Cholesterol

and Keto
What you
need to
know
One would be hard
pressed to find a more
controversial topic in health and
medicine than cholesterol. This
should be surprising given that
there have been tens of billions of
dollars spent on researching
cholesterol and its effects on
health. Yet we still have more
questions than answers. This
article is largely in response to
thousands of questions from
confused people buried under
hoards of information.
Some health experts think we
should have cholesterol as low as
possible. Some have suggested
even children should be
considered for cholesterol
lowering statin drugs. Prescribing
statins to kids might be a boon for
pharmaceutical companies—as
you’ll see it’s entirely unclear
whether statins actually help and
might actually hurt the people
they’re supposed to benefit.
Conversely, seemingly credible
health experts dismiss the whole
notion of cholesterol as irrelevant.
This cocksureness may be ok for
their individual lives but for the
many people who are
understandably confused about
cholesterol and its role in health
and disease, these polar extremes
can be both frustrating and scary.
I’ll do my best to unpack the topic
of cholesterol but I’ll tell you
upfront that much of this story
depends on some fairly unique,
individual factors. To better
understand, let’s look at what
cholesterol is, what it does, and
explore the relationship between
cholesterol and cardiovascular
disease.
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What is
Cholesterol?
Cholesterol is a waxy substance primarily
found in animal based products such as
meat, dairy, and seafood, although there are
similar compounds produced by both plants
and fungi. Cholesterol is an integral part of
every cell in your body. Without it life
would grind to a halt pretty quickly.
As I’m sure you’re aware, your circulatory
system is filled mainly with water (good ol’
dihydrogen monoxide) but interestingly, for
our life process to work we need to move a
dizzying number of substances around the
body via our circulation. Some things
dissolve easily in water (sodium chloride for
example
example, better known as table salt), while
some substances do not mix well in water at
all. This is the case with cholesterol. It’s
waxy nature allows it to dissolve well in
olive oil or gasoline, but not that great in
water or blood.
What’s a living organism to do? It wraps
cholesterol in a neat little package called a
“lipoprotein.” The proteins carry the
cholesterol inside of the lipoprotein,
keeping it away from the water portion of
our blood. However, the proteins eventually
dissolve due to the chemistry of the protein
in contact with the water.
© Robbwolf.com All Rights Reserved. 3
What is Cholesterol?

This may sound like a lot of academic geek-
speak and most cholesterol research has
largely ignored this, but knowing the
lipoprotein molecule moves cholesterol
(and other substances) around the body is
arguably the most important element of the
story as it is likely not cholesterol, but rather
the lipoprotein carrier that may be the
largest factor in the atherogenic process.
You’re most likely familiar with terms like
“HDL” and “LDL.” Although researchers
and medical practitioners have focused on
the cholesterol fraction of these substances,
they’ve ignored the lipoproteins. A good
analogy here is that lipoproteins are like
cars, busses, and motorcycles (different
sizes and functions) and cholesterol is the
passenger on these vehicles.

Cholesterol

Lipoproteins

When you get routine blood work, you’ll

likely be tested for things like HDL, LDL,
Small LDL particles
triglycerides, glucose, etc. For the vast
majority of tests, what is reported is the
cholesterol (passengers) and not the
lipoproteins (vehicles).
This is a particularly important point to
consider as two people may have the
same cholesterol levels but remarkably LDL-C=120mg/dl
different lipoprotein counts.
Take the graphics on the right, where we
have two people (represented here as Large LDL particles
bridges) with the same cholesterol levels
(120mg/dl respectively). The person on
the top has relatively few, larger
lipoproteins while the person on the
bottom has a much higher lipoprotein
count. However, both have the same
relative cholesterol levels. If “we” (our
doctor) only look at cholesterol levels, we
may miss a huge part of this story, which LDL-C=120mg/dl
can have dire consequences.

