Populations with Cardiovascular Disease

Costa et al. (2012)

“Dietary sodium intake was estimated from a 62-itemvalidated FFQ. . . . Significant correlations were found between sodium intake and percentage of fat and calories in daily intake. . . . Overall, for the first 30 days and up to 4 years afterward, total mortality was significantly associated with high sodium intake.”

Kono et al. (2011)

“Cumulative risk analysis found that a salt intake of greater than the median of 4,000 mg of sodium) was associated with higher stroke recurrence rate. Univariate analysis of lifestyle management also found that poor lifestyle, defined by both high salt intake and low physical activity, was significantly associated with stroke recurrence.

O’Donnell et al. (2011)

“For the composite outcome, multivariate analysis found a U-shaped relationship between 24-hour urine sodium and the composite outcome of CVD death, MI, stroke, and hospitalization for CHF.” In other words, both higher (>7,000 mg per day estimated intake) and lower (<2,990 mg per day estimated intake) intakes of sodium were associated with increased risk of heart disease and mortality.

Studies on Populations with Prehypertension

*Cook et al. (2007)

In a randomized trial comparing a low sodium intervention with usual intake, lower sodium intake did not significantly decrease risk of mortality or heart disease events.

*Cook et al. (2009)

No significant increase in risk of adverse cardiovascular outcomes was associated with increased sodium excretions levels.

Other

“Several other studies discussed in this chapter analyzed data on health outcomes by blood pressure and found no statistical interactions (Cohen et al., 2006, 2008; Gardener et al., 2012; O’Donnell et al., 2011; Yang et al., 2011).”

Studies on Populations with Diabetes

Ekinci et al. (2011)

Higher sodium intakes were associated with decreased risk of all-cause mortality and heart disease mortality.

Tikellis et al. (2013)

“Adjusted multivariate regression analysis found urinary sodium excretion was associated with incident CVD, with increased risk at both the highest [> 4,401 mg/day] and lowest [<2,346 mg/day] urine sodium excretion levels. When analyzed as independent outcomes, no significant associations were found between urinary sodium excretion and new CVD or stroke after adjustment for other risk factors.”

Other

“Two other studies discussed in this chapter analyzed the data on health outcomes by diabetes prevalence and found no interaction (Cohen et al., 2006; O’Donnell et al., 2011).”

Studies in Populations with Congestive Heart Failure

Arcand et al. (2011)

High sodium intake levels (≥2,800 mg per day) were significantly associated with acute decompensated heart failure, all-cause hospitalization, and mortality.

Lennie et al. (2011)

“Results for event-free survival at a urinary sodium of ≥3,000 mg per day varied by the severity of patient symptoms.” In people with less severe symptoms, sodium intake greater than 3,000 mg per day was correlated with a lower disease incidence compared to those with a sodium intake less than 3,000 mg per day. Conversely, people with more severe symptoms who had a sodium intake greater than 3,000 mg per day had a higher disease incidence than those with sodium intakes less than 3,000 mg per day.

Parrinello et al. (2009)

“During the 12 months of follow-up, participants receiving the restricted sodium diet [1840 mg/day] had a greater number of hospital readmissions and higher mortality compared to those on the modestly restricted diet [2760 mg/day].”

*Paterna et al. (2008)

The lower sodium intake group [1840 mg/day] experienced a significantly higher number of hospital readmissions compared to the normal sodium intake group [2760 mg/day].

*Paterna et al. (2009)

A significant association was found between the low sodium intake [1,840 mg per day]) and hospital readmissions. The group with normal sodium diet [2760 mg/day] also had fewer deaths compared to all groups receiving a low-sodium diet combined.

The NaCl Debacle Part 1: Salt makes you fat?

Don’t look now, but I think the Institute of Medicine’s new report on sodium just bitch-slapped the USDA/HHS 2010 Dietary Guidelines.

In case you have a life outside of the nutritional recommendation roller derby, the IOM recently released a report that comes to the conclusion that restricting sodium intake to 1500 mg/day may increase rather than reduce health risks. Which is a little weird, since the 2010 Dietary Guidelines did a great job of insisting that any American with high blood pressure, all blacks, and every middle-aged and older adult—plus anyone who has ever eaten bacon or even thought about eating bacon, i.e. nearly everybody—should limit their salt intake to 1500 mg of sodium a day, or less than ¾ of a teaspoon of salt. The American Heart Association was, of course, aghast. The AHA thinks EVERYBODY should be limited to less than ¾ teaspoon of salt a day, including people who wouldn’t even think about thinking about bacon.

