We have been led to believe that all fat is bad for us yet that has never been the case
Crash course in Cholesterol, and Statins
Debunking the Dogma About Fat, how we got here, the beginnings.
For
half a century, health agencies and experts have recommended vegetable
oils over saturated fats for cooking. They have told the public that
vegetable oils are cardiac-protective. However, research suggests that
these oils may not be as beneficial as they seem.
When
the term "cooking oil" is mentioned, the immediate image that comes to
mind for most people is pale and yellow liquid in large transparent
bottles labeled "vegetable oil."
Though
vegetable oils are a staple cooking oil for many now, they are only a
recent invention. For thousands of years until only a few decades ago,
common fats used in cooking were animal fats such as lard, tallow,
butter, and suet, all of which tend to have a higher saturated fat
ratio.
The switch to vegetable oils can be traced back to researcher and physiologist Ancel Keys, who hypothesized in the 1950s that
replacing animal fats higher in saturated fats with vegetable oils,
which tend to be higher in polyunsaturated fat, would lower blood
cholesterol levels and in turn, reduce heart disease.
This
idea, and various market changes, led to the widespread adoption of
this dietary shift. And based on all the available evidence, it seems
that the hypothesis is completely wrong..
While
vegetable oils do lower blood cholesterol (which isn’t a good thing),
they don’t lower coronary heart disease mortalities at all. In
fact, many vegetable oils put consumers at untold risk of other harm.
Nevertheless,
Keys' hypothesis has persisted. Starting in the 1960s, the American
Heart Association put forward recommendations to switch from animal fat
to vegetable oils.
The idea influenced the first edition of Dietary Guidelines for Americans in February 1980. Both the American Heart Association and the Dietary Guidelines for Americans, valid from 2020 to 2025, have disastrously recommended polyunsaturated fatty acid consumption over saturated fat.
In
the 1950s, several randomized controlled clinical trials began testing a
diet low in animal fat; participants switched from consuming animal
fats, such as milk and cheese, to a polyunsaturated vegetable-fat diet. While these studies saw reductions in cholesterol levels, long-term and follow-up studies showed that those who had traded animal fats for vegetable oils and proteins often suffered from higher overall mortality, (more deaths) often with increased cancer deaths.
Starting in the 1980s, several studies also linked low blood cholesterol with cancer,
though it hasn't been determined why this link exists. Low blood
cholesterol is also linked to dementia, Alzheimer’s and numerous other
health issues. The use of Statins (the most profitable drug until 2020)
has caused terrible damage to health with no obvious benefit except
profit. We will discuss that in a different later in this email.
"The people on the high vegetable oil died at higher rates from cancer, and there were a series of very high-level meetings at
the National Institutes of Health throughout the 1980s trying to
understand this very concerning outcome," investigative journalist Nina
Teicholz said. "Those concerns were not resolved.” The connection
between seed oil oxidation and inflammation, and its relation with
cancer, was first extensively outlined in Teicholz's book, New York
Times bestseller "The Big Fat Surprise." Teicholz is the first to label
seed-derived vegetable oils as "seed oils" and spent a decade
researching fats and oils to write her book.
Although
other health experts have also linked vegetable oil with obesity and
diabetes, Teicholz said the evidence is usually from observational
studies. In contrast, the cancer link was seen in randomized controlled
trials, making it a more robust methodology.
Saturated Fats Are More Suitable for Cooking. Fats
high in saturated fat tend to be the most stable when cooked, this is
because they are much less reactive with heat and oxygen at the
molecular bond level.
Vegetable Oils Continue to Be Recommended Despite Health Risks: 3 Main Reasons
Though
research repeatedly shows that vegetable oils, otherwise known as seed
oils, are harmful when cooked, dietary guidelines and health
organizations continue to promote polyunsaturated vegetable fats over
animal fats. Nina Teicholz, an investigative journalist who had
spent a decade researching fats and oils, gave three major potential
reasons why the recommendation has not changed despite a lack of
evidence of vegetable oils' purported benefits and discrepancies in
studies that point to possible cancer risks.
