We’ve all heard the story. Maybe we’ve even been the protagonist.
Person goes full keto. They lose a bunch of weight, normalize their pre-diabetic glucose numbers, resolve their high blood pressure readings, have more energy, feel great, and have nothing but high praise for the new way of eating.
Except for one thing, everything seems perfect: their cholesterol is sky-high. It throws a wrench into the whole operation, installs a raincloud over the procession, spoils their confidence.
“Could I be killing myself?”
“Are my health improvements just a mirage?”
In other words, are the apparent benefits of keto merely superficial if your cholesterol skyrockets?
The evidence is pretty clear that for the majority of adults who go keto, their cholesterol numbers improve.
In obese adults with type 2 diabetes, a ketogenic diet improved blood lipids and boosted fat loss compared to a low-calorie diet.
In lean, healthy adults without any weight to lose (and who didn’t lose any weight during the course of the diet), total cholesterol went up from 159 to 208 mg/dL and triglycerides fell from 107 to 79 mg/dL. A lipophobic doc might freak out at the rise in TC, but given that the triglycerides dropped, I bet the change reflects a rise in HDL and an overall positive, at worst-neutral effect.
Another study of lean adults with normal cholesterol numbers found that going keto improved their lipids, reducing triglycerides, increasing HDL, and leaving LDL unchanged. Those with small pattern B LDL particles (the “bad kind”) saw their LDL particle size increase, on average. All told, keto was beneficial.
But you aren’t everyone. You aren’t the average of a population. And, given the number of readers I have and the number of people trying a ketogenic diet, there are bound to be some people whose lipid profiles go in the other direction.
I don’t give medical advice here, and I always encourage people to partner with the physicians for health solutions. That said, let me share some thoughts on the keto-cholesterol question….
I’m not just talking about high total cholesterol or high LDL-C. I’m talking about what appears to be the real, legit risk factor for a cardiac event: elevated LDL particle number. According to experts like Dr. Peter Attia and Dr. Chris Masterjohn, atherosclerosis occurs when LDL particles infiltrate the endothelial lining of our arteries. Thus, it’s not high LDL cholesterol that increases the risk of atherosclerosis—LDL-C is the cholesterol found inside the particles— it’s a high number of LDL particles in circulation. The more LDL-P, the greater the chance of them becoming oxidized and infiltrating the arterial wall. There are many factors to consider, like oxidative stress, inflammation, and fatty acid composition of the LDL particles, but all else being equal, a greater number of LDL particles seems to increase the risk of a heart attack.
I asked Dr. Cate Shanahan for her input on this topic, and she provided a beautiful explanation:
But when you stop eating so many carbs insulin politely steps aside, and your insulin levels plummet. Now your body fat can more easily and more often release its stores of fatty acids into your bloodstream.When your body fat releases stored fatty acids, any unused fatty acids quickly get picked up by the liver and packed into VLDL lipoprotein. VLDL is a precursor to LDL. So in reducing your insulin levels and increasing your body’s use of fat, you will raise your VLDL, LDL and total cholesterol. You are simply trafficking in fat more often now. And now, because your body stabilizes fat carrying lipoproteins with cholesterol, there is a need for more cholesterol in your blood. These are not bad consequences. They are in fact happy signs your diet is doing what its supposed to be doing.
If you’re actively losing weight, you will probably experience a rise in cholesterol. This is the transient hypercholesterolemia of major weight loss, and it’s a well-known phenomenon. Once your weight stabilizes, cholesterol should normalize—although to a lesser extent than other diets, given Dr. Cate Shanahan’s explanation of increased “trafficking in fat.”
The thyroid is a barometer for your energy status. If you have plentiful energy to spare, thyroid function is normal. If your body perceives low energy availability, thyroid function may down-regulate. Since the thyroid plays a big role in regulation of LDL receptor activity, its downregulation can lower LDL receptor sites. Fewer LDL-receptors clear LDL particles from the blood. Folks with genetic predispositions to heart disease often have low LDL receptor activity, causing elevated LDL particles. Folks with genetic variants that increase the activity and expression of LDL receptors have lower heart disease rates. Although genes often have different effects that may affect disease risk via other pathways, that’s pretty strong evidence that LDL receptor activity regulates, at least in part, one’s LDL-P and heart disease risk.
Read this post for maintaining thyroid function on keto, and check out Elle Russ’ Paleo Thyroid Solution for an even deeper, more thorough dive into thyroid health.
Some keto people pride themselves on gorging. Some are doing it for a good cause—a quest to find the fabled metabolic advantage. Some are doing it to show off and for keto cred—look how much salami I can eat! Some are using keto to deal with unresolved issues with food itself.
Everything I say about doing keto presupposes that you are eating like a normal person. You’re eating as much as you need to fuel your brain and daily activities, fitness and performance goals. You’re leaving the table satiated, not stuffed. For most people, this happens without even trying. It’s why keto is so effective for weight loss.
Genes aren’t destiny, but they do modify and regulate our response to a given environmental input.
Some people are dietary cholesterol hyper responders. Unlike the majority of the population, they absorb tons of dietary cholesterol and do not down-regulate their endogenous production to accommodate. The result is an increase in cholesterol synthesis and absorption, leading to a spike in blood cholesterol.
Some people are sensitive to saturated fat. In response to it, they produce elevated numbers of LDL particles. If your keto diet is high in saturated fat and you have a genetic sensitivity to it, your cholesterol will probably skyrocket.
Some people have genes that reduce the activity of their LDL receptors. This will necessarily boost LDL particle numbers.
This topic—genetic variance and how it affects keto—could be an entirely separate post, so I’ll leave it at that (and probably come back to it in the future).
Huh? Too much butter, Sisson? Is such a thing even possible?
