Bite Back with Abbey Sharp - The SURPRISING Truth About Butter, Saturated Fat & Health (The Research SHOCKED Me!) | Fat Wars Part 2
Episode Date: September 22, 2026In today’s episode of Bite Back with Abbey Sharp, we’re back with Fat Wars — Part Two, turning our attention to butter, beef tallow, coconut oil, and the saturated fat comeback. We unpack the sc...ience behind saturated fat, cholesterol, and heart disease, including LDL, ApoB, and the controversial studies used to defend saturated fat. Plus, we explore why not all saturated fat sources are created equal and why what you replace butter with may be the most important part of the debate. Did butter deserve a correction, or has wellness culture taken its comeback too far? Here’s a run down of what we discussed in today’s episode: How Butter Made Its Big Comeback Cholesterol 101: LDL, HDL & ApoB Explained Are “Big Fluffy” LDL Particles Actually Safe? Does Raising HDL Cancel Out High LDL? Does Saturated Fat Really Cause Heart Disease? The Controversial Studies Behind Butter’s Comeback The Most Important Question: What Replaces Butter? Butter vs. Refined Carbs, Whole Grains & Unsaturated Fats Butter, Coconut Oil, Beef Tallow & Cheese: Are They Different? The Fat Wars Verdict: What Does the Evidence Say? 👩🏼💻 RESEARCH LINKS: https://ers.usda.gov/amber-waves/2016/july/butter-and-margarine-availability-over-the-last-century https://www.fda.gov/food/food-additives-petitions/final-determination-regarding-partially-hydrogenated-oils-removing-trans-fat https://www.journalofdairyscience.org/article/S0022-0302(82)82217-0/pdf https://share.google/zlXtL8n5q0i6u3MFA https://www.researchgate.net/publication/10785457_Effects_of_dietary_fatty_acids_and_carbohydrates_on_the_ratio_of_serum_total_to_HDL_cholesterol_and_on_serum_lipids_and_apolipoproteins_A_meta-analysis_of_60_controlled_trials https://pubmed.ncbi.nlm.nih.gov/1386252/ https://pubmed.ncbi.nlm.nih.gov/12716665/ https://pmc.ncbi.nlm.nih.gov/articles/PMC7652325/ https://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0241993 https://pubmed.ncbi.nlm.nih.gov/16685042/ https://pubmed.ncbi.nlm.nih.gov/16685042/ https://pubmed.ncbi.nlm.nih.gov/40289348/ https://www.bmj.com/content/346/bmj.e8707 https://www.researchgate.net/publication/301279770_Re-evaluation_of_the_traditional_diet-heart_hypothesis_Analysis_of_Recovered_data_from_Minnesota_Coronary_Experiment_1968-73 https://www.researchgate.net/publication/281188515_Intake_of_saturated_and_trans_unsaturated_fatty_acids_and_risk_of_all_cause_mortality_cardiovascular_disease_and_type_2_diabetes_Systematic_review_and_meta-analysis_of_observational_studies https://pubmed.ncbi.nlm.nih.gov/20071648/ https://www.researchgate.net/publication/359350267_Abstract_27_Is_Butter_Back_A_Systematic_Review_and_Meta-analysis_of_Butter_Consumption_and_Risk_of_Cardiovascular_Disease_Diabetes_and_Total_Mortality https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2831265 https://pmc.ncbi.nlm.nih.gov/articles/PMC12095860/ https://pubmed.ncbi.nlm.nih.gov/41397264/ https://link.springer.com/article/10.1007/s11883-006-0021-0 https://pubmed.ncbi.nlm.nih.gov/31728492/ https://pubmed.ncbi.nlm.nih.gov/26429077/ https://www.cochrane.org/evidence/CD011737_effect-cutting-down-saturated-fat-we-eat-our-risk-heart-disease https://pubmed.ncbi.nlm.nih.gov/41397264/ https://pubmed.ncbi.nlm.nih.gov/29511019/ https://www.researchgate.net/publication/337567817_Impact_of_coconut_oil_consumption_on_cardiovascular_health_a_systematic_review_and_meta-analysis https://www.sciencedirect.com/science/article/abs/pii/S0308814625007666 https://pubmed.ncbi.nlm.nih.gov/1845606/ https://pubmed.ncbi.nlm.nih.gov/28251937/ — DISCLAIMER:The content in this episode is for educational and entertainment purposes only and is never a substitute for medical advice. 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Removing butter is not the intervention. What you put on the plate in its place is.