1. Bureaucracy Versus Science
The
anti-saturated fat nutrition recommendation comes from the American
Heart Association (AHA) researcher and physiologist Ancel Keys'
Diet-Heart Hypothesis, originally put forward in the 1950s. Keys'
original assumption was that fat, which raised blood cholesterol levels,
caused coronary heart disease. He later narrowed the fat type to
saturated fat.
While the hypothesis has been since debunked, Keys' published
a study that compared heart disease and fat consumption in a half dozen
countries (Australia, USA, Canada, UK, Japan, and Italy).
The
more fat, the more heart disease. The trend line was unmistakeable.
Just one little problem, keys left out countries where people eat a lot
of fat but have very little heart disease, like Holland and Norway. He
also left out countries where people don’t eat much fat, but do have
lots of heart disease like Chile.
In fact, Keys had reliable data from 22 countries, but only showed the 6 that fitted his story. The
results were all over the place. But you can’t make a big splash in the
scientific community with a trend line that is all over the place. So
keys did what any dedicated researcher would do that wanted to make a
name for himself. He threw out the data that didn’t fit his story and
published his results that did.
Unfortunately,
this anti-saturated fat recommendation has evolved over the decades
from an incorrect diet recommendation to health dogma and national
policy. Congressional backing of this diet was the final nail in the coffin.
The
1977 Dietary Goals for the United States, authored by a Senate select
committee, followed the AHA's guidance to reduce total and saturated fat
intake, and began nationalizing the low-fat, low-cholesterol diet.
Soon after, in 1980, the National Institutes of Health published its first edition of Dietary Guidelines for Americans.
A whole section was dedicated to reducing cholesterol and fats. With
this, the hypothesis and dietary recommendation was taken out of the
realm of science and into the world of politics and government. From
there, the bureaucracy took over and the machine of government turned
dogma into policy and programs.
Bureaucratic
powers, however, are antithetical to scientific reasoning. Good
science requires skepticism to survive and involves challenging
preconceived hypotheses and conclusions to get closer to the truth.
Bureaucracies, however, are designed to execute on rules and guidelines,
not challenge them.
Such
is the case with the AHA, the main mouthpiece in this area, heavily
funded by those companies who profit heavily from this advice.
The
AHA has recommended against animal fat consumption for nearly half a
century. Retracting such a cornerstone recommendation would pose a
problem for the AHA, hence why many leading researchers dedicate their
lives and careers to finding evidence to support their dogma, and steer
popular opinion.
2. Financial Incentives
A
sizeable financial empire spanning the food and pharmaceutical
industries has been built on the Diet-Heart Hypothesis. This is a
significant reason why many researchers, health organizations, and the
industry resist considering that animal fats may not be that harmful. Vegetable
oils have been with the AHA since the association's rise to
prominence. Founded in 1924 at the outset of the coronary heart disease
epidemic, the AHA remained a fringe and underfunded research
organization for decades.
Then in 1948, things changed. Procter
& Gamble (P&G) designated the AHA to receive all the funds from
its 'Truth or Consequences' contest on the radio. The funds totalled
over $1.4 million, equivalent to $20 million today.
According
to the AHA's official history book, titled "Fighting for Life" by
William W. Moore, AHA's director from 1972 to 1980, P&G executives
presented the cheque at a luncheon, and "suddenly the coffers were
filled, and there were funds available for research, public health
progress, and development of local groups—all the stuff that dreams are
made of!" It was this funding that launched the organisation. I’m confident the AHA were “grateful”.
P&G
was the first company to sell hydrogenated seed oil as food. Its
product Crisco was initially made from hydrogenated cottonseed oil. I’m
sure you can join the dots. P&G are the first company to try to sell
an industrial product as food, they award a massive amount of money to
the AHA, and then the AHA says that this new product is the healthy
choice, and not the natural fats (nutrient dense tallow and butter)
which have been used for centuries.