Maybe. Subjecting cream to the butter-making process strips it of something called milk fat globule membrane (MFGM). And when you compare equal amounts of dairy fat through either cream (with MFGM intact) or butter oil (with MFGM absent), you get very different metabolic effects. Those who ate 40 grams of dairy fat through butter oil saw their lipids worsen, including ApoB, a surrogate for LDL particle number. Those who ate 40 grams of dairy fat through cream saw their lipids unchanged, and in the case of ApoB even improve. That’s 4 tablespoons of butter compared to 4 ounces, or a half cup, of heavy cream.
Caveats apply here. The subjects weren’t eating a low-carb or ketogenic diet; they just added the butter or cream on top of their normal diet. But in keto people who are genetically susceptible, huge amounts of butter may be responsible for rising LDL-P.
I still love butter. It doesn’t affect my lipids like that. But your mileage may vary, and it’s something to think about if you’re in that situation.
Kidding… It’s true that swapping out some of your animal fats for polyunsaturated seed oils will almost certainly lower your cholesterol levels. It does this by increasing LDL receptor activity, but, being far more unstable than other fats, omega-6 PUFAs also increase the tendency of the LDL particles to oxidize. And since oxidized LDL are the ones that end up wedging in the arterial walls and causing issues, loading up on PUFAs might not be the right path.
You know what just occurred to me? This is an aside, but maybe linoleic acid (the primary fatty acid in seed oils) up-regulates LDL-R activity because the body recognizes the inherent instability of linoleic acid-enriched LDL particles and wants to clear them out before they can cause trouble. I hope some researchers take this idea further.
Half a package of cream cheese for a snack.
Dipping an entire stick of pepperoni into homemade alfredo sauce and calling it dinner.
I’m not saying cream cheese is bad. It’s great. Nor am I suggesting you never eat pepperoni, dipped in alfredo sauce or not. But the amounts are unreasonable. And turning those into regular meals is a bad idea. There’s no reason you can’t go keto while eating a hamburger patty or ribeye over a Big Ass Salad. Far more nutrients, far more micronutrients, and it tastes way better.
Maybe if you’re a nomadic horselord sweeping across Europe in the early Bronze Age, you need to eat an entire lamb intestine stuffed with marrow and organs, and you should wash it down with a quart of creamy mare milk. Such a meal would provide the calories you need to see your enemies driven before you and go great with the lamentations of their women. But you’re not a Yamnaya nomad. You’re you.
You probably don’t need that much food, that many calories, and that much fat—since there’s plenty of it on your body already, waiting to be liberated and converted into energy. Therein lies the beauty of keto. That’s what this is all about: Getting better at burning your own body fat.
The overzealous and protracted drive to demonize all sources of saturated fat as evil has led to a vociferous backlash from the other direction. But just because the supposed experts got the saturated fat issue wrong doesn’t mean the opposite is true: That all the fat we eat should be as saturated as possible.
For one thing, eating nothing but saturated fat is very hard to do using whole foods. Very few animals exist in the world, past or present, with only saturated fat. The only exception I can recall is the coconut, a curious sort of beast that spends most of its time hanging from a tree impersonating a large hairy drupe. Your average slab of beef fat runs about 50% saturated fat, 45% monounsaturated fat, and 5% PUFA. That differs from cut to cut and depending on the diet of the animal, but not by much. It’s similar for other ruminants like bison and lamb. And the most prominent saturated fatty acid in ruminant fat is stearic acid, a fat that converts to monounsaturated oleic acid in the body and has an effect on cholesterol indistinguishable from MUFA or PUFA.
Or take the fatty acid composition of game meat—the type humans encountered and consumed for our entire history.
I could go on, but you get the idea: Humans have been consuming a wide range of fatty acids for millennia. It probably makes sense to emulate that intake.
Once again, the folks whose cholesterol goes nuts on keto are outnumbered by those whose cholesterol improves. But if you’re one of the unlucky ones in the former category, try broadening your fatty acid intake (to, ahem, possibly include more nuts):
They even have a version of keto called the Spanish ketogenic diet, which features a lot of extra virgin olive oil, olives, fish, and red wine. It works great and might be a good alternative for people whose cholesterol goes wild on saturated fat-heavy keto.
Maybe, maybe not.
But be honest about it. You can’t oscillate between championing positive changes to blood lipids on a keto diet and pooh-poohing negative changes to blood lipids on a keto diet.
You can’t use positive changes to prove the efficacy and safety of the ketogenic diet, then turn around and claim that negative changes don’t count because keto dieters are understudied. What if those “positive” changes are actually negative in the context of a ketogenic metabolism? After all, keto dieters are largely understudied in both directions. If what’s unhealthy in a normal dieter might be healthy in a keto dieter, what’s healthy in a normal dieter may be unhealthy in a keto dieter.
I write these things as a strong proponent of spending a significant time in ketosis. As someone who frequently hangs out in a ketogenic state. As someone who wrote a book about keto and is writing another. But also as someone who insists on maintaining strict intellectual honesty and integrity.
We simply don’t know what very high cholesterol numbers mean in the subset of ketogenic dieters who experience them. I strongly suggest not being too flippant about them.
True: There aren’t any perfect studies examining the utility of conventional cardiovascular risk factors in people eating the type of keto diets you see in the ancestral health space. Maybe your elevated LDL particle number doesn’t mean what it means in the average overweight adult eating the Standard American Diet. Maybe your inflammation is low enough that the risk of atherosclerosis and oxidative modification of LDL is low. But I wouldn’t take that risk, not until we have more data.
What do you think, folks? How did keto affect your blood lipids? Did you make any changes, and if so, did they work? Thanks for stopping in today.
Note: This information isn’t intended as and shouldn’t be considered medical advice. Always consult your doctor in the management or treatment of any health issue.
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