© Robbwolf.com All Rights Reserved. 4

What is Cholesterol?
Some people have what appears to be
normal, low cholesterol, yet they have quite
high
Road A. Discordance scenario A: low cholesterol, high lipoprotein
Arguably, these people may be ticking CVD
time bombs since their doctor is only
looking at cholesterol and not considering
lipoproteins in the least. At our clinic we
frequently see this type of person frequently
in police, military, and re personnel. We
suspect this type of discordance is driven in
large part by insulin resistance borne or bad
sleep and high stress.
Road B. Discordance scenario B: high cholesterol, low lipoprotein
Both of these situations are classified as a
type of “discordance.” But the first case of
low/normal chol+high lipoproteins MAY
explain why nearly half of the people who
suffer a heart attack have low/ normal
cholesterol (but these folks may be running
around with high lipoproteins...I’ll get to
why that’s important in a moment). The
people who have “high cholesterol”+ low
lipoprotein counts are often the people who
are told to go on a statin. However, this
recommendation is not only typically not
information
high lipoprotein counts (see graphic below).
These are often the folks who die in their
30s and 40’s due to a cardiac event.
Conversely, we see people with what
appears to be high cholesterol but low
lipoprotein counts (below).
well-supported by research, it’s a decision
based on inadequate information, i.e.
without the lipoprotein number or other
inflammatory markers, which may be a
critical piece of this story.
The consensus within mainstream
lipidology is that atherosclerosis (a disease
in which plaque builds up inside your
arteries) is a “gradient driven process.” In
simple terms this suggests that if one has
more lipoproteins, there’s a greater
differently
© Robbwolf.com All Rights Reserved. 5
What is cholesterol?

likelihood of an “accident.” And by accident to mainly focus on the lipoprotein number.

we’re talking about a lipoprotein and/or its
cholesterol passengers getting stuck in the
cells that line our vascular system. This is
the beginning of an atherosclerotic plaque.
Going back to our vehicle analogy, this
makes sense—the more cars, busses, and
motorcycles on the road, the greater
likelihood of complications.
I’ve seen a small number of anecdotal
examples of people with HIGH
lipoproteins but low insulin resistance and
inflammation who underwent additional
screening such as carotid intima- medial
thickness (CIMT) and appeared to be 100%
atherosclerosis free. They

However, without knowing an individual’s They showed no signs of atherogenic

lipoprotein count, I’m hard pressed to see
how any healthcare provider can default to
either the position “you’re totally safe from
Cardiovascular disease (CVD), regardless of
cholesterol levels” (a very common position
within the ardent low-carb camps who
attribute all of CVD to insulin
dysregulation) or the other extreme of “we
must put you on a statin” even if you’re a
woman and the research suggests higher
cholesterol may in fact confer a longer life
for you.
disease process. Now, this is NOT
information coming from a medical trial, it’s
small in number and observational in
nature...most people would scoff at even
considering this information. But I’ve seen
enough emerging trends to at least put a bit
of thought into the possibility that yet again,
we might be faced with a “not one size fits
all” scenario. I’ll provide some guidelines
and resources shortly to help you make a
more informed decision about your unique
situation.

Our best current understanding is that Keep this in mind for a moment as we
lipoprotein count, not cholesterol amount, consider what cholesterol and lipoproteins
is likely the primary driver to CVD actually do in the body.
potential. The frightening part of this is that
the vast majority of healthcare providers are
either unaware of lipoprotein testing or
neither use nor understand it’s implications
Further, if an individual is insulin resistant
and inflamed, lipoprotein count may be
much more of a factor. Said another way, if
we had two people, both with the same
lipoprotein counts and cholesterol levels,
but one person is insulin resistant and the
other is say, eating a low carb diet...we have
two VERY different disease potentials. Yet
our mainstream healthcare system assumes
these people should get the same treatment
based entirely on looking at cholesterol
levels.
I’d like to point out that this is a
controversial position in the lipidology
world, as most of these very smart scientists
and doctors are of the opinion that we need
to

