This is the second installment in a short-ish series looking at roadblocks to fat loss, even when it seems like you’re doing “all the right things.” If you missed part 1, you can check it out here, and here’s a link to a post about the complexity of weight loss in general.
Since we covered some of the “duh” stuff last time—the stuff that most of you are already aware of and were probably angry with me for even writing—this time, let’s get into some issues that might resonate with more of you, and, perhaps most importantly, provide you with information you can apply immediately if they do resonate.
In the series I wrote about insulin (which general consensus says totally kicked butt, by the way), I frequently used the word lipolysis. I explained that that’s just a fancy way to say “breaking down fat.” (“Lipo” for fat, and “lysis,” for splitting apart.) I further explained that lipolysis is the splitting of a triglyceride into its component pieces: a glycerol molecule and three fatty acids. The reason lipolysis is such an important process is that it is the method by which body fat is released from adipose tissue (fat cells), in order to travel through the blood to arrive at a destination where it can be burned for energy, such as in muscle cells. (10-second refresher: triglycerides are too large to pass through the cell membrane. In order for them to get out of the fat cell—which is what we want and need to happen in order to burn that fat—they have to be broken down into smaller pieces.)
As we also covered in the insulin posts, insulin gets in the way of lipolysis. (Scientifically speaking, insulin inhibits the enzyme hormone-sensitive lipase, which is what starts the lipolysis ball rolling.) This is one of the mechanisms by which low-carb diets work: keep insulin levels low, and lipolysis is free to proceed. Keep insulin levels high, and that fat ain’t goin’ nowhere, no-how.
But here’s the thing. And pay attention, because this is a very big thing:
Lipolysis is not the same thing
as burning fat
The breaking down of triglycerides so that they can be released from adipose cells is not the same thing as burning (oxidizing) fatty acids. Think of it this way: Lipolysis is like cutting a gigantic fallen tree into less-gigantic logs that you can transport to your backyard to chop up for firewood. The process called beta-oxidation is like taking those still-somewhat-large logs, chopping them into small logs, and stacking them by the fireplace. Burning fat is when you take one of those small logs, put it in the fireplace, and set fire to it. So you can see that lipolysis is great, but it’s only the beginning of the fat burning process.
You may have heard somewhere along the way that mitochondria are our cells’ fuel burning factories. Mitochondria are sometimes referred to as the cellular “energy generators,” because they take the end products of glycolysis (the first step in the breakdown of carbohydrate) and beta-oxidation (breaking down fat), and they convert these into ATP, which is the “universal energy currency of the cell.”
In case anyone is having scary flashbacks to high school or college biochemistry, let’s stop here and take a breath. Don’t be overwhelmed. All I’m saying is, the mitochondria are where the majority of food “calories” are actually turned into energy. (Way back in this post I explained that the human body does not run on “calories.” The only thing the body can use to “get stuff done” is ATP.)
At this point, we are interested in two things that take place inside the mitochondria. The first is beta-oxidation, and the second is the Krebs cycle. (I explained more than you would ever want to know about mitochondrial structure and the Krebs cycle back in this post from the cancer series.) As I mentioned a minute ago, beta-oxidation is taking one long-ish fatty acid and breaking it up into smaller pieces. (Chopping the logs into small firewood.) The Krebs cycle is the fireplace, with a rip-roaring fire burning inside it. (Putting the firewood into the fireplace and burning it.) The reason we are interested in these two things is because if they aren’t humming along effectively, you will have a hard time losing body fat. So, the question we should be asking ourselves now is, what are some things that might compromise beta-oxidation and the Krebs cycle?
The first one that jumps to mind is…
Mitochondria aren’t magicians. They don’t oxidize fats and produce ATP out of thin air. They need lots of helper molecules to do what they do. Specifically, they need vitamins B2 (riboflavin), B3 (niacin), and B5 (pantothenic acid), iron, carnitine, manganese, and coenzyme Q10. They probably need a whole lot more than that; those are just the ones I know of off the top of my head. (If you want me to open my biochem textbook, the least you could do is buy me dinner first! ;D)
I won’t bore you with the details on where and why each of these nutrients is required. I could definitely geek out on all that, but for our purposes here, it’s enough just to know you need ‘em. I will point out one thing, though: if you are on a statin drug, you most definitely should also be taking a CoQ10 supplement. (Refer to this post about mitochondrial dysfunction for details, and check out this post to see just how awful statins are, in general.)
