What if Everything You Thought You Knew Was Wrong?
Our industry is famous for blurring the line between fact and opinion, and debating the details of things that simply aren’t yet clear.
Take the spinal flexion debate, for example. Lead researcher in spine biomechanics, Dr. Stuart McGill, showed that repetitive bending of the spine can cause damage to discs. As a result, many of us (including myself) have since eliminated crunches and other abdominal flexion exercises from our programs.
But Bret Contreras and Brad Schoenfeld recently published this great article in the Journal of Strength and Conditioning that calls a few things into question. For example, they make the point that much of Dr. McGill’s research on spinal flexion was done using model pig spines, and therefore limited by the removal of musculature and supporting tissues. And as is consistent with Wolff’s Law, when stress is applied to a living tissue (provided it doesn’t exceed its physiological capacity and is allowed time to recover), the tissue remodels and grows stronger – suggesting that a live human spine may be more resilient to repeated bending cycles than that of a dead pig.
In addition, a living human creates intra-abdominal pressure to support the spine during movement, something a stack of pig bones just can’t do.
They also point out that McGill’s research on human workers used continuous cycles of loading (rather than the intermittent ones used during training, where periods of rest are allowed and remodeling can take place) and far more of them than would ever be performed in one session at the gym; that individual genetics and structure play a role as well; and that spinal movement is needed to drive nutrients into the discs – all good points, some of which I’ve discussed here before.
Even Stuart McGill will tell you that every back is different and ANY repetitive load on the spine is harmful, including those resulting from static postures (i.e., staying in one position for too long). Therefore, it may just be that some spinal movement (including flexion) is beneficial, and too much is harmful (not a hard thing to believe). Problem is, we really have no way of knowing just how much is too much.
The saturated fat debate is another example, and one that I’ve recently been discussing with a colleague. We’ve thought for years that saturated fat was a primary contributor to heart disease – mainly because it’s made of triglycerides, and it’s pretty clear that high triglycerides are a risk factor for CVD. But many now refute the claim that eating saturated fat can lead to heart disease and instead point to refined sugar as the culprit. The most common argument I hear usually comes from advocates of a Paleolithic-style of eating. It goes something like this:
1. Our ancestors ate a lot of saturated animal fats and didn’t have the high rates of heart disease we see today; and
2. They didn’t eat a lot of refined sugar; so therefore,
3. Sugar (not saturated fat) causes heart disease.
As examples to support this argument, they usually either allude to African tribes (who hunt and kill their own meat) or Eskimos (who eat mostly animals, including a buttload of heart-healthy fatty fish like salmon).
But this logic seems somewhat flawed to me. First, we need to stop using the terms “saturated fat” and “animal fat” interchangeably; they aren’t the same thing. A saturated fat is simply a fatty acid with no double bonds between its carbons; it is “saturated” with hydrogen atoms. An animal fat is a fat from an animal. All fats contain a proportion of saturated and unsaturated fatty acids; and while animal fats do contain a higher percentage of saturated fatty acids, they are not one in the same.
And herein lies the problem: Our ancestors hunted and killed wild animals; they didn’t raise them in factories or buy them at the grocery store. The animals ate grass (not processed corn feed, i.e., GMO refined sugar), moved around more (i.e., exercised), spent their days outside (synthesizing more vitamin D) and weren’t pumped full of hormones and antibiotics. As a result, their fatty acid profiles were better. Today’s conventional animal (the kind most of the research involves) is a different beast. The animals our ancestors ate contained less saturated fat and more essential Omega-3 unsaturated fatty acids, more like today’s organic animals.
READ: LESS saturated fat, MORE Omega-3 unsaturated fats – which we already know are cardioprotective. This doesn’t disprove that saturated fats don’t contribute to heart disease. If anything, it shows that replacing saturated fat with Omega-3s can reduce the risk of heart disease – which is already a recommendation – and that eating vegetables (not grains), exercising and increasing vitamin D levels can improve the health of animal species (of which humans are one).
