A Brief Primer on Trans Fats
Yes, I struggled long and hard to find a way to make a clever title conflating trans fats with transgenderism, but failed. Probably for the best, as these posts are already getting me into the kind of trouble I fled Facebook to avoid.
Last week, I was interviewed by a couple of Carleton University journalism students about the epidemiology of trans fats as a health factor. I will stream that interview from this site when I get their permission. But I thought I would take a moment to describe to lay people why there is such a concern over trans fats in our foods.
What Are Trans Fats?
When we say “trans fats” what we mean are “trans fatty acids”, or TFAs. A fatty acid molecule is a chain of carbon atoms forming a spine, with hydrogen atoms sticking out like vetebra; an oxygen-hydrogen group is tagged at the end to make it officially an acid.
Saturated fatty acids have all their carbon bonds individually bonded to separate hydrogen atoms. Unsaturated fats have many of those carbon bonds as double bonds, where they bond to each other rather than to hydrogen atoms.
Saturated and unsaturated fats behave differently in the world. Animal fats (lard, tallow, etc) tend to be saturated. Vegetable fats (oils, etc) tend to be unsaturated. Saturated fats are solid at room temperature. Unsaturated fats are liquid at room temperature.
This means that if you want to make a flaky pie crust or something as delicious, you would typically use lard or butter to keep it together at room temperature. But it would go rancid in a couple of days, as bacteria want to feast on the delicious stuff. It’s a little harder to make a pie crust out of an oil.
So about 150 years ago, chemists figured out that if they bubbled hydrogen through unsaturated fats, you can force some of those double bonds to release, and to bind to the hydrogen atoms instead, essentially saturating those carbon atoms. We call that process hydogrenation.
If the new hydrogen atoms bond on the same side of the carbon chain, we say it’s a cis atom. Cis-fats tend to bend in the middle. If the new hydrogens bond on opposite sides of the carbon chain, we call it a trans fatty acid, which still remains straight and linear.
I’m not a chemist, but I think I got that part right. If not, I’m sure the chemists among you will let me know.
It turns out that this new trans fatty acid –TFA– has an important property of saturated fats: it’s solid at room temperature, as its melting point has risen. In addition, it doesn’t seem to have much of a taste to it, whereas lard, tallow and butter definitely taste lardy, tallow-y, and buttery.
Another intriguing property of TFAs is that bacteria don’t seem to be as attracted to them as they are to regular saturated fats. Foods made with TFAs don’t go rancid as quickly, and therefore have a much longer shelf life.
I Don’t Like To Read. Can You Summarize That?
So let’s add it all up:
(1) TFAs are cheaper than regular saturated fats because they can be made from inexpensive vegetable oil rather than expensive animal flesh;
(2) TFAs have less of a taste than do regular saturated fats, so they can be easily substituted into scores of foods without changing their flavours;
(3) TFAs grant foods a much extended shelf life.
The sum: of course industrial food producing companies would much prefer to use TFAs than regular saturated fats! They expand product lines and product lifespan, saving the companies millions upon millions of dollars!
So TFAs Are Artificial?
Trans fats do occur naturally. Animals that are part of our food chain –cows, pigs, sheep– seem to create minute amounts of TFAs naturally. Perhaps less than 1% of fat produced by an animal can be considered TFAs, I believe I’ve read somewhere. But the science remains unclear on whether such naturally occurring TFAs have the same properties as the ones industrially created.
So What Are The Health Risks?
Frankly, there is a mountain of good epidemiological evidence that eating TFAs is associated with a significant elevated risk of heart disease. Specifically, it seems that TFAs might cause an elevation in serum LDL (the “bad” cholesterol) and a decrease in serum HDL (the “good” cholesterol), via metabolic pathways upon which I am not qualified to either expound or describe.
As we all (should) know, high LDL and low HDL are a recipe for atherosclerosis, which in turn is how we get heart attacks and strokes.
Crisco, which originally was almost 100% TFAs, arrived on the market in 1911 . By 1996, up to 10% of recommended daily limit of fat consumed by Americans was made up of TFAs, from sources like Crisco and its heirs.