Why are the AHA and USDA/HHS so freaked out about salt?  And how did the IOM reach such a vastly different conclusion than that promoted by the AHA and the Dietary Guidelines?  Fasten your seat belts folks, it’s gonna be a bumpy blog.

First, it is helpful to examine why the folks at AHA and USDA/HHS are so down on salt.  The truth: we have no freakin’ idea. Salt has been around since what, the dawn of civilization maybe? It is an essential nutrient, and it plays an important role in preserving food and preventing microbial growth (especially on bacon). But Americans could still be getting too much of a good thing. Everybody at the AHA seems to think that Americans consume “excessive amounts” of sodium. (Of course, just about anything looks excessive compared to less than ¾ of a teaspoon.) But do we really consume too much sodium?

Back in 2010, Dr. Laurence I-Know-More-About-Sodium-Than-Your-Kidneys-Do Appel (or as his friends call him, “Low-Sodium Larry”), one of the leading advocates for a salt-free universe, acknowledged that “The data is quite murky. We just don’t have great data on sodium trends over time. I wish that we did. But I can’t tell you if there’s been an increase or decrease.”

Well, Low-Sodium Larry, I can, and I am about to make your wish come true.

According to recent research done by that wild bunch of scientific renegades at Harvard, in the past 60 years sodium intake levels have . . .drumroll, please . . .  not done much of anything.

Hey, that doesn’t sound right! Everyone knows that it is virtually impossible to get an accurate measure of sodium intake from dietary questionnaires; people are probably just “under-reporting” their salt intake like they “under-report” everything else. Low-Sodium Larry has previously insisted that one of the reasons the data is so murky is that few epidemiological studies measure sodium intake accurately and that, “really, you should do 24-hour urinary sodium excretions to do it right.”

The guys at Harvard looked at studies that did it right.  This systematic analysis of 38 studies from the 1950s to the present, found that 24-hour urinary sodium excretion (the “gold” standard—omg, I could not resist that—of dietary sodium intake estimation) has neither increased nor decreased, but has remained essential stable over time. Despite the fact that Americans are apparently hoovering up salt like Kim Kardashian hoovers up French fries—and with much the same results, i.e. puffing up like a Macy’s Thanksgiving Day balloon—for whatever reason we simply aren’t excreting more of it in our urine.

According to that same study however, despite the lack of increase in sodium excretion (which is supposed to accurately reflect intake—but that can’t be right), high blood pressure rates in the population have been increasing. Duh. Everyone knows that eating lots of salt makes your blood pressure go up. But have the rates of high blood pressure in America really been going up?

Age-Adjusted Prevalence of Hypertension (2009 NIH Chart Book)

Well, no.  Not really. The Harvard dudes cite a report that goes back to 1988-1994 data, and yes, rates of high blood pressure have been creeping slowly back up since then. This is because from 1976-1980 to 1988-1994, rates of high blood pressure plummeted for most segments of the American population.

We don’t know why rates of high blood pressure fell during the 70s and early 80s. It may have been that the Dietary Guidelines told people to eat more potassium-filled veggies and people actually tried to follow the Dietary Guidelines, which would have had a positive effect on high blood pressure. On the other hand, it could have been largely due to the sedating influence of the soft rock music of that era blanketing the airwaves with the mellow tones of England Dan and John Ford Coley, Christopher Cross, Ambrosia, and the like (youtube it, you young whippersnappers out there). We also don’t know why rates are going back up. Rising rates of obesity may be part of the problem, but it is also entirely possible that piping the Monsters of Lite Rock through every PA system in the country might save our health care system a lot of time and trouble.

This is what we (think we) know:

  • High-sodium diets might possibly maybe sometimes be a contributor to high blood pressure.
  • Rates of high blood pressure are going (back) up.
  • Obesity rates are definitely going up.