© Robbwolf.com All Rights Reserved. 6

What’s
the role of
cholesterol and
lipoproteins?
Most healthcare providers look at
cholesterol like a ticking time-bomb, poised
to kill us with a “widow maker” heart attack
or stroke. But like we talked about before,
cholesterol is found in ALL animal species
and every critter on earth would die if it did
not obtain cholesterol either from its diet or
making it itself (the only two ways of
obtaining the cholesterol necessary for life:
eat it or make it). Seems like a lot of effort
for all of biology to make something that’s
going to kill the host!
Lipoproteins help shuttle cholesterol and
other fat soluble substances throughout the
body
body. This ‘shuttling’ plays a key role for
growth and repair in the body as well as in
the innate immune system. It’s the “first line
of defense” the body uses in dealing with
everything from bacterial and viral
infections to cancer.
It’s worth noting that people with the life
threatening condition called sepsis (caused
by a bacterial infection), those with
HIGHER lipoprotein and cholesterol levels
have a much better likelihood of surviving
the septic process than those with low levels
of cholesterol and lipoproteins. There’s also
research which suggests that people with
higher
© Robbwolf.com All Rights Reserved. 7
What’s the role of cholesterol and lipoproteins?

higher cholesterol and lipoproteins may

have a lower risk for certain cancers likely
due to the immune supporting features of
the lipoproteins..
Phew! That’s a lot of info. But it’s important
to have a little background of this material
to understand what your individual story
may be with regards to cholesterol,
lipoproteins, and disease potential.
We’ll explore how and why these substances
may play a role in CVD but it’s worth
knowing that these molecules have critical
roles in the body and they’re not just a
nuisance waiting to kill us. Additionally,
understanding the functions of lipoproteins
may help us understand why levels may be
higher or lower due to infections, stress, or
hormonal changes such as low thyroid.
Let’s take a look at where the idea that
cholesterol causes CVD came from.
Perhaps we can better understand the reality
and dispense with some of the fiction :)

© Robbwolf.com All Rights Reserved. 8

What’s the
history of
cholesterol
and why does
my doctor think
it’s going to kill me?
In the 1940’s and ‘50’s researchers and A few integral pieces of
medical providers noticed increasing rates
of CVD in certain countries, including the
research during the 40s and
US. Several factors came together at this 50s
time which painted cholesterol and fat
Familial Hypercholesterolemia (FH):
(particularly saturated fat) in a poor light.
People with a specific genetic mutation
It’s a complex, convoluted story and both
which causes them to have exceptionally
myself and many other people have gone
elevated cholesterol and lipoprotein
deep in this history at various points. I’ll
numbers were observed to die from CVD at
provide links if you want to dig into this in
relatively young ages (in some cases late 20’s
detail. For now, you just need the big
but more often the early 30’s). Autopsies of
picture to understand how we arrived at our
these individuals demonstrated large
current state of a airs with cholesterol.
amounts of atherosclerotic plaquing
throughout the arterial system of FH
affected

© Robbwolf.com All Rights Reserved. 9

What’s the history of cholesterol?