Today, the AHA has awarded over 120 AHA
"heart-check" marks to vegetable oil products. These logos are
displayed on product labels certifying the AHA has approved them as
heart-healthy. While many of these oils are olive oil, they also include
canola, soy, and vegetable. Only four dairy heart-checks were given, unfortunately these are to soy milk (estrogenic) or a brand of nonfat milk with above-average sugar content
It’s
an nice little ‘earner’. The AHA charges food makers fees to use their
logo but the association's financial returns don't appear to detail the
exact revenue from the heart check program.
Over
the decades, the pharmaceutical industry has also made billions of
dollars selling drugs that lower LDL cholesterol, deemed "bad
cholesterol" and the primary cause of coronary heart disease. Animal fat
increases all cholesterol levels, including LDL, while vegetable oils
decrease cholesterol levels. This is an even bigger ‘earner’.
3. Egos and Established Notions Are Hard to Challenge
Over
half a century, the belief that saturated fat is bad for the heart has
become a dogma among doctors and nutritionists. Therefore, arguments
that contradict the Keys' Diet-Heart Hypothesis are met with extreme
resistance. Researchers and journalists who publicly challenge this
dogma have been subject to attacks and backlash.
This
response is not new. As far back as the hypothesis' inception, some
researchers whose work challenged Keys' lost their academic careers. For
example, the late Dr. George Mann from Vanderbilt University, a
professor and biochemist who challenged the Diet-Heart Hypothesis, This
research path cost him his NIH funding and entrance to reputable
journals for publication.
Keys
himself openly dismissed and criticized those who put forth other
causes for heart disease. While one may interpret Keys' actions as one
of a guilty researcher trying to hide his deceit.
The
late Professor John Yudkin, a physiologist and nutritionist at the
Queen Elizabeth College in the United Kingdom, asserted that sugar could
lead to heart disease. His hypothesis was ridiculed and marginalized.
Keys called Yudkin's hypothesis "a mountain of nonsense", even though,
decades later, research indicated that Yudkin's idea is very much on the
right track.
Mann
was also the associate director of the Framingham Heart Study from 1948
to 1955. Initiated in 1948, the large ongoing study investigates
epidemiology and risk factors for cardiovascular disease.
During
Mann's time as the associate director of the observational study,
researchers found that rather than decreasing coronary heart disease
risk, low cholesterol levels were unexpectedly associated with an
increase in coronary and total mortality. The study also observed "no
relationship" between coronary heart disease and the diet of the
participants interviewed.
In
1972, Mann co-authored a study on the African Maasai people who
consumed a diet high in meat, milk, and animal blood but had low blood
cholesterol and little to no heart disease. However, Mann speculated
that exercise could be what protected these people from heart disease.
In
his 1977 commentary "Diet-Heart: End of an Era," Mann lamented the
fastidious establishment of Keys' hypothesis as dogma despite the lack
of evidence.
Keys dismissed Mann's paper in a letter published in 1978, accusing Mann of "deliberately" distorting data. (Pot-Kettle-Black)
For
half a century, health agencies and experts have recommended vegetable
oils over saturated fats for cooking. They have told the public that
vegetable oils are cardioprotective. However, much research suggests
these oils are devastating for health.
While
saturated fat has historically faced criticism due to its association
with blood cholesterol levels and coronary heart disease, emerging
studies have provided a more nuanced understanding of this topic,
including this fat's potential advantages in high-temperature cooking.
Big Pharma's Take
Over
the decades, the pharmaceutical industry has also made billions of
dollars selling drugs that lower LDL cholesterol, deemed "bad
cholesterol" and the primary cause of coronary heart disease. Animal fat
increases all cholesterol levels, including LDL, while vegetable oils
decrease cholesterol levels.