Ergo pro facto summa cum laude, it is clear—using the logic that seems to undergird the vast majority of our public health nutrition recommendations—salt makes you fat.  The USDA/HHS has been faced with rapidly rising rates of obesity which, until now, they have only been to pin on the laziness and gluttony of Americans.  But if salt makes us fat, that might explain why the USDA/HHS doesn’t want us to eat it.

After all, the biomechanics of this is pretty straightforward. If you eat too much sodium (which we must be), but you don’t pee it out (which we aren’t), you must be retaining it and this is what makes your blood pressure and your weight both go way up. They didn’t really cover the physics of this in my biochemistry classes so you’ll have to ask Dr. Appel how this works because he knows more about sodium than your kidneys do. But I think it must be true. After all, this is the mechanism that explains the weight loss behind carbohydrate-reduced diets, right? I myself reduced my carb intake and lost 60 pounds of water weight!

And besides, taking the salt out of our food will give food manufacturers the opportunity to make food more expensive and tasteless while adding synthetic ingredients whose long-term effects are unknown—just what the American consumer wants!

For a while there, we thought the whole idea was to reduce sodium in order to reduce blood pressure in order to reduce diseases of the circulatory system, like heart failure, stroke, and coronary heart disease . That didn’t seem to work out so well, because the whole time that sodium intake was staying stable (if we want to believe the urinary sodium excretion data) and high blood pressure rates were going down (although they are starting to go back up), rates of those diseases have gone up:

Age-Adjusted Prevalence of Heart Failure (2009 NIH Chart Book)

Age-Adjusted Prevalence of Stroke (2009 NIH Chart Book)

Age-Adjusted Prevalence of Coronary Heart Disease (2007 NIH Chart Book)

So if reducing blood pressure to reduce cardiovascular disease isn’t the answer, then we must need to reduce blood pressure to reduce obesity! By jove, I think we’ve got it!

The USDA/HHS must have known the “salt makes you fat” notion would be a tough sell, I mean, what with the lack of any shred of supporting science and all that. (But then, the “salt causes high blood pressure which causes cardiovascular disease” argument hasn’t exactly been overburdened by evidence either, and that never seemed to stop anyone.) So the 2010 Dietary Guidelines brought together the American Heart Association’s Superheroes of Sodium Slashing, Low-Sodium Larry and his bodacious salt-subduing sidekick, Linda Van Horn, both of whom had been preaching the gospel of sodium-reduction as a preventive health measure with little conclusive evidence to support their recommendations.  The USDA/HHS knew that with Linda and Larry on the team, it didn’t matter how lame the science, how limited the data, or how ludicrous the recommendation, these two could be counted on to review any and all available evidence and reliably come up with the exact same concrete and well-proven assumptions they’d been coming up with for years.

The Sodium-Slashing Superheroes–Drs. Lawrence Appel and Linda Van Horn– ready to make the world safe for bland, unappetizing food everywhere! (Drawings courtesy of Butcher Billy)

So here’s the cliffhanger:  Will Linda and Larry be able to torture the science on salt into confessing its true role in the obesity crisis?

Tune in tomorrow, when you’ll hear Linda and Larry say: “Science? We don’t need no stinkin’ science.”

A Heaping Dish of Humility and a Side of Caution

This was not on the menu at the ”Is Nutrition Research Keeping Pace with Policy and Consumers” panel at the Consumer Federation of America’s National Food Policy Conference.

I’m not sure what I expected, but I was encouraged by the fact that during other presentations at the conference, I had heard murmurs that perhaps we don’t really know what we mean what we say “healthy food” and that the public has some real concerns about what they are being told about nutrition.  So I was manifestly disappointed to hear just another rallying cry for the status quo from the academics and policymakers on this panel.

A panelist from the National Cancer Institute asserted–despite those rumors heard elsewhere in the conference–that we “do have consensus” about what constitutes a healthy diet: “lean meat, whole grains, more fresh fruits and vegetables, and reduced saturated fat, sugar, trans-fats, and sodium.”  Linda Van Horn, who chaired the 2010 Dietary Guidelines Advisory Committee, told the audience that:  ”We know what the problem is in obesity.  It’s the calories.  The calories.”  She went on to let us all know that if we just had policies that would help Americans follow the recommendations that are already in place, we could reverse the obesity crisis.  Sigh.  Make the healthy choice the easy choice for poor stupid fat Americans?  Again?  Already?