Where Is Your Evidence, Deonandan?
In 1990, a study in the New England Journal of Medicine showed the link between TFAs and serum cholesterol changes.
In 2004, Denmark became the first country to ban TFAs outright.. Three years later, the mortality rate from cardiovascular disease declined by an average of 14.2 deaths per 100,000 people per year, suggesting that the Danish ban saved two lives per day.
In 2006, another study in the NEJM suggested that for every 2% of calorie intake that comes from TFAs, one’s heart disease risk increases by 23%. That’s a lot.
In 2017, a JAMA study found that people living in areas that restrict trans fats in foods had fewer hospitalizations for heart attack and stroke compared to residents in areas without restrictions (a significant 6.2% difference).
Also in 2017, a Japanese study found a more direct connection between TFA consumption and cell death. So TFA’s bad effects are not just through its effects on cholesterol, but directly as a kind of poison.
So Why Has It Taken So Long For TFAs To Be Banned?
It may surprise you to learn….. Oh, who am I kidding? No one is surprised by this. In the 1980s, the food industry employed clever scientists to routinely attack, and thus effectively suppress, research showing a connection between TFA consumption and poor health.
Whaaaaa?
Surely science is immune from such efforts, no? The truth shall always come forth, no? Well, no. I myself was once offered the job of defending evil corporate interests who were being sued by people that those corporations’ products had harmed. I didn’t take the job, because if I had, how could I sleep at night?
The answer, as I tell all my students, is: “On a bed of money.” That’s how I would sleep at night.
Okay, how can one poke holes in TFA research? Simple. The gold standard for cause-and-effect research is the randomized controlled trial (RCT), which involves randomly assigning a product (e.g., a drug) to one group, and compelling another randomly selected group to be denied that product; control both groups’ environments to keep all factors equivalent; then assess their health states at some point later.
The major problem with using RCTs to assess causality for things like cigarettes and TFAs is that you have to compel some people to use them. I would have to randomly select 20-30 children and compel them to eat only TFAs for a couple of decades, while restricting their access to other factors that might cause heart disease (like, I don’t know, food), while doing the same to a control group.
It’s neither practical nor ethical.
Therefore, in absence of RCTs, we assess causality by using a suite of other tools, including both observational and ecological studies. The studies linked above are good examples of these. An observational study simply observes what people do naturally, i.e. interviewing a bunch of heart disease patients to determine their eating history, and computing an association between their disease state and how much TFA they probably consumed.
An ecological study is even looser. That’s when the unit of analysis is a population rather than an individual. When we look at population rates of hospitalization in regions with TFA bans versus those without TFA bans, that’s a loose kind of ecological study.
A keen asshole epidemiologist can easily argue that these are non-ideal forms of evidence. But a better epidemiologist will argue back that the sheer mountain of such evidence, its reproducible nature, its dose-response relationship, and the degree of statistical effect all combine to provide sufficient evidence to make policy change.
What’s Happening Globally?
The WHO has called for a global ban on TFAs. They argue that presently TFAs are responsible for 500,000 deaths annually. And, they say, if we ban it all, we can save more than 10 million lives by 2023.
But Why Is This Controversial?
The obvious first level pushback is that any ban on anything impinges on your Zod-given right to eat shit and to be an asshole. A more nuanced argument has to do with the practicality of a ban, and the uncertain history of previous food bans
An asshole
Some critics argue that while it’s true that TFAs increase the risk of heart disease and death, the amount of actual risk is small compared to other things we could and should be focusing on. This is especially true at the global level, where, one can argue, calorie production and access should be the focus, not calorie restriction.
In other words, TFA supporters argue, 500,000 deaths due to TFA consumption is small compared to the millions of deaths that could result if we reduce our ability to produce and store foods.
I would argue that this is a weak position. Most food insecurity is the result of economic and political access, and is not a function of the industry’s ability to produce or store product. Moreover, food wastage is indeed a big problem worldwide, having to do with poor shelf life and inefficient transportation methods. But the solution is not a “fake” food that can withstand transportation, but rather a more rational supply chain that allows for greater reliance on local produce.
What do you think? Leave your comments below.