The
biggest blockbuster drug of all time are LDL cholesterol-lowering
medications: statins. Saturated fat has to remain the bogeyman because
saturated fats tend to raise your LDL cholesterol, so that was always
part of the assumption of why saturated fats are bad.
This is a classic Hegelian Dialectic.
The
funding from pharmaceutical companies, including Pfizer, Merck, and
AstraZeneca, made up 3.8 percent of the American Heart Association's
total revenue in 2021–22, a total of nearly $34 million.
Pfizer, Merck, and AstraZeneca are all major players in the statin industry.
Funding
from non-pharmaceutical corporations made up almost 18 percent of the
AHA's funding that same year, totalling over $157 million. While the AHA
provides the names of all its pharmaceutical benefactors, the
organization declined to give names of the other corporations and
donation values.
Statins
are one of the most widely prescribed drugs on the planet. Whether they
have been of great benefit to humankind is a difficult question.
Until
2021 they were the most profitable drug sold in history. To give you an
idea of how profitable, there are approximately 67 million people in
the UK, and Statins are one of the most commonly prescribed drugs in the
UK: around 8 million adults in the UK take them, and by reducing the
parameters for prescribing of Statins for Cholesterol reduction, big
Pharma and the NHS hope to get at least 10 million people on this drug..
NHS Business Services Authority published the official statistics in June 2022.
The key findings showed that:
*
The cost of prescription items dispensed in the community in England
was £9.69 billion, an increase from £9.61billion in 2020/21.
* The number of prescription items dispensed in the community in England was 1.14 billion.
* Atorvastatin (a statin medication) was the single most dispensed drug in England in 2021/22 with 53.4 million items.
However when you add up all the different available statins, this number is significantly higher.
NHS
spending on statins is currently about £500 million per annum and
rising at an annual rate of 30%. This is all paid for by our taxes, not
just income tax, but the tax on fuel, wine, food etc etc.
The
Global Statin market size reached USD 15.38 billion in 2022. Looking
forward, it is predicted to rise to USD 22.21 billion by 2030
So do you think Big Pharma is being benevolent?, or does self interest and profit play a major part?
A few interesting facts
Highest life expectancy in Europe. The Swiss
Highest cholesterol in Europe. The Swiss
The highest fat rich diets in Europe. The Swiss and French
The lowest cardiovascular disease in Europe. The Swiss and French
Statin
drugs came out in 1987. To facilitate the sale of them, we were made
afraid of Heart disease, and more specifically; Cholesterol.
Additionally
In the 1980’s a new but separate fear was promoted, Alzheimer's disease
is a neurodegenerative disease that usually starts slowly and
progressively worsens and is the cause of 60–70% of cases of dementia
disease. It didn’t exist in any measurable number prior, not even by a
different name. It has several potential causes, one of which is a fat
and cholesterol deficiency.
Your brain is mainly made of cholesterol. And statins disrupt your liver making cholesterol.
Is Cholesterol the bogeyman, and doesn’t it cause Heart attacks and Strokes?
Cholesterol is
essential for all animal life, with each cell capable of synthesizing
it by way of a complex 37-step process. All animal cells (exceptions
exist within the invertebrates) manufacture cholesterol, for both
membrane structure and other uses, with relative production rates
varying by cell type and organ function. About 80% of total daily
cholesterol production occurs in the liver and the intestines.
We hear about HDL and LDL and HDL is ‘Good’, LDL is ‘Bad’. However, nothing the body makes is bad. HDL
is the carrier and returns any excess Cholesterol back to the liver to
be recycled. LDL is the repairer and the deliverer. It also delivers
Cholesterol to the brain.
40
years ago a total cholesterol level of 8-9mmol/L was considered normal.
Now you are pushed to take prescribed statins if it is under 5mmol/L.
Human physiology hasn’t changed in 40 years, but the rate of Cardio
Vascular Disease has increased. Statins haven’t made anything better.
Our body produces cholesterol in the liver, Your liver makes cholesterol
for a purpose. It isn’t a mistake.