And–yes–in case you are wondering, I was quivering with rage by the time the panel finished talking (yogic breathing sadly not helping).  When my turn to ask a question arrived, I reminded the panel of the changes that we’ve already made in our diets–reduced red meat and egg consumption, increased whole grains and fresh fruits and vegetables, switched whole milk for low fat milk–and yet obesity and chronic disease continue to rise.  My question to them was, “When are nutrition experts and policymakers going to quit blaming the consumer for not following the food rules and start thinking about whether or not the advice we’ve been given is truly effective?”

After the panel, the gentleman next to me said “Good question.”  Yeah, I thought so too, but I got a truly lousy response from Dr. Van Horn:  ”We may have reduced red meat, but we’ve increased sugar.”  Have we? Why might that have happened–if indeed it has?*  ”No one is blaming the consumer; the fault lies with the food industry.”  This, at a conference devoted to showing consumers how their choices have driven the actions of industry. To blame industry is to blame the consumer; it’s just a sneaky and, frankly, dishonest way of doing it.

Ironically, the next day BMJ published an editorial with a completely different perspective. In it, Gary Taubes  (science writer and champion for the return of common-sense and intellectual rigor in the world of nutrition science)** suggests that instead of yet another round of “making the healthy choice the easy choice” for poor stupid fat Americans who haven’t the good sense to lose weight and stay healthy the way they’ve been told to for the past 35 years, perhaps nutrition experts might try a different tact:

“We believe that ultimately three conditions are necessary to make progress in the struggle against obesity and its related chronic diseases—type 2 diabetes, most notably. First is the acceptance of the existence of an alternative hypothesis of obesity, or even multiple alternative hypotheses, with the understanding that these, too, adhere to the laws of physics and must be tested rigorously.

Second is a refusal to accept substandard science as sufficient to establish reliable knowledge, let alone for public health guidelines. When the results of studies are published, the authors must be brutally honest about the possible shortcomings and all reasonable alternative explanations for what they observed.

Finally, if the best we’ve done so far isn’t good enough—if uncontrolled experiments and observational studies are unreliable, which should be undeniable—then we have to find the willingness and the resources to do better. “

While I find plenty to disagree with here (high glycemic grains?  really?), Taubes outlines some fascinating aspects of the history of obesity research and sheds some light on why the calories in-calories out hypothesis won out over the endocrinological (say it 5 times fast) one—and what nutritional mayhem has ensued since.  (Read the whole thing.  You’ll be glad you did.  I’ll wait here.)

His editorial reminds us that when it comes to the question of what dietary pattern will prevent obesity and chronic disease, we really don’t know much.  And it makes clear that what is needed now is a view toward a future where we will approach this question with much more humility and caution than we have in the past.

I’m going to suggest now–and you dear readers help me remember–that this time next year, we need to take Consumer Federation’s Food Policy Conference by storm.  It isn’t expensive (I think registration is $90, cheaper still if you are a student).  We are, after all, consumers.   The meeting is full of industry reps, policymakers, journalists, as well as academics.  It’s a small enough venue that I believe we can make our voices heard.  We can let them know that the current definition of “healthy food” doesn’t work for all of us & we, as consumers, want different choices and different information.

I get the impression that the current crop of nutrition experts and academics isn’t interested in trying this new dish–humility with a side of caution.  Since these folks seem to want to persist in keeping the public’s health on a trajectory where they can be the solution to the problems they have caused, perhaps we can find some ways to  ”make the reasonable choice the easy choice” for them.

I’ll rent the hotel room & anybody who wants to can bring a sleeping bag–paleo sleepers can spread their bearskins on the floor.  Let’s do it.

*The truth is we don’t really know how sugar intake has changed.  Dietary data and food availability data offering conflicting views.  A mean of 15.8% of consumed calories was from added sugars in this study; data from 2010.  This study estimated that 26% of calories were from added sugar; data from 1977-1978.

**Full disclosure:  I know, and usually actually like, Gary Taubes.  But he does not pay me to say nice things about him & I disagree with him as much as I agree.

TMAO? LMAO.

Move over saturated fat and cholesterol. There’s a new kid on the heart disease block: TMAO.

