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
“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.
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
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
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
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.
What Could Be Causing LDL Elevations On Keto? Weight Loss
I asked Dr. Cate Shanahan for
her input on this topic, and she provided a beautiful
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.”
Low Thyroid Function
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
post for maintaining thyroid function on keto, and check out
Elle Russ’ Paleo
Thyroid Solution for an even deeper, more thorough dive into
Eating Too Damn Much
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).
Too Much Butter
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.
So, What Can You Do If You See An Increase in LDL? Start Chugging
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
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
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.
Stop Being a Keto Caricature.
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
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 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.
Balance Your Fats
The overzealous and protracted drive to demonize all sources of
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
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
African kudu (antelope family): 35% SFA, 24% MUFA, 39%
African impala (antelope family): 51% SFA, 15% MUFA, 33%
- Elk: roughly 40% SFA, 30% MUFA, 30% PUFA
- Moose: roughly 33% SFA, 33% MUFA, 33% PUFA
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):
Focus on monounsaturated fats and fat from meat, rather
than isolated sources of saturated fat like butter and coconut
oil. You probably don’t have to eliminate those fats.
Just don’t make them the centerpiece of your diet.
Eat more avocados, avocado oil, olives, olive oil, and
mac nuts for monounsaturated fat. Salads are a great
nutrient-dense way to incorporate high-MUFA foods.
Eat more fish. A couple portions of farmed
Atlantic salmon were enough to
improve LDL-P in overweight men and women. And compared to plain
keto, keto +
omega-3s from fish has a superior effect on inflammation and
Eat more kudu and impala (if you can get it).
Sort of kidding. But really, eat them if you can.
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.
Are Traditional Lipid Markers Even Relevant for Keto Dieters?
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
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
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
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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