Your
body is made of trillions and trillions of cells walls are a minimum of
30% cholesterol. Some are 60% cholesterol. Without cholesterol the
cells don’t work properly. Your brain is 75% cholesterol by
weight. The white matter, ‘myelin’ is cholesterol. You can’t make sex
hormones without cholesterol. Testosterone, estrogen, progesterone,
cortisol and adrenal hormones are all steroid hormones which are 95% by
weight, cholesterol.
We
also ended up with Low testosterone, which in men, causes erectile
disfunction, and women causes difficulties relating to menopause (low
libido pre menopause and muscle wasting, joint pain and incontinence
post menopause).
If
you don’t have enough cholesterol you get erectile disjunction, you get
menopause, you get adrenal exhaustion, you get cognition diseases.
Statins have been prescribed since 1987, which coincides with the rise
in Alzheimer’s cases.
Vitamin
D3 is created by 7 DHC (dehydrocholesterol) cholesterol plus UVB
radiation. And Vitamin D is about as good as it gets for overall health.
(Put simply, sunshine hitting your skin which contains cholesterol)
Which food source has the highest amount of cholesterol. A clue, its purpose is to enable the brain to develop.
Breast milk.
Cholesterol
is essential, and doesn’t cause Heart disease. In fact, cholesterol
tries to fix inflammation in our arteries in a similar way that firemen
turn up at a house fire to put out the fire, you see a burning building,
you will probably see firemen and fire engines. The firemen didn’t
cause the fire, they are there to help put it out. (apologies to Lady
Firemen)
Cholesterol
has been the bogey man for several generations, it was supposedly going
to kill you either by Heart disease or a stroke, and this has been
proven to absolutely and positively untrue.
The
biggest blockbuster drug of all time are LDL cholesterol-lowering
medications: statins. Saturated fat has to remain the bogeyman because
saturated fats tend to raise your LDL cholesterol, so that was always
part of the assumption of why saturated fats are bad.
Cholesterol isn’t the problem, as such, Statins cannot be the answer.
We need to have a refresher on statins at this stage. What actually do statins do, and how.
Statins have been prescribed since 1987, and achieve
what they set out to do. They stop the liver from doing its job
properly. The liver makes cholesterol according to what the body
requires.
They
will actively block the enzyme that creates cholesterol, known as
hydroxy-methylglutaryl-coenzyme A reductase (HMG-CoA). However, strange
symptoms have always been present with statins that we haven't been able
to explain fully.
We
already know that by blocking HMG-CoA, we block the production of CoQ10
(same pathway), which is an amazing molecule that helps us make energy,
and is extremely important for heart health (where we find most CoQ10).
This is why people supplement it.
There's
more to the story though than CoQ10 and statins though. Patients who
are on Statins also suffer from myopathy myalgia, increased
calcification of the soft tissues (gall bladder, joints, arteries etc)
and osteopenia. This is likely due to the reduction in Vitamin K2, and
the effect this has.
What
exactly is going on here? Well recent research has revealed some
interesting insights. What we know now is that these symptoms
collectively stem from something else, including the blocking of CoQ10.
Statins
block a compound known as Geranylgeraniol (GG). GG is a substance that
is made in the human body via a biochemical pathway called the
mevalonate pathway. This is the same biochemical pathway that makes
cholesterol. Guess what else GG does?
GG
allows us to actually make CoQ10 (we need this) and Vitamin K2-MK4 (we
need this also, it’s the only biochemical synthesised form of Vitamin K2
in the human body). Vitamin K2 in partnership with Vitamin D3 regulates
our calcium by putting it into the bone where it needs to be, and pulls
it out of the soft tissues. GG is literally making K2 in over 25 organs and tissues in the body, and Statins block the creation of GG.
If we don’t have enough Vit K2, we suffer from calcium deposits in soft tissues, and not in the bones. This isn’t a good thing.