TMAO is not, as I first suspected, a new internet acronym that I was going to have to get my kids to decipher for me, while they snickered under their collective breaths. Rather, TMAO stands for Trimethylamine N-oxide, and it is set to become the reigning king of the “why meat is bad for you” argument. Former contenders, cholesterol and saturated fat, have apparently lost their mojo. After years of dominating the heart disease-diet debate, it turns out they were mere poseurs, only pretending to cause heart disease, the whole time distracting us from the true evils of TMAO.

The news is, the cholesterol and saturated fat in red meat can no longer be held responsible for clogging up your arteries. TMAO, which is produced by gut bacteria that digest the carnitine found in meat, is going to gum them up instead. This may be difficult to believe, especially in light of the fact that, while red meat intake has declined precipitously in the past 40 years, prevalence of heart disease has continued to climb. However, this is easily accounted for by the increase in consumption of Red Bull—which also contains carnitine—even though it is not, as some may suspect, made from real bulls (thank you, BW).

Here to explain once again why we should all be afraid of eating a food our ancestors ignorantly consumed in scandalous quantities (see what happened to them?  they are mostly dead!) is the Medical Media Circus! Ringleader for today is the New York Times’ Gina Kolata, who never met a half-baked nutrition theory she didn’t like (apparently Gary Taubes’ theory regarding carbohydrates was not half-baked enough for her).

Step right up folks and meet TMAO, the star of “a surprising new explanation of why red meat may contribute to heart disease” (because, frankly, the old explanations aren’t looking too good these days).

We know that red meat maybe almost probably for sure contributes to heart disease, because that wild bunch at Harvard just keeps cranking out studies like this one, Eat Red Meat and You Will Die Soon.

This study and others just like it definitely prove that if you are a white, well-educated, middle/upper-middle class health professional born between 1920 and 1946 and you smoke and drink, but you don’t exercise, watch your weight, or take a multivitamin, then eating red meat will maybe almost probably for sure increase your risk of heart disease. With evidence like that, who needs evidence?

Flying like the Wallenda family in the face of decades of concrete and well-proven assumptions that the reason we should avoid red meat is because of its saturated fat and cholesterol content, the daring young scientists who discovered the relationship between TMAO and heart disease “suspected that saturated fat and cholesterol made only a minor contribution to the increased amount of heart disease seen in red-meat eaters” [meaning that is, the red-meat eaters that are white, well-educated, middle/upper-middle class health professionals, who smoke and drink and don't exercise, watch their weight, or take a multivitamin; emphasis mine].

Perhaps their suspicions were alerted by studies such as this one, that found that, in randomized, controlled trials, with over 65 thousand participants, people who reduced or changed their dietary fat intake didn’t actually live any longer than the people who just kept eating and enjoying the same artery-clogging, saturated fat- and cholesterol-laden foods that they always had. (However, this research was able to determine that a steady diet of broiled chicken breasts does in fact make the years crawl by more slowly.)

You can almost ALWAYS catch something on a fishing expedition.

Our brave scientists knew they couldn’t just throw up their hands and say “Let them eat meat!” That would undermine decades of consistent public health nutrition messaging and those poor stupid Americans might get CONFUSED—and we wouldn’t want that! So, instead the scientists went on a “scientific fishing expedition” (Ms. Kolata’s words, not mine) and hauled in a “little-studied chemical called TMAO that gets into the blood and increases the risk of heart disease.” Luckily, TMAO has something to do with meat. [As Chris Masterjohn points out, it also has something to do with fish, peas, and cauliflower, but--as I'm sure these scientists noticed immediately--those things do not contain meat.] Ta-da! Problemo solved.

Exactly how TMAO increases the risk of heart disease, nobody knows. But, good scientists that they are, the scientists have a theory. (Just to clarify, in some situations the word theory means: a coherent group of tested general propositions, commonly regarded as correct. This is not one of those situations.) The researcher’s think that TMAO enables cholesterol to “get into” artery walls and prevents the body from excreting “excess” cholesterol. At least that’s how it works in mice. Although mice don’t normally eat red meat, it should be noted that mice are exactly like people except they don’t have Twitter accounts. We know this because earlier mouse studies allowed scientists to prove beyond the shadow of a doubt that dietary cholesterol and saturated fat cause heart disease mice definitely do not have Twitter accounts.