affected individuals. This finding, plus what conviction that saturated fat was a root
I’ll share with you shortly, was pretty cause of CVD, even he fully exonerated
damning for cholesterol. It’s worth noting dietary cholesterol as a factor in this story.
however, that FH may not have been a Despite all this, most healthcare providers
problem until relatively recently. There’s still claim that dietary cholesterol is a CVD
research that suggests FH was in fact a risk.
survival advantage in the pre-antibiotic era.
Rabbit Model: Researchers fed rabbits
(strict herbivores) a diet of oxidized The perfect storm
cholesterol mixed into a chow formula.
These rabbits developed significant These three stories, Familial
amounts of atherosclerotic lesions, where hypercholesterolemia, rabbit studies, and
normally the rabbits developed little, if any, Ancel Keys’ influence, came together in a
of this disease process. perfect storm. A storm that not only greatly
oversimplified the cholesterol/CVD link
Ancel Keys and the Seven Countries but also has driven research, governmental
Research: A charismatic researcher, Ancel policy, and public behavior in directions
Keys championed the notion that saturated that are both expensive and injurious.
fat was the primary driver of CVD based on Again, this is a surface-level history, I’ll
his early epidemiological research famously provide links at the end for you to explore
titled The Seven Countries Study. While this topic further. Let me now shift gears to
Keys definitely presented a compelling talk about what our best understanding of
argument for his case, there are the atherogenic process is. I think this will
fundamental issues with his research. For put a lot of the moving parts into
one, correlation does not always prove perspective.
causation. In this case it’s worth mentioning
that research initiated by Keys himself
suggested that saturated fat did not in fact
increase CVD rates. This research hugely
contradicts the claims of Keys’ Seven
Countries Study. But—get this—it was
“lost” for decades. And by “lost”, I mean it
appears the results were effectively buried.
In brief, during the study, the researchers
fed a group of mental patients two different
diets: one contained large amounts of
saturated fat, the other replaced saturated
fat with polyunsaturated vegetable oils. The
vegetable oil group did in fact see reduced
cholesterol levels but their rates of CVD
and all cause mortality were actually
WORSE than the saturated fat group. All of
this was uncovered only a few years ago and
it puts a rather large thumb in the eye of
many of the saturated fat/cholesterol cause
CVD claims. It’s also worth mentioning that
although Keys remained unswayed in his
conviction