This
is a big breakthrough in understanding of the effects of statins and it
helps explain why patients suffer from symptoms like increased
calcification, arteriosclerosis, and muscle myopathy. GG is also
required for the making of skeletal proteins. Without it, we can't
deliver new muscle proteins properly.
Vitamin
D3 can come from supplements or sunshine, but only if you have a ready
supply of cholesterol in your skin, and per a normal functioning body.
When the cholesterol in your skin reacts with UVB light it creates the
required Vit D3. Statins are robbing your body of more than just
cholesterol, and Vitamin K2, you are now low on Vitamin D3, the free
sunshine drug.
The argument in favour of
limiting saturated fat intake is based on evidence that shows that
replacing saturated fat with unsaturated fat decreases the risk of
cardiovascular events. But usually, overall mortality rates don't
significantly improve. The core studies showing this link were carried out in the 1960s and ’70s, forming the foundations against saturated fat intake.
These
studies include the Los Angeles Veterans Administration diet study
conducted in the 1960s. More than 800 men aged 55 or older participated
in the trial.
Half
the participants replaced two-thirds of the animal fat in their diets
with vegetable oil, while the other half continued to consume animal
fat. After six years, the first group saw a 13 percent drop in
cholesterol levels, and only 48 men died from heart disease during the
study compared with 70 in the group that consumed animal fat. The caveat to this finding is that the overall mortality between the two groups was about the same, but more cancer cases were reported in the group that consumed vegetable oils.
Another highly cited study is the Anti-Coronary Club study conducted in the 1950s.
The researchers didn't intervene in the control group members' diets,
but the experimental group was told to reduce their animal fat intake,
consume as much fish and poultry as they liked, consume one ounce of
corn oil per day, and cook with polyunsaturated fat. As a result of the
intervention, participants' cholesterol levels dropped and hypertension
improved. However, more deaths were reported among this experimental group.
"The
intervention studies were done in the ’60s and ’70s ... and certainly
the intervention studies suggested that there was a small benefit, but
it wasn't statistically very strong," nutrition researcher Peter
Clifton, who is a professor at the University of South Australia said. Mr.
Clifton, who recommends replacing polyunsaturated fats with saturated
fats, said more robust evidence supporting the diet-heart hypothesis
comes from cohort studies that follow large populations.
One such cohort study published in 2015 examined
more than 120,000 men and women. The researchers found that those who
replaced 5 percent of their saturated fat intake with polyunsaturated
fat and whole grains had fewer cardiovascular events. Another 2014 cohort study published
in Circulation followed more than 2,700 people and found that high
levels of linoleic acid, an omega-6 fatty acid, in the blood were
associated with fewer cardiovascular events. A problem with cohort studies is that, unlike randomized controlled trials, they can't prove causality.
Since
researchers can't control factors in participants' lives, including
dietary choices, any relationship is linked only by association. Cohort
studies also take a long time, so participants may be lost during
follow-up, which can introduce bias into the findings.
The Evidence Against the Saturated Fat and Heart Disease Link
Scientists
who challenge the current dietary recommendations to reduce saturated
fat intake emphasize the limited evidence supporting such
interventions. They often cite the large randomized controlled
trials that show that lowering saturated fat or replacing it with
polyunsaturated fat had no effect or even caused harm.
Opposition
to the link between saturated fat and heart disease includes the Sydney
Diet Heart Study, the Minnesota Coronary Survey, and the Women's Health
Initiative Dietary Modification Trial.
In the 1990s, the Women's Health Initiative Dietary
Modification Trial involved nearly 49,000 postmenopausal women who had
to reduce either their saturated fat intake to less than 10 percent or
make no change in their diet. The study found that reducing fat didn't
affect the women's heart disease or weight loss.
The Sydney Diet Heart Study was conducted between 1966 and 1973. It put 458 men who had had a heart attack on a diet that
replaced their saturated fat with soy oil. While the men's LDL
cholesterol dropped, their risk of death increased by more than 60
percent, and their risk of heart disease increased by 70 percent.