Welcome to another episode of Bite Back with Abby Sharp, where I dismantle diet culture rules,
call out the charlatans spinning the pseudoscience, and help you achieve food freedom for good.
At some point in the past 20 years, butter stopped being a banal ingredient in your grandmother's
muffin recipe and started to take on its own cultural
identity. It became a symbol of real food, a stand-in for wholesome tradition, a badge of purity, and a
profound moral statement, which is kind of extraordinary when you consider where butter was sitting
culturally just a few decades ago. For most of the second half of the 20th century, butter was practically
the poster child for what nutrition experts told us not to eat. It was a fat, and fat, fat,
apparently made us fat, but even worse, it was a bad fat.
And so in its place came margarine.
Cheaper, lower and saturated fat, scientifically engineered, and aggressively marketed as the
enlightened heart-conscious alternative.
And the people ate it up.
Like literally.
Between 1942 and 1972, butter availability in the United States dropped from more
than 16 pounds per person per year to just five, while margarine overtook it in sales by the late
50s and ultimately peaked by the mid-70s. But then the story started to unravel. Because a lot of those
old-school margarins were made with partially hydrogenated oils, which could contain
industrial trans fats. And unlike the increasingly complicated conversation around saturated,
fat, the evidence on artificial trans fat became unequivocally clear. Transfat raises bad LDL cholesterol,
lowers good HDL cholesterol, and increases the risk of cardiovascular disease. Eventually, the FDA
determined that partially hydrogenated oils were no longer recognized as safe and largely removed
them from the American food supply. Suddenly, the supposedly scientific replacement for butter didn't look so
clever anymore. And so began Butter's Great Redemption arc. By 2005, Americans were once again
consuming more butter than margarine, giving way to the Atkins resurgence, followed by paleo,
keto, and eventually carnivore. And by 2014, Time magazine put a giant curl of butter on its cover
with two very large words, eat butter. And culturally, the case seemed like it was close.
Butter had not simply been welcomed back into the kitchen, it had been exonerated, vindicated, almost martyred as it became proof that nutrition authorities everywhere had lied to us.
And this is where I think the story gets really interesting, because there was such a legitimate and much-needed course correction happening here.
For years, we had dramatically oversimplified dietary fat by encouraging folks to focus on total grade.
grams of fat, far more than the important question, which was what was going to replace that fat.
We sold highly refined low-fat products as inherently healthier, even when the removed fat
had simply been replaced with refined starches and added sugars.
And we allowed foods containing industrial trans fat to wear a heart health halo simply because
they were saturated fat-free.
Those were real public health mistakes that we need to call out and own.
But we're now facing a very different mistake, where the very valid acknowledgement that
we were wrong to demonize all dietary fat morphed into the more muddy, we were wrong about saturated
fat, which has now become eating more saturated fat is actually healthy.
More specifically, that butter, tallow and coconut oil are superior to
handmade vegetable or seed oils, and anybody who's telling you otherwise is repeating debunked
nutritional dogma. Those are four very different claims. Correcting an overly simplistic
nutrition message does not mean that every piece of science underneath that message was wrong.
So while we were certainly in need of a correction, does it warrant a full-blown butter coronation?
Well, today we're going to be building on what we discussed in part one of
the Fat Wars series here to figure out where the pendulum should actually stop. Is saturated
fat genuinely harmful? Does butter really raise your heart disease risk? What about its impact
on HDL and so-called fluffy LDL? Do coconut oil, beef tallow, cheese, and butter all behave the same
way just because they're rich in saturated fat? And perhaps most importantly, if you eat less
butter, what are you eating instead? Because that question turns out to change almost everything we think
we know about fat. All right friends, one last thing. If you are new to bite back, welcome. I would really,
really love if you would hit subscribe or follow wherever you're watching or listening right now,
and if you would share this podcast with a friend who is always going on about their latest
fad diet. Also, if you prefer short of form content, absolutely check me out at Abby's Kitchen on
IG and TikTok. All right, friends, get yourself a glass and wine or some coffee and your favorite
snack, because we are going deep with this one. All right, friends, let's dive in. Okay, so to set the
stage, we got to do like a little biology lesson and talk about cholesterol and heart health,
seeing as the historical argument against saturated fats are that they increase the risk of heart
attack and stroke. So very quickly, cholesterol is an essential waxy lipid molecule that is essential
for cell membrane structure, bile acid production, cell signaling, hormone production, and honestly,
so much more. The problem isn't that cholesterol exists in the body. The problem, when we're
talking about atherosclerosis, is prolonged exposure to too many APOB-containing lipoprotein
particles that can enter and become retained in the artery wall, delivering cholesterol
that ultimately contributes to plaque. So let's just unpack that very complicated sentence.