…Aaaaand, because I can’t help myself, I’ve just decided that I will go ahead and explain the whys and wherefores of these nutrients, as they relate to burning fat—and, ultimately, losing weight. ‘Cuz, really, you can’t lose weight without burning fat at the cellular level. (Screw the treadmill; it’s far more important what’s going on in your mitochondria.) If you don
’t care about what these nutrients actually do inside us, you can stop reading here. You’re good to go, and the rest will only bore you. If, on the other hand, you want to know the whys and hows, here goes:
Carnitine is an interesting one. If you speak any Spanish, this might remind you of the word carne. Indeed, red meat is the richest source. (Lamb and beef, specifically. As if you needed more good reasons to eat those!) Carnitine is not technically an “essential nutrient,” because we can make it from the amino acids methionine and lysine, but it’s still possible to have an insufficiency. The big deal with carnitine is that it is a required cofactor for the enzymes that transport fatty acids into the mitochondria. If mitochondria are like exclusive nightclubs that everyone is trying to get into, think of carnitine as the guy who knows the bouncers. If you’re attached to carnitine, you can go to the front of the line and get inside. No carnitine, no entry. (In fact, ketogenic diets are contraindicated for individuals with inborn errors of carnitine metabolism; that's how crucial carnitine is for burning fat.)
Moving on, let’s see about pantothenic acid (B5). B5 is the main building block for a molecule called coenzyme A (usually shortened to CoA). Coenzyme A is crucial for the production of ATP from all fuel sources—glucose, fatty acids, ketones, etc. After lots and lots of intracellular wheeling & dealing, all three of these fuel sources eventually end up as something called acetyl-CoA, which is one of the substances that makes ATP production possible. (“That’s when you fell and hit your head and had the vision for the flux capacitor, which is what…makes…time travel…possible.” :D Hopefully my overseas readers have seen this movie and don’t think I’ve completely lost my mind!) Specifically, acetyl-CoA can catch a ride through the Krebs cycle. But even before we get to acetyl-CoA, the process of beta-oxidation also requires coenzyme A. So we need CoA to break the long fatty acid chains into smaller fatty acid chains. In general, just about all cellular energy production requires coenzyme A. (In the mitochondria, anyway. CoA is not required for glycolysis, which is the converting of glucose to pyruvate, with a net yield of 2 measly ATP.)
And how about B2 and B3? Riboflavin and niacin are other essential helper molecules required for the continued flow of the Krebs cycle and electron transport chain. So you can see why insufficiencies in some of these nutrients will result in fatigue--and difficulty losing weight. If you have sub-par levels of these nutrients, then you literally cannot produce energy effectively--that is, you cannot "burn fat." Your ability to generate ATP from pretty much any type of fuel is compromised. This is why nutritional strategies for tackling chronic fatigue, fibromyalgia, and adrenal exhaustion typically include high doses of B-vitamins—B5, in particular, but usually all B-vitamins.
Yet another nutrient important for energy generation is magnesium. As illustrated in a past post about glycolysis, magnesium is essential for converting glucose into pyruvate, and the subsequent conversion of pyruvate into acetyl-CoA is an important step that eventually helps keeps the Krebs cycle humming along nicely. (This might be what’s behind a phrase you may have heard – “fat burns in the flame of carbohydrate” – but it’s pretty oversimplified.) As you can see in this diagram of glycolysis, no less than six molecules of magnesium (circled in blue) are needed to turn just one molecule of glucose into a net of 2 measly ATP. It’s not surprising that many diabetics and individuals with metabolic syndrome are magnesium-deficient. (Frankly, most people are probably low on Mg.)