Look, just because the scientists can’t explain how TMAO does all the bad stuff it does, doesn’t mean it’s not in there doing, you know, bad stuff. Remember, we are talking about molecules that are VERY VERY small and really small things can be hard to find–unless of course you are on a scientific fishing expedition.

What will happen to the American Heart Association’s seal of approval now that saturated fat and cholesterol are no longer to be feared?

Frankly, I’m relieved that we FINALLY know exactly what has been causing all this heart disease. Okay, so it’s not the saturated fat and cholesterol that we’ve been avoiding for 35 years. Heck, everybody makes mistakes. Even though Frank Sacks and Robert Eckel, two scientists from the American Heart Association, told us for decades that eating saturated fat and cholesterol was just greasing the rails on the fast track to death-by-clogged-arteries, they have no reason to doubt this new theory. And even though they apparently had no reason to doubt the now-doubtful old theory, at least not until just now—as a nation, we can rest assured that THIS time, they got it right.

Now that saturated fat and cholesterol are no longer Public Enemies Number One and Two, whole milk, cheese, eggs, and butter—which do not contain red meat—MUST BE OKAY! I guess there’s no more need for the AHA’s dietary limits on saturated fat, or for the USDA Guidelines restrictions on cholesterol intake, or for those new Front of Package labels identifying foods with too much saturated fat. Schools can start serving whole milk again, butter will once again be legal in California, and fat-free cheese can go back to being the substance that mouse pads are made out of. Halla-freaking- looyah! A new day has dawned.

But—amidst the rejoicing–don’t forget: Whether we blame saturated fat or cholesterol or TMAO, meat is exactly as bad for you now as it was 50 years ago.

“Broccoli has more protein than steak”—and other crap

Of all the asinine things that I read about nutrition—and let me tell you, I read a lot of them—this one has got to be the asininniest: Broccoli has more protein than steak.

I’ve seen this idiotic meme repeated many times, but the primary source of this stupid—see also: delusional, ludicrous, and absurd—notion seems to be Dr. Joel Furhman. My mom—bless her little osteoporotic soul—keeps his books down at the beach cottage. I don’t think she does it to taunt me, but you never know. I was a bad kid, and payback may be in order. My family has forbidden me to read Dr. Furhman’s books, to pick them up, or to even glance at the covers because the resulting full-on nutrition-rant kills everybody’s beach buzz.

However, as of last week, I have officially maxed out my tolerance for just ignoring this nonsense. So, note to my family: Read no further, it will kill your beach buzz.

According the Dr. Furhman’s book, Eat to Live, a 100-calorie portion of sirloin steak has 5.4 grams of protein, and a 100-calorie portion of broccoli has 11.2 grams of protein. This is rubbish. According to the USDA’s Agricultural Research Service’s Nutrient Data Laboratory database, 100 calories of broiled beef, top sirloin steak has exactly 11.08 grams of protein and 100 calories of chopped, raw broccoli has exactly 8.29. I’m not sure what universe Dr. Furhman lives in, but in my universe, 8.29 is less than 11.08.

I can explain the discrepancy in numbers by the simple fact that Dr. Furhman and I used different sources for our information. Dr. Furham wrote his book—the one that contains the piece of drivel under consideration—in 2005, but he chose to reference a nutrition book written in 1986 (Adams, C. 1986. Handbook of the Nutritional Value of Foods in Common Units, New York: Dover Publications). Just to put things in perspective, in 1986, the internet and DVDs had not yet been invented, no one knew who Bart Simpson was, and it would be another couple of years before Taylor Swift even draws her first ex-boyfriend-bashing breath.

Here’s what I can’t explain: Why, oh why did he dig up a reference nearly two decades old and not just use the USDA internet database, which is—and has been since the 1990s—available to anyone with a library card and a half a brain? While I do not wish to speculate on exactly which of these tools Dr. Furhman might be lacking, suffice it to say that it would take less than 10 minutes for any blogger interested in the truth of the matter to find a more recent source of information—assuming of course that bloggers who perpetuate this particular fiction are interested in the truth.