The Minnesota Coronary Survey,
conducted at about the same time, followed 9,000 people and reported
similar findings: LDL cholesterol levels fell while risks of death and
cardiac events increased.
In 2020, 12 researchers came together to publish a state-of-the-art review in the Journal of the American College of Cardiology (JACC).
"Whole-fat
dairy, unprocessed meat, and dark chocolate are SFA-rich [saturated
fatty acid-rich] foods with a complex matrix that are not associated
with increased risk of CVD [cardiovascular disease]. The totality of
available evidence does not support further limiting the intake of such
foods," the authors wrote.
Regarding
cohort studies, the perceived benefits of replacing saturated fats with
polyunsaturated fats "could be attributed to a possible beneficial
effect of polyunsaturated fatty acids and not necessarily to an adverse
effect of SFAs," according to the authors.
"The effect of saturated fat and raising LDL cholesterol is pretty small. So it's not a really powerful fat," Mr. Clifton said. There are also large meta-analyses with findings that support both sides of the argument, such as the 2020 Cochrane Review.
Cochrane
Reviews are recognized as the gold standard in research. The authors
examined 15 randomized, controlled trial findings on replacing saturated
fat with polyunsaturated and monounsaturated fat. The study concluded
that this replacement reduced the risk of a cardiovascular event by 17
percent but didn't affect overall mortality.
The authors of this commentary emphasized findings that show that reducing saturated fats didn't reduce total
mortality, cardiovascular mortality, coronary heart disease mortality,
fatal and nonfatal heart attacks, and coronary heart disease events.
Another
argument put forward by the authors of the JACC report is that not all
saturated fatty acids are equal, so health professionals should look at
the sources rather than the overall consumption of saturated fat.
Lauric
acid, a type of medium-length saturated fat commonly found in coconuts,
strongly raises LDL cholesterol; therefore, some studies suggest that
it elevates cardiovascular risk. However, studies on unrefined coconut
oil suggest that it has an overall cardioprotective effect.
Butter is high in palmitic acid, another saturated fat with a potent LDL cholesterol-raising effect. However, a meta-analysis on butter has shown it to have a cardioprotective effect. About 70 percent of dairy is saturated fat, yet studies have shownthat
high dairy consumption is heart-protective. Milk has short-chain
saturated fat, which is linked to cardioprotective effects.
Beef
has also been shown to have a relatively neutral effect on heart
disease. Although beef is often associated with having high saturated
fat, monounsaturated and polyunsaturated fats make up about 50 to 60 percent of beef fat.
Contrary to popular belief, the primary source of saturated fat may not be animal-based food but processed food, as argued by obesity researcher Zoe Harcombe, who holds a doctorate in public health nutrition.
The
2020–2025 Dietary Guidelines for Americans shows that processed food
accounts for 42 percent of saturated fat consumed by Americans aged 1
year and older. On the other hand, animal-based food, including milk,
meat, and poultry, makes up 27 percent (pdf).
Saturated fats are often added to processed food to prolong their shelf life and improve their texture.
Processed
foods are also high in sugar, and professor Benjamin Bikman (a hero of
mine), a cell biology expert at Brigham Young University with a
doctorate in bioenergetics, explained that the combination of saturated
fat and refined carbohydrates is the most toxic.
Sugar
in the blood oxidizes LDL cholesterol. This forms small, dense LDL
cholesterol more prone to atherosclerosis. Sugar also increases
triglyceride levels in the blood vessels. Oxidized LDL cholesterol and
raised blood triglyceride levels are risk factors for heart disease. To make things more complicated, research has shown that LDL cholesterol may not be the best predictor for cardiovascular risk.
So, 'Bad' Cholesterol May Not Be So?