LDL, commonly called bad cholesterol, isn't actually cholesterol itself.
LDL is a lipoprotein particle that carries cholesterol and other lipids throughout the blood.
HDL is another lipoprotein involved in transporting and exchanging cholesterol throughout the body,
including pathways that ultimately return cholesterol towards the liver.
The measurement LDLC tells us how much cholesterol is being carried inside those LDL particles,
while APOB gives us a sense of the total number of atherogenic particles,
including LDL, remnants, and LPA.
Simply put, cholesterol is the cargo, LDL is the delivery truck,
LDLC tells us how much cargo is in the LDL fleet, and APOB tells you roughly how many
atherogenic trucks are on the road. While there's way more nuance that we're going to dive into,
the reason for the long-standing saturated fat fears is the repeated finding that a diet-rich
and saturated fat raises LDL cholesterol. And just to complicate things right out the gate,
saturated fat is not actually one fat. It's a family of different fatty acids,
and some particularly meristic and palmitic acid are potent LDL razors,
while others like stearic acid may have a much smaller effect.
We're going to come back to why that means that butter and coconut oil or beef tallow
are not metabolically interchangeable, but that brings me to another nuance worth untangling,
particle size. Because like saturated fats, LDL particles are also not all identical.
LDL particles exist across a spectrum of sizes, although they're often broadly discussed as either small and dense or large and buoyant, or what the internet affectionately calls big and fluffy.
Research suggests that it's these small dense LDL particles that are most strongly associated with insulin resistance and an increased risk of coronary heart disease.
Some, but not all trials, suggest that increasing saturated fat increased the massed,
of large LDL particles, leading a lot of carnivore enthusiasts to claim that even if their
animal and butterfilled diet did increase their LDL, if that LDL was suddenly all the big fluffy
stuff, then it's all good, right? Maybe not. First of all, it seems that the most striking,
kind of small to large particle shift seen in a lot of these keto-style dietary patterns
occurs with carbohydrate restriction and reductions in triglycerides.
Not necessarily because saturated fat itself has some unique LDL fluffing capability.
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Second, particle size might not be the most important consideration. Particle size may tell us something
about the metabolic context, but the total concentration of circulating APOB containing particles
may be far more telling. According to a recent 2025 analysis of more than 207,000 people,
they found that as soon as the total APOB particle number was accounted for, LDL particle size,
subclasses stopped predicting coronary disease. So like back to our cargo truck analogy,
a big truck may carry more cholesterol than a small one, but it still has an APOB license plate
and can still enter the artery wall.
So if your saturated fat diet turns your LDL into bigger trucks,
but also puts more trucks on the highway,
don't worry they're fluffy, isn't exactly reassuring.
But what about saturated fat's impact on our so-called good HDL levels?
Because yes, saturated fat can raise LDLC,
but it can also raise HDLC.
So do these two things just cancel each other out?
Again, no.
Cardiovascular biology is not a scoreboard where one point for HDL erases one point for LDL and
the match ends the draw.
Higher HDLC is associated with lower risk, but simply raising HDLC has not been shown to
protect us from heart disease.
Meanwhile, if a dietary change is increasing the number of APOB containing particles
circulating in your blood, that is an atherogenic change.
and a simultaneous rise in HDLC does not magically neutralize it.
So we've established something that is actually pretty difficult to argue with in the research.
And that is that certain saturated fats, particularly pulmetic and meristic acid,
can raise LDL and in some cases also APOB.
But of course, nobody actually cares that much about lowering a number on a blood test
just for the satisfaction of watching the number go down.
The question we really care about is, does that increase in LDL translate into more actual heart
attacks, strokes, and cardiovascular deaths? And this is where the evidence gets considerably messier.
Because we can lock people into controlled feeding studies for like a few weeks,
carefully manipulate the fat in their diets, and watch their LDL change. What we cannot
realistically do is randomly assign thousands of people to eat butter or olive oil for 30 years,
and wait to see who has a heart attack.