© Robbwolf.com All Rights Reserved. 10

How
good arteries
go bad
The atherogenic process, where plaque
causes vascular blockage and a heart attack
or stroke occurs, is a remarkably complex
process and has required decades to unravel.
Because one could easily write a book on
this topic alone, I’ll take some liberties and
opt for the simple story but, again, I’ll
provide references for you to dig into this
topic in greater detail if you so choose.
Think of CVD like an injury
People don’t typically think about the
development
development of CVD in terms of an injury
but the processes are effectively the same.
For example, if we get a cut, a number of
things occur at that site: clotting, immune
response, localized inflammation, scar
formation, and some degree of tissue
remodeling. The same process occurs in our
arteries. An injury may occur due to non-
laminar ow of blood through certain parts
of the arterial system. This type of blood ow
is turbulent and is often an outgrowth of
high blood pressure. The turbulence tends
to cause a low-grade injury to the artery,
which causes a cascade of events similar to
that
© Robbwolf.com All Rights Reserved. 11
How good arteries go bad
that of a cut described above.
As one of the first stages in healing,
lipoproteins, mainly from the LDL class,
enter the vascular lumen (the cells in direct
contact with the blood) and deposit
cholesterol. This in itself should not be a
problem. The trouble occurs if the
inflammatory environment is sufficiently
high—immune cells will make their way to
this site and begin to engulf both the
cholesterol fragments and the surrounding
tissues. This IS an issue when it progresses,
getting worse over time.
The end stage of this process is effectively a
scab in the arterial wall. Above the scab are
the contents of circulation, below the scab
are a mix of immune cells, cholesterol, and
various pro-inflammatory substances. If the
scab remains intact one could argue
“nothing bad happens” although the whole
atherosclerotic process is itself
inflammatory in nature and can worsen
conditions such as insulin resistance.
If the scab ruptures (and the likelihood of
this occurring grows with increased systemic
inflammation, insulin resistance, and
interestingly, significant blood sugar
swings), the contents of the scab are
dumped into the circulation—that’s when
things get bad. Massive clotting and
inflammatory cascade are initiated with the
end result most often being some kind of
occlusive heart attack or stroke.
This is a significant piece of the story but
there are a few more details.
Size vs quantity
Lipoproteins are constantly moving in and
out of the vascular epithelium in order to
shuttle cholesterol and other nutrients
around the body. In theory this is a
reasonably seamless process but there’s an
argument
argument that the “gradient driven effects”
(the total number of lipoproteins present)
are a large factor in atherosclerotic potential.
The idea again is simply more lipoproteins
mean more problems. A reasonable
assumption but there are important details,
for example relatively large LDL-particles
appear to be less atherogenic. These large
particles are cleared faster which might be
important since cholesterol carried by the
LDL-particles is at constant risk for
oxidation. Oxidized cholesterol is quite
inflammatory and atherogenic.
Insulin resistant individuals tend to have a
larger number of small, dense lipoproteins.
So, small, dense lipoproteins are bad, right?
Well... the smaller particles are actually
better at helping us deal with chronic and
acute infections! The scientific literature is
fairly clear that chronic infections, ranging
from gingivitis in the mouth to small
intestinal bacterial overgrowth (SIBO),
increase the likelihood of an atherogenic
profile.
Infections are by nature pro-inflammatory.
But what may be happening here is: if the
body is under a long term stress of
infection, the lipoproteins may shift towards
a smaller, more dense pro le to help mitigate
the toxic effects of low grade sepsis. That’s
good. The downside? These small, dense
particles are likely much more problematic
for the circulatory system.
Not to muddy the waters, but worth
mentioning: thyroid hormone is a critical
component of lipid metabolism and
hypothyroid is strongly associated with an
increased atherogenic potential. In the
hypothyroid individual LDL-particles are
not cleared rapidly, tend to build up in the
circulation, and are prone to oxidation.
Interestingly, chronic stress and infection
can dramatically alter effective thyroid
hormone levels. I’ll talk about this a bit
more
© Robbwolf.com All Rights Reserved. 12
How good arteries go bad
more later, but part of my reticence to
buy into what the mainstream
lipidologists are promoting is although
elevated lipoprotein levels likely present
an increased risk for atherogenic
processes, there are a lot of factors,
anything from infection to low vitamin
D levels to hormonal disturbances, that
may be the cause of elevated
lipoproteins.
Two-year pilot study: police
and fire
Let’s put all of this information into clinical
context. I serve on the board of directors
for a medical clinic in Reno, NV that
specializes in metabolic risk assessment and
lipidology. This clinic implemented a two-
year pilot study with the Reno Police and
Fire departments which looked like this: 35
individuals were identified as being at high
risk for CVD and type 2 diabetes based on
advanced testing (disordered lipids and
insulin resistance being the primary factors)
and a comprehensive Health Risk
Assessment (HRA).
The high risk individuals were placed on a
low-carb paleo diet coupled with efforts to
improve sleep (a huge factor) and exercise.
Based on changes in the blood work of
these individuals it’s estimated the pilot
study saved the city of Reno upwards of
$22MM with a 33/1 ROI. Pretty impressive
stuff and, as I mentioned, lipidology
program with a focus on advanced testing
(looking specifically at LDL-P, not just
cholesterol) was a cornerstone of this
program.
When I arrived on the scene I was quite
impressed with the program but a few
elements made me curious. Although
people generally saw dramatic
improvements
improvements in their advanced testing, this
was not across the board. In some cases we
had wacky situations in which an individual
lost weight, felt great, improved
performance, and reversed insulin
resistance...only to see LDL-P INCREASE.
This was perplexing at best—everything but
one parameter improved.
Due to the clinic’s lipidology focus, the
standard treatment was a low dose statin.
Now by low dose, I really do mean low. The
average dosage for a statin like Crestor
would be in the 20-30mg/day range. In our
case, the doctors were recommending 5mg.
Quite small, but I just have this sneaky
feeling people do not have statin
deficiencies.
I sat down with our staff and looked at
some of the other elements in these folks’
medical histories and found what was likely
subclinical hypothyroid in some cases,
SIBO in other cases, and a mix of both
problems in others. Our doctors and
dieticians starting digging into that. In a
number of situations we addressed either
thyroid or infections and brought LDL-P
down from numbers like 2,000 to 1,000.
Not all cases resolved this well, but quite a
few did. For the folks whose LDL-P was
still elevated we do recommend additional
screening to help better understand their
situation. I’ll talk about this more in a
moment.
Statins! The dirty deets
This is a good time for an aside to talk
about statins in a bit more detail.
Statins are quite good at reducing the
production of both cholesterol and
lipoproteins. They bring these numbers
down but have generally only shown
efficacy in preventing heart attacks
(presumably, the intended purpose) in a
very
© Robbwolf.com All Rights Reserved. 13
How good arteries go bad