But wait—before you foam at the mouth too much, Adele—8.29 grams of protein is fair bit of protein.  There is only a difference of a couple of grams of protein between broccoli and steak.  Yes, I would agree, those numbers are a lot closer than you might expect, and this might actually be nutritionally important, if—Big If—all protein were created equal. Which it isn’t.

While I am a big fan of coming at nutrition from an individualized perspective, and I am aware that nutrition scientists don’t have any monopoly on truth, we have managed to nail down a few essential things that human must acquire from the food that they eat. In terms of essentiality, after calories and fluid comes protein—or more specifically, essential amino acids (there are more essentials, but they are not the topic of this particular rant). Because these amino acid requirements are so important (a particular form of starvation, kwashiorkor, involves not overall calorie deprivation, but protein deficit in the context of adequate or near-adequate calories), the World Health Organization has established specific daily requirements of the essential amino acids that are necessary for health.

Let’s see how similar caloric intakes of steak and broccoli stack up when comparing how these two foods provide for essential amino acid requirements. A 275-calorie portion of steak (4 ounces) has 30.5 grams of protein and comes very close to meeting all the daily essential amino acid requirements for a 70 kg adult. A 277-calorie portion of broccoli is not only way more food—you’ll be chewing for a long time as you try to make it through 9 ¼ cups of broccoli—exactly NONE of the daily essential amino acid requirements for an adult are met:

EssentialAmino acids (g) Daily requirement 70 kg adult (g) Essential amino acids (g) in 275 calories of steak (4 oz or 113.33 g) Essential amino acids (g) in 277 calories of chopped, raw broccoli (9.25 cups)
histidine 0.70 0.975 ( +0.275) 0.48 (-0.22)
isoleucine 1.400 1.391 (-0.009) 0.643 (-0.757)
leucine 2.730 2.431 (-0.299) 1.05 (-1.68)
lysine 2.100 2.583 (+0.483) 1.099 (-1.001)
methionine 0.70 0.796 (+0.096) 0.309 (-0.391)
cysteine 0.28 0.394 (+ 0.114) 0.228 (-0.052)
threonine 1.050 1.221 (+0.171) 0.716 (-0.334)
tryptophan 0.280 0.201 (-0.079) 0.269 (-0.011)
valine 1.82 1.516 (-0.304) 1.018 (-0.802)

In reality, it takes twice that much broccoli, or over 18 cups, containing nearly twice as many calories, in order to get anywhere near meeting all essential amino acid requirements.  While I’m willing to concede that individual amino acid requirements may vary considerably, I am not willing to concede that similar caloric amounts of steak and broccoli provide a similar supply of those requirements.  I’m no broccoli basher (it’s sooo yummy baked with cheese & a little bacon on top), but as a protein source, even a lot leaves a lot to be desired.

Oh yeah? Well then, “how on earth do animals like elephants, gorillas and oxen get so big and strong eating only plants? A diverse plant-based diet can obviously support a big, powerful body.“ Sure it can. If you’re an elephant or a gorilla or an ox.

In general, human bodies don’t work very efficiently without a regular dietary supply of all essential amino acids: “It would be difficult to find a protein that did not have at least one residue of each of the common 20 amino acids. Half of these amino acids are essential, and if the diet is lacking or low in even one of these essential amino acids, then protein synthesis is not possible” [Emphasis mine; reference: Campbell & Farrell's Biochemistry, 6th edition]. Protein synthesis allows us to grow, heal, reproduce, and function in general. One of the specific outcomes of protein deficiency in humans is stunting, i.e. where humans who would otherwise grow bigger, don’t.

Dr. Furhman seems to think that those of us who “believe” that food from animals provides a more biologically complete source of protein than food from plants “never thought too much about how a rhinoceros, hippopotamus, gorilla, giraffe, or elephant became so big eating only vegetables.” Hmmm. I have to say, I’m thinking the same thing about Dr. Furhman. Maybe he is unaware that humans aren’t really all that much like rhinoceroses, hippos, gorillas, giraffes, or elephants. But then maybe he just hangs out with a different crowd than I do.

Once again, armed with a library card and half a brain, it is not too difficult to figure out—assuming you did think about how those animals got so big eating only plants and didn’t just mindlessly parrot Dr. Furham’s poorly-researched blather—that, as Gomer Pyle would say, surprise! surprise! Humans and other large mammals ARE different.