So to answer the heart disease question,
we're kind of forced to combine several different types of evidence.
Short or controlled feeding studies,
longer-term observational cohorts,
and the relatively small number of older randomized control trials
that actually measured cardiovascular events.
And sometimes they don't tell us a perfectly neat story.
If you've been on carnivore talk,
you've maybe heard about two famous trials
that the seed oil skeptics love to cite.
the Sydney Diet Heart Study and the Minnesota Coronary Experiment.
In Sydney, 458 men who had already experienced a coronary event
were randomized to an intervention intended to replace saturated fat sources
with polyunsaturated safflower oils.
The control group did not receive the same dietary intervention.
When previously unpublished data were recovered and reanalyzed years later,
the intervention group had lower cholesterol,
but higher all cause cardiovascular and coronary mortality.
I'm sorry, what?
Then in Minnesota, more than 9,000 institutionalized participants
were randomized to a diet that replaced saturated fat with corn oil and corn oil margarine.
Cholesterol dropped substantially, but mortality did not.
And again, in a secondary analysis, they found that the greater reductions in cholesterol
were actually paradoxically associated with higher mortality.
Obviously, these unexpected findings deserve attention,
but they also warrant further scrutiny.
Sydney was a relatively small study in men who had already experienced coronary disease,
and its intervention produced a very unusual high linoleic acid dietary pattern
without a corresponding omega-3 increase.
Minnesota involved institutionalized populations,
many participants were not exposed to the experimental diets for very long, and both studies
were conducted in the 60s and 70s in an entirely different cardiovascular treatment era.
The exact composition of historical margarins also wasn't characterized with the precision
that we would expect today.
That said, I would not simply waive these trials away by blaming trans fats.
I mean, they are offering legitimate randomized data points that deserves
to live in the evidence-based. They just probably shouldn't get to be the entire evidence-based,
especially because we've accumulated way more research since then. So one 2015 meta-analysis
of observational studies found no clear association between saturated fat intake and all-cause
mortality, cardiovascular disease, or coronary heart disease outcomes. An earlier 2010 cohort
meta-analysis reached a similar conclusion. And a 2016
review, provocatively titled Butter Back, found that eating an additional tablespoon of butter
per day was essentially neutral for cardiovascular disease, with only a very weak association with
total mortality. Those papers were enormously influential in butter's rehabilitation, and understandably,
but there are two big glaring issues with them. One, again, they were largely observational
studies where butter consumption would travel alongside loads of other behaviors. And,
that researchers can't perfectly separate.
And two, most importantly, simply asking whether people ate more or less saturated fat
tells us nothing about what replaced those calories.
In other words, is heart disease lower specifically because you added saturated fat
or because you've reduced your sugar or refined carbs?
Thankfully, we've just recently got some new hints here.
In 2025, researchers followed more than 221,000 adults from three major U.S. cohorts for up to 33 years.
The people with the highest butter intake had about 15% higher total mortality than those with the lowest,
while higher plant oil intake was associated with lower mortality.
Statistically, replacing 10 grams of butter per day with plant oil was associated with about 7,000.
17% lower total mortality. Now remember, this is an observational study. Association, not proof
of causation. And importantly, that specific butter to plant oil substitution did not produce a statistically
significant reduction in cardiovascular mortality. So I wouldn't turn this into like
butter kills. But it certainly complicates the idea that modern long-term research has completely
exonerated butter while condemning vegetable oils. So then we move to look at the more valuable
randomized control trials, which is honestly where things get even more chaotic. One 2025 systematic
review of nine randomized control trials found no statistically significant reduction in cardiovascular
mortality, total mortality, myocardial infarction, or coronary events from reducing saturated fat. The authors went
And so far as to conclude that saturated fat restriction could not currently be recommended for
preventing cardiovascular disease and mortality.
But then a larger 2025 risk stratified review looked at 17 randomized control trials and more
than 66,000 adults.
And it felt something a little more nuanced.
For people who started at low cardiovascular risk, the absolute benefit of reducing or modifying
saturated fat over about five years was very small. For people at higher cardiovascular risk,
the potential absolute benefit became more meaningful. And critically, when saturated fat was
specifically replaced with polyunsaturated fat, the risk of non-fatal heart attack was about 25% lower.