Does that mean the Paleo lovers are wrong in that we should eat organic animals? Of course not. We absolutely should, for all the reasons just described. It simply means we can’t disprove that saturated fat can contribute to heart disease using this line of reasoning. We can justifiably argue that most of the studies suggesting a link between saturated fat and heart disease don’t control for other important factors like food quality, dietary sugar consumption, caloric intake and/or adiposity, but that still doesn’t disprove a correlation between saturated fat consumption and heart disease. The most it does is justify the healthy level of skepticism currently circulating.
Now, let’s look at the sugar argument. Excess sugar intake leads to high insulin levels and a subsequent tendency for this sugar to be stored in the body as fat (i.e., triglycerides); and as we said, high triglycerides are a risk factor for CVD (this is the link between diabetes and heart disease).
Well, we do see elevated triglyceride levels drop when people decrease their intake of refined sugar; can’t argue with that. But does that mean sugar is the culprit? Not exactly… We also see a drop in triglyceride levels when we lose weight, regardless of how we do it. Links, associations, if you will, have been shown between sugar intake and heart disease AND between saturated fat intake and heart disease. There is an even bigger link between overweight and heart disease.
When we replace saturated fat with monounsaturated, polyunsaturated and Omega-3 essential fats, lipid profiles improve and heart disease risk factors decrease. Does that mean saturated fat is the cause of heart disease? No. It could just mean those other fats are cardioprotective – which we’ve already said. When we replace saturated fat with carbohydrates, however, we don’t see drastic improvements in cardiovascular health. Does that mean carbohydrates are the cause of heart disease? No. It could just mean those other fats are cardioprotective! But we do see a correlation between high triglycerides and high intakes of refined sugar, so carbohydrates are likely a strong contributor.
But is there any reason to think both sugar and saturated fat can’t BOTH be problematic? Could TOO MUCH saturated fat lead to heart disease? Yep. Could TOO MUCH sugar? Sure. Unless they’re burned for energy, they both get stored in the body as triglycerides (a major difference being that we do need some saturated fats for nervous system health whereas we don’t need refined sugars), so it’s hard to argue that either of them can’t contribute to heart disease – either directly or indirectly. The “too much” is the bigger problem here.
Adiposity is a CVD risk factor in and of itself, and likely contributes much more to heart disease than either saturated fat or refined sugar. Excess fat changes our physiology (which is highly individual to begin with), and this is probably why we see controversy in the literature. It also causes inflammation, which we now know is at the root of atherosclerosis and a host of other diseases. We can argue within that as much as we want, but it shouldn’t change the primary recommendation: To lower CVD risk, we first need to stop being so fat!
Some do argue that the problem is refined sugar and saturated fat in combination, and that’s all fine and well. Heck, it’s probably even true (at least to some extent). But it isn’t going to help the general population if they overconsume either sugar or saturated fat, don’t exercise and wind up overweight. They’re still at risk for heart disease.
BOTTOM LINE: In the grand scheme of things, the fields of nutrition and exercise are still relatively new and the research is still relatively lacking. There are a lot of nitty gritty details about health that we still don’t “know.” Do I think they’re important? Of course. Moreover, they’re fun to debate for those of us interested. But do I think they’re that important to focus on given the current and desperate state of our nation? Probably not.
We can’t neglect what actual experience tells us. There are plenty of people walking around who have done crunches forever and will never have a low back problem (and an equal number who will), and just as many who will abstain and still have low back pain. Likewise, there are people who can decrease their saturated fat intake, lose weight and improve heart health; the same can be said for those who reduce sugar. There are a lot of other factors to consider and we just don’t know exactly how they all interact. But if we stop for a second and focus on what we do know, the “big picture,” if you will, we can still make some sound recommendations to help people improve their health. Not loading the spine TOO MUCH in any manner, not eating TOO MUCH saturated fat OR refined sugar OR food in general, and not carrying TOO MUCH bodyfat are good places to start – and probably all we should reasonably expect the general population to understand and apply.
What constitutes “too much?” The verdict is still out…
Filed under: exercise research, fat loss, fitness commentary, health, nutrition