While non-ruminants (like humans) must get their essential amino acids from their diet, ruminants (like giraffes) “may also acquire substantial amounts of these amino acids through the digestion of microbial protein synthesized in the rumen” (see: Amino Acids in Animal Nutrition, edited by J.P. Felix D’Mello). This may come as a bit of a shock to Dr. Furhman and his readership, but humans don’t actually have rumens and utilizing this particular approach to the acquisition of essential amino acids from plant matter ain’t gonna work for us.

You can get plenty of protein from a plants-only diet by eating like a hippo.

Other non-ruminant grazers—see elephants, rhinos, and hippos—have a different eating strategy. The “eat for volume and low extraction.” In other words, the relatively low availability of protein in the food is overcome by the high volume consumed. In that regard—assuming you aspire to an elephant-like, rhino-like, or hippo-like bod—it may be possible to get sufficient protein from a strictly plant-based diet. If you don’t mind eating all the time. And pooping. Less than half of what is consumed by the high-volume grazers is utilized by the body; the rest—like a handsome stranger—is just passin’ through (see: Nutritional Ecology of the Ruminant, by Peter J. van Soest). If the idea of literally flushing over half of what you eat down the toilet doesn’t bother you, then this strategy actually might work.

ooooh! Can we? Please?

So what about gorillas? This particular primate-to-primate comparison has been tossed all around the internet. Why can’t we just eat plants like gorillas do? Gorillas, although not so good at Jeopardy, are big and strong and they’re vegans, so we should all be vegans too, right? Aside from the fact that we don’t really know exactly what gorillas are eating much of the time, it does seem that they eat a lot of bugs along with their plants. So unless you have a particularly fastidious gorilla, some dietary protein won’t be vegan. Compared to humans, gorillas also have a much larger proportion of the gut devoted to fermentation—again, another source for microbes to contribute to the nutritional completeness of a plants-only diet. And, again, a high volume of food is consumed to compensate for the low nutritional value of it. You won’t have to worry about half your food going down the toilet, though. Those who want to live like gorillas can just eat that poop instead of flushing it. This provides the body with another opportunity to extract nutrition from the substance formerly known as food and may also help explain the willingness of Dr. Furhman’s readers to swallow what he’s shoveling.

I have nothing against a plants-only diet—in whatever form it takes—if that’s what a person want to do and it makes him/her happy. I have no more interest in converting a vegan to omnivory than I do in having a vegan attempt to convert me to swearing off bacon. I am also aware that there is more—much more—to food choices than the nutritional content of the food chosen.

But I’m afraid this is just one of those situations where ideology has been sent to do the work of science. Ideology has its place, and science has its flaws. Truth, facts, and beliefs can be hard to define and harder still to separate. I get all that. But – to quote Neil deGrasse Tyson – “The good thing about science is that it’s true whether or not you believe in it.” Unfortunately, for all those gorilla-wannabees out there, the reverse also applies: Believing in something doesn’t make it true. You can believe all you want that broccoli is a better source of protein than steak, but your ribosomes don’t have access to a keyboard and they might vote differently.

Now, dear readers, if you ever run across some library-card-challenged blogger out there perpetuating Dr. Furhman’s little myth, you have a link to help spill some sunshine on the matter.

Meat is Bad and The World is Flat: Thoughts from the Critical Nutrition Symposium

Reblogged from Emily Contois:

Click to visit the original post
  • Click to visit the original post
  • Click to visit the original post
  • Click to visit the original post

While this post's title might sound like April foolery, it isn't. Not really. You see, on March 8, I had the pleasure of attending the Critical Nutrition Symposium at UC Santa Cruz, organized by Julie Guthman, author of Weighing In. The event was spawned from a roundtable discussion at last year's Association for the Study of Food and Society…

Read more… 847 more words

A beautifully-written summary by Emily Contois regarding the recent Critical Nutrition Symposium held at UC-Santa Cruz. Organized by Julie Guthman, author of Weighing In, this symposium brought together food scholars from around the country (plus me) and invited us and the audience to participate in a thought-provoking and nuanced conversation about food, nutrition, culture, and ways of knowing.