Antioxidant Nutrient Deficiencies
Another key nutrient for healthy mitochondrial function—and ATP production, in particular—is iron. (For details, check out this post about mitochondrial dysfunction.) Iron’s role in mitochondrial function is two-fold: First, it’s an essential part of the cytochrome proteins that are part of the electron transport chain. Second, iron is a cofactor for catalase, which is an enzyme that converts hydrogen peroxide into water and oxygen. Hydrogen peroxide is great for whitening your teeth, but it's not something you want a lot of to accumulate inside your cells. Where does hydrogen peroxide come from inside your cells? It comes from the action of the enzyme superoxide dismutase (SOD). Inside the mitochondria, SOD takes highly damaging superoxide radicals (one type of “free radical”) and converts them into hydrogen peroxide. Superoxide radicals are a normal byproduct of the electron transport system. Sometimes, oxygen radicals just kind of “leak out,” and SOD is there to contain the situation before it gets out of hand. Hydrogen peroxide is still damaging in itself, but it’s not quite as bad as superoxide. So SOD and catalase work hand-in-hand: SOD turns oxygen radicals into hydrogen peroxide, and catalase turns hydrogen peroxide into oxygen and water. The nutrient cofactor required for mitochondrial SOD is manganese. While manganese and iron are not directly involved in lipolysis or beta oxidation, iron is required for the electron transport chain, and both nutrients are needed for healthy mitochondria. If your mitochondria are highly damaged from free radical assault, there’s a good chance your fat-burning capability will not be optimal. (As an aside, manganese is the cofactor for mitochondrial SOD. The SOD found in the cytoplasm uses copper & zinc.)
Pretty neat, huh? We all know we “need” vitamins and minerals, but most of us have no idea what they actually do for us. We just eat good food, pop a few pills, and hope for the best. Having even a rudimentary understanding of these cellular processes helps us appreciate the roles of various nutrients, and might guide us on our paths to fat loss.
Now, it’s not just overt deficiencies or subclinical insufficiencies that can stand in the way of fat loss. It’s possible to have imbalances that compromise optimal cellular function. As just one example, copper excess inhibits catalase activity. (Probably because copper and iron [and zinc] have a delicate interrelationship, and tipping the scales too far in one direction can upset the balance of the others.)
If you are especially concerned about your nutrient status, check with your healthcare practitioner about doing some assessments. I don’t have a lot of experience in this area, myself (virtually none, actually), but I’m told a hair tissue mineral analysis can be quite revealing.
Poor Digestive Function
It would be nice if eating a healthy diet were enough to keep mitochondrial fat-burning going strong. In fact, if you’re following a Paleo, Primal, or LCHF strategy, then you’re probably already consuming lots of nutrient-dense foods. The purists among you might even go out of your way to eat exclusively grass-fed meats, free-range eggs, organic produce, etc. (You wouldn’t even think about doing “80/20.” You’re more like 110/-10.) But what if you’re not absorbing the nutrients these foods contain? Remember: we are not what we eat, but rather, what we digest and absorb. If your digestive function is compromised, then you will not necessarily be getting the nutrients you think you are. Just because you’ve put something down your piehole doesn’t mean the vitamins, minerals, amino acids, and fatty acids will make their way to where they need to go.
I won’t bore you with the specifics here. If you’re interested in learning about healthy digestion, I wrote a very detailed—and funny, if I do say so myself—series on digestion a while back. It’s a whirlwind tour of the digestive process and the GI tract, starting in the brain and ending at the
bunghole anus. It starts here: Digestion for (not-so) Dummies.
How can you tell if your digestion isn’t up to snuff? *Shrug.* There are lots of signs to tip you off: heartburn/acid reflux, bloating, gas, diarrhea, poor hair and nail growth, greasy stools (and/or oily slicks in the toilet bowl…ick), very dry skin, achy joints—almost like machine parts that need oiling. (You can see where I’m going with those last three – poor absorption of dietary fats.)
If you are on prescription or over-the-counter antacids, or have had your gallbladder removed, there’s a good chance your digestive function isn’t as effective as it could/should be. I can’t give personalized recommendations on this blog, so work with your healthcare professional to see if you might benefit from supplemental HCl (hydrochloric acid/stomach acid), bile salts, pancreatic enzymes, etc.
You can download some tips for supporting healthy digestion here: Digestive function.
Now that we’ve come to the end of this post, those of you who know about the role of the thyroid in regulating metabolic rate are probably thinking, “Amy, jeez…how can you possibly talk about nutrient deficiencies that affect fat loss and not mention iodine, selenium, and vitamin A? Don’t you know anything?” Yes. Yes, I do. I know enough to know that when we’re talking about stubborn fat loss, thyroid function warrants its own post. (Two or three posts, actually.) So that’s where we’ll go next time. All of you out there -- and I know there are many of you -- who are on thyroid meds, and have been for years, but still feel like crap-ola and are no slimmer than when you started, stay tuned.
Remember: Amy Berger, M.S., NTP, is not a physician and Tuit Nutrition, LLC, is not a medical practice. The information contained on this site is not intended to diagnose, treat, cure, or prevent any medical condition.