very specific population: men between the

ages of 55-65 who have suffered a previous
cardiac event. This is a remarkably small
segment and yet statins are routinely
recommended to a whole host of
populations which they’ve shown no clinical
relevance. To the degree statins help with
CVD, it appears to have little to do with the
cholesterol lowering effects and everything
to do with anti-inflammatory effects.
Additionally, we’re now seeing a remarkable
number of research findings suggesting
statin use may increase risk for type 2
diabetes, obesity, insulin resistance, and
neurodegenerative disease. I’ve talked at
length with the folks at our clinic about all
of this and it’s just an area of relative
unknown. Which one of these biomarkers
should we believe? How do we balance one
risk factor for another? In the next section
let’s look at how we might triage all of this
and what we can do, ranging from diet to
additional screening to hopefully minimize
our CVD risk as it related to cholesterol and
lipoproteins.

© Robbwolf.com All Rights Reserved. 14

Things
to do
1. Reduce blood pressure
This may be a surprising recommendation
as, looking through the literature, efforts to
reduce blood pressure (mainly via a low fat
diet and drugs) does not typically reduce
blood pressure much, if at all. What’s
missed is the likely reason behind the
consistent elevated blood pressure seen in
modern Westernized countries. And that is
the elevated insulin levels that cause an
increase in the hormone aldosterone, which
causes the kidneys to retain sodium. If we
reduce insulin levels by improving sleep and
finding
finding an appropriate carbohydrate load,
we tend to see a remarkable decrease in
blood pressure. One of the ironic criticisms
of low carb diets is that in the early stages
most of the weight loss is “just water
weight.” That “water” is excess fluid
volume due to elevated insulin, which is at
the root of hypertension. If you recall,
elevated blood pressure can damage the
arteries, which expedites the atherosclerotic
process.
© Robbwolf.com All Rights Reserved. 15
Things to do
2. Get advance testing
Standard blood work doesn’t tell us enough
to begin to understand the real risks if all
we’re looking at is total, HDL, and LDL
cholesterol. standard
At a minimum I recommend getting an
LDL-P (LDL particle count test) in addition
to standard testing. In many cases we may
see that the total cholesterol is “high” but
the lipoproteins are low. In the case where
both cholesterol and lipoproteins are
elevated to concerning levels we do still
have options that should be explored.
3. Check thyroid, vitamin D,
and gut health
This track can be tricky since not many
doctors know what to look for with these
tests. In most doctors offices a “thyroid
test” involves nothing more than a TSH
(thyroid stimulating hormone) level, which
doesn’t tell us much except for in very
extreme cases. If you’re generally looking,
feeling, and performing better on your
version of a low carb diet but have elevated
lipoproteins, I don’t think it wise to ignore
this. I recommend connecting with
providers from organizations like the
Institute for Functional Medicine and
The Kresser Institute. When contacting
these people, or interviewing other
providers, ask them if they’re familiar with
how thyroid, vitamin D, and gut health
(SIBO) can affect lipoprotein and
cholesterol levels. If familiar, they should be
easily conversant and likely able to provide
some examples of people they’ve worked
with. If the provider is not familiar, you’ll
likely hear a long silence in which the
person thinks you’re nuts. Unfortunately,
this person will not be any help to you and
you’ll need to keep looking.
4. Additional screening
Something that’s not often discussed is that
the studies behind cholesterol and
lipoprotein levels and their relationship to
the atherosclerotic process are correlative.
Correlation can be helpful in looking further
into a process, but all too often it is
presented as gold standard “proof” of
causation. Unfortunately, this story is not
that simple.
The medical establishment tries to look at
easily tracked biomarkers and hope they
have a real, predictive relationship to the
disease process we’re concerned with. This
is a reasonable approach, but not a
complete approach. There’s evidence to
suggest that at least in some situations
(inflamed + insulin resistant) atherosclerosis
is a gradient driven process (worse with high
lipoproteins, better with low lipoproteins).
But we do have anecdotal observations that