Hmm. Okay. Well, how the heck the two reviews published months apart,
still appear to tell us very different things?
Well, that's nutrition research for you, baby.
Different inclusion criteria, populations,
baseline risk, interventions, amounts of saturated fat actually reduced,
and most notably different replacement nutrients,
which means different results.
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Which brings us to the most important question we need to ask to get to the bottom of the fat wars.
If we're saying saturated fat is good or bad for heart health, what are we comparing it to?
Because when you remove butter, something else is going to replace it that is going to influence the health outcome.
Or maybe you remove the butter and you don't replace those calories at all, creating an energy deficit,
potentially changing body weight and a bunch of other risk factors at the same time.
So anytime someone quotes a study that found that reducing saturated fat doesn't prevent heart disease,
What we then need to find out is what filled the butter gap.
One likely reason so many observational studies that helped rehabilitate saturated fat found little or no association with heart disease is that they didn't adequately account for the replacement.
If the comparison nutrient is essentially whatever else people happen to eat, including refined starch and sugar, the benefit of eating less saturated fat can disappear.
That doesn't mean that saturated fat is something.
how heart protective, it might mean that the replacement sucked. The replacement is not just some
minor statistical nuance. The replacement is the experiment. So when researchers actually account for
what is filling that saturated fat gap, a lot of the apparently contradictory research starts to
make more sense. So let's start with carbohydrates. Because according to a major meta-analysis
of 60 trials, if you replace saturated fat with,
With carbohydrates, LDL will generally come down somewhat.
But if those carbohydrates are predominantly refined starches and added sugars,
you simultaneously lower HDL, raise triglycerides, and promote the kind of chronic
disease causing lipoprotein profile that we really don't want.
So you've kind of improved one number while likely worsening others.
Now let's talk about unsaturated fat.
That same meta-analysis found that when people replaced
saturated fat with unsaturated fats, LDL came down without the same triglyceride penalty,
and the total cholesterol to HDL ratio also improved. But again, blood work is not really the
endpoint we're ultimately interested in. We want to know whether people actually have fewer heart
attacks. And we've got data on that too. One landmark analysis pooled data from 11 prospective
cohort studies involving almost 345,000 people to see what happened.
when 5% of calories from saturated fat were hypothetically exchanged for something else.
When those calories were replaced with polyunsaturated fat, aka those seed oils that we love to
hate, coronary events were about 13% lower and deaths from coronary heart disease were about 26% lower.
But when saturated fat was replaced with carbohydrate as a broad category, there was no
cardiovascular benefit. Coronary events were actually modestly higher in that particular analysis.
Now, that study didn't do a very good job distinguishing Ebola steel cut oats from a Pop-Tart.
And as you can probably imagine, that distinction matters. But a massive 2015 prospective study
did. They found that when 5% of calories from saturated fat were replaced with polyunsaturated fat,
again, that's the seed oils, coronary heart disease risk was about 25% lower. When it was replaced
with mono-unsaturated fats, those are the things that we find in olive oil or avocado oil,
the risk was 15% lower. And when it was replaced with whole grains, the risk was 9% lower. But when
folks replaced their butter for sugar or refined starches, they saw no significant reduction in heart
disease risk. But again, all observational. So let's talk about the randomized control trials.
According to a large 2020-Cockering review, a 15 long-term randomized trials and 56,000 people,
reducing saturated fat, did not clearly reduce total mortality or even cardiovascular mortality. But it did
lower the risk of combined cardiovascular events by roughly 17%. Even more impressive, though, were the
results of a 2025 systematic review with 17 randomized control trials. Again, the impact on mortality
and cardiovascular events didn't seem like anything to write home about until they look specifically
at comparison nutrients. When saturated fat was being replaced by polyunsaturated fat, non-fatal
heart attacks were about 25% lower. And that benefit was much more potentially meaningful
for people who already started at high cardiovascular risk.
So the evidence isn't telling us butter is poison,
or even that eating less saturated fat is automatically healthier.
It's telling us something much more nuanced and hierarchical.
If you replace butter with refined starch and sugar,
you may accomplish very little.
With whole grain carbohydrates or plant proteins,
now you're getting a little improvement.