call into question the notion that this is a
100% airtight case. My good friend, Rocky
Patel MD related an interesting experience.
I’ll pull a quote from his blog post:
“I had my CIMT done in 2006 on the Standard
American “heart healthy diet” eating low fat, higher
carb. You know those espoused by the ADA and
AHA. My lipids were “normal” at this time. My
thickness was 0.6 mm (about the 50th percentile). I
also had two small “road bumps “ (minimal
plaques) at my left carotid bulb both measuring 1.2
mm. I was not happy. I also had similar findings on
a study in 1/2010.
Flash-forward to June 2012, about 4 months into
CNS (a cyclic low carb diet), my CIMT showed a
thickness of 0.445 mm (13th percentile) and I had
the vascular age of a 16 year old! And oh by the
way, the “road bumps” were gone. All the while
carrying an LDL-P of over 2500 consistently for
over a year. I have also had a CT Coronary
Calcium score that was zero.”
© Robbwolf.com All Rights Reserved. 16
Things to do
Rocky had some clear carotid artery
thickening and as he said, a few “bumps”
when he was eating a low fat, high carb diet.
He did not know his LDL-P at this point,
but his cholesterol was “low.” While eating
a cyclic low carb diet Rocky saw both his
cholesterol and LDL-P elevate to rather
alarming levels. Yet, when he had a CIMT
performed, he appears to have REVERSED
both carotid artery thickening and plaquing
in this area, all while running an LDL-P that
would make just about any lipidologist
shudder. But, it would appear that a direct
measure of disease process indicates “no
problems.”
Are there in fact no problems? No one
really knows. No one. The people who are
strongly wed to the gradient driven
paradigm will conveniently ignore the
remarkable changes Rocky experienced
despite having very high LDL-P numbers.
Conversely, there are folks who completely
and totally dismiss LDL-P so long as one is
eating a low carb (low insulin) diet.
Personally, I don’t feel comfortable being
smugly sure about either of these positions.
The fact Rocky saw elevated LDL-P and
cholesterol while reversing CVD
processes... that’s damn interesting.
Confusing, but interesting.
Rocky has played with adding more carbs to
his diet and he reported that he starts to see
signs of blood sugar dysregulation and just
feels poor relative to consistently eating low
carb. We know pretty clearly that being
insulin resistant, heading towards diabetes
leads to increased CVD risk. From this
perspective it makes sense for someone like
Rocky to stick with a low carb diet as it has
arguably brought his IR and diabetes risk
down considerably. What’s unclear is if the
apparent reversal of the vascular changes
Rocky experienced while seeing an LDL-P
in the 2,500s is a net win.
LDL-P intrigue
Let me share a somewhat similar story for
more perspective. Dave Feldman is an
engineer by training who became interested
in ketogenic diets several years ago. Dave
jumped into this process as only an engineer
can—bringing a remarkable amount of
analytical scrutiny to the ketogenic diet in
general but to the story of cholesterol and
lipoproteins in particular.
Historically Dave has had fairly high relative
cholesterol and lipoproteins. In general
eating a ketogenic diet has pushed these
numbers up, but Dave has done a series of
self experiments on himself and others in
which he’s able to shift his LDL-P from as
low as 800 to as high as 3,500 in just a
matter of DAYS. Now, if you talk to people
knowledgeable about cholesterol and
lipoproteins, they’ll say it takes weeks and
months to see any appreciable shift in
lipoprotein numbers.
Side note: I haven’t seen research in which people
look at lipoproteins at an hourly or daily level, so
this may be a huge blind spot in lipidology. There
may be a host of assumptions out there that are
wrong or incomplete. I’ve tried to get commentary
from some top lipidologists about what Dave is
reporting and I can’t get anything back. Some folks
who follow Dave’s work online have dismissed it as
“anecdotal.” Yes, it’s one guy tinkering, not a
randomized controlled trial, but I’m a bit amazed
that people can respond in this way. At a minimum
one would expect a “Wow, that’s crazy...I sure hope
there’s research soon that will look at this.”
The reason I’m sharing this specific story is
for two reasons: First, it questions many
assumptions that are made about lipidology
and lipoproteins. There’s an assumption
these numbers take weeks and months to
change. If it may only be hours, what else
might
© Robbwolf.com All Rights Reserved. 17
Things to do