With mono-unsaturated fats,
particularly from plant foods like olive oil, nuts, and avocado, and you'll likely see a reduction
in risk. And finally, if you replace your butter with foods rich in polyunsaturated fats like
nuts, seeds, fatty fish, and unsaturated plant and seed oils, that is where we see the clearest
cardiovascular win. So once again, removing butter is not the intervention. What you put on the plate
in its place is. Now there's one last tiny little wrinkle here because I have been using saturated
fat and butter somewhat interchangeably for this podcast, and metabolically, that isn't entirely fair.
Saturated fat is a family of different fatty acids, and different foods contain different
combinations and permutations of them. Butter, for example, contains a lot of pulmitic and meristic
acid. Two of the saturated fats, particularly at fault for raising elizabeth.
ldl. Coconut oil is actually more saturated than butter over 90%, but roughly half of it is a
medium chain triglyceride called loric acid with far less palmitic acid. And that different
fingerprint seems to matter. And one randomized control trial comparing 50 grams per day of butter,
coconut oil and olive oil, butter raised ldial significantly more than either coconut or olive oil.
Now before the coconut oil lobby pops the champagne, when
researchers have pooled clinical trials, coconut oil still raises LDL by about 10 milligrams
per deciliter compared to other vegetable oils. So coconut may behave somewhat better than butter
in some direct comparisons, but still likely worse than canola, soybean, or olive oil. And then there's
the uber trendy beef tallow. It's actually only about 50% saturated, with more than 40% of the same
heart-healthy mono-saturated fat that is olive oil.
claim to fame. And while we definitely need a lot more robust research for like
officially ranking the healthfulness of each oil and fat, one tiny study found that
butter produced the highest LDL followed by beef tallow and then cocoa butter and
then olive oil. But just because one saturated fat may produce a more favorable
lipid response than another doesn't automatically make it a superfood.
Tallow raises LDL less than butter is not the same claim as Tallow is
better for cardiovascular health than unsaturated plant oils. And then there's one more tiny little twist
to throw in the mix here. Even foods containing very similar saturated fatty acids don't necessarily
behave identically. Take cheese, for example. If saturated fat were the only thing that mattered,
you might expect dairy fat eaten as cheese to affect cholesterol exactly the same way as dairy
fat eaten as butter. But it doesn't. In a randomized control trial of 92 adults,
LDL was about 3.3% lower after the cheese diet compared to the butter diet. Why?
Likely because of the food matrix of cheese where the calcium, protein, fermentation, physical structure,
and the way that fat is packaged within that food affects our body's response. So now we have two
separate layers of nuance. Different saturated fatty acids can behave differently and the same
fatty acids can behave differently depending on the food matrix, their
packaged in. So this is just another reminder that nutrition labels kind of flatten a lot of biology
into one number, and honestly, the devil is actually in the details. So where does this leave us?
The way I see it, the problem with the low-fat era wasn't necessarily that we identified saturated
fat as something worth moderating. The mistake was acting as though anything was healthier
simply because it contained less of it. A fat-free cookie wasn't car.
protective because somebody removed the butter. And conversely, your salad doesn't become dangerous
because you dressed it in canola oil. What we've learned over decades of research is that the
health effect lives heavily in the substitution. Compared with what is the question that actually
makes the seemingly contradictory saturated fat evidence makes sense. And that doesn't mean
we need to swing the pendulum straight back to 1993 and start counting fat grams.
So here's my evidence-based bottom line take. Use unsaturated fats including olive oil,
avocado oil, and yes, those demonized seed oils as your everyday default more often than fats
dominated by saturated fat. Two, let better coconut oil and tallow be foods that you use when
their flavor or culinary function actually adds something you value, not because wellness
culture convinced you their medicine. And three, aim to get most of your fats from nutrition,
nutrient dense whole foods like avocado nuts seeds and fatty fish because butter does not need to be
poison in order for olive or canola oil to often be the better cardiovascular choice and seed oils
doesn't need to be a superfood for replacing some of your butter with it to make sense butter deserved
a correction but not a coronation and on that note i'm going to make myself some avocado toast for
breakfast if you are not already i would really appreciate you subscribing or following to the podcast
wherever you are listening or watching.
And also, please leave me a five-star review.
It really does make all the difference in helping me get the word out.
And as you can probably see, this is a lot of work.
There were, I don't even know how many citations in this one,
but, you know, your girl was deep in the stacks.
But until next time, signing off with Science and Sass.
I'm Abby Sharp.
Thanks for listening.
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