might we be wrong about? And second, The first two steps involve simple dietary
although Dave has had elevated lipoproteins strategies to hopefully reduce LDL-P,
for quite some time, his CIMT and similar ideally without damaging other aspects of
screening put him in the “no risk” category our health. The 3rd step involves screening
for CVD. So, similar to Rocky, Dave had for actual disease process. None of these
CORRELATES of CVD that suggest he options are any type of guarantee and we
has problems brewing but when looking for don’t have a lot of data to go on at this
specific disease process we see either none point.
or in Rocky’s case, what appears to be
reversal of disease process. I wish I had a The thinking behind the advanced screening
definitive answer to all this. I do not. like the 3D CAT scan is that if there’s no
established disease process, perhaps the
And the folks who are staunchly in one lipoprotein levels are not an issue. While
camp or the other are confusing to me as there’s logic behind this, there’s no concrete
there is enough evidence (IMHO) to data. Using a low dose statin will likely bring
question just about everything in this story. down lipoprotein levels, but are we making
On one hand we have the more lipidology a Faustian bargain, trading CVD potential
oriented folks who default to statins to for increased diabetes and
knock down the LDL-P. On the other hand neurodegenerative potential? This is of
we have people who say that so long as particular concern for people with the
insulin levels are low, there’s no dangerous APOE 4/4 and 4/3 genotypes, as they
LDL-P level. appear to be at particular risk for both
neurodegenerative disease and CVD.
What makes sense to me is if every other
parameter of your health appears to
improve—from inflammation to blood
glucose to insulin—but your LDL-P
remains elevated one could do the
following:
1. Try adding a few more carbs while
reducing fat and see if that positively
affects LDL-P without negatively
impacting other important markers, not
the least of which is how you feel.
2. Try adding monounsaturated fat
sources and limit saturated fat sources.
3. Get a screening like CIMT or a much
more powerful intervention called 3D
Coronary CAT scan. During this
procedure they 3D image all the
coronary arteries of your heart to assess
them for blockage. This technique has
proven to be incredibly powerful in
predicting coronary events. You can find
out more about this procedure from Dr.
Eric Harrison MD at his website
CardiacCareCritique.com

© Robbwolf.com All Rights Reserved. 18

So
where does
that leave us?
My personal bias is that doing whatever we
can to reduce both insulin and inflammation
is where we get the greatest benefit. We can
achieve this by sleeping better, getting
reasonable amounts of exercise, and finding
a dietary carbohydrate load that works for
us. Beyond this things are a bit of a guess, at
least until we have more and better data.

Want to dive deeper into the world of

cholesterol? Check out Peter Attia, M.D.’s
10-part series

© Robbwolf.com All Rights Reserved. 19

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