For
decades, low-density lipoprotein (LDL) cholesterol was one of the most
critical indicators that doctors measured for heart disease. Now,
doctors and researchers are challenging whether LDL cholesterol, also
known as "bad cholesterol," is really as bad as we once feared. Research
shows that measuring LDL cholesterol doesn't always effectively assess a
person's cardiovascular risk and that other tests may be more useful.
Low-Density Lipoproteins Versus LDL Cholesterol. Many
people with normal LDL cholesterol levels may experience heart attacks,
cardiovascular research scientist James Di Nicholantonio explains.
The number and size of LDL particles, rather than LDL cholesterol, may be a more relevant risk factor.
Studies have shown that
LDL cholesterol levels predict higher cardiovascular risk 40 percent of
the time, while apolipoprotein B (apoB) concentration, the summation of
all LDL particles and their precursors, is associated with elevated
risk 70 percent of the time.
Other studies comparing
LDL cholesterol levels against cholesterol levels in LDL and its
precursors, apoB number, and LDL particle number, also found that the
latter two tend to be stronger predictors of risk, while LDL cholesterol
is the weakest.
So what's the difference between LDL particles and LDL cholesterol?
An
LDL particle is a type of lipoprotein made by the liver. Its primary
function is to deliver triglycerides from the liver to other cells in
the body. Transporting cholesterol is more akin to an LDL's side hustle.
The cholesterol that an LDL transports is called LDL cholesterol.
High-density lipoprotein (HDL) and LDL cholesterols contain the same cholesterol;
their carriers are what differ. LDL cholesterol can also leak into
blood vessels, causing atherosclerosis, thereby earning its "bad"
reputation.
On
the other hand, HDL particles can venture into atherosclerotic plaques
to absorb the cholesterol trapped inside, preventing further plaque
formation and helping to prevent heart disease. Hence, HDL cholesterol
is considered "good.” Therefore, nutritionist Jonny Bowden says labeling HDL and LDL cholesterols as good and bad cholesterol is wrong.
Mr.
Bowden, who co-authored the bestselling book "The Great Cholesterol
Myth," compared measuring the number of LDL particles to counting the
number of passengers traveling in cars on a road. We know that more cars
mean more congestion and traffic accidents, but more passengers doesn't
necessarily indicate this. Conversely, traffic could still be congested
even if passenger numbers are low or average.
"My
LDL [cholesterol] was like 100 (2.6mmol/L), maybe 110 mg/dL(2.8mmol/L)"
(very, very close to to the perceived ideal of lower is better), Mr.
Bowden said. "Then I got the particle tests, and they showed an entirely
different picture."
The test showed that he carried many small, dense LDL particles in his blood and was at high risk for cardiovascular events.
There are two types of LDL particles: large and buoyant, and small and dense. The
small and dense LDLs are much more atherogenic (contributive to
atherosclerosis), whereas the large, buoyant LDLs are less so. These two
types of LDLs can be measured through advanced lipid testing.
About
80 percent of total LDL cholesterol level comprises the more harmless
large, buoyant LDLs, with atherogenic small, dense LDL making up the rest. Interestingly, fats increase large, buoyant LDLs and decrease small, dense LDLs, whereas refined carbohydrates increase small, dense LDLs.
Professor Erik Froyen from California State Polytechnic University, who
has a doctorate in nutritional biology and whose research investigates
mechanisms by which fatty acids impact cancer and cardiovascular disease
risk factors, has also demonstrated this in his work.
Research suggests that intake of refined carbohydrates is more relevant than saturated fat in causing coronary heart disease.
Mr.
Bowden compares large, buoyant LDLs with large volleyballs that float
along in the water, moving with the tide, while small, dense LDLs are
like small golf balls that get stuck between rocks, where they start
oxidizing and accumulating to form atherosclerotic plaques. Individuals with more large, buoyant LDLs are said to exhibit a pattern A type
of cholesterol profile, and these people are at low risk of
atherosclerosis. On the other hand, those with more small, dense LDLs exhibit a pattern B cholesterol profile and are at risk of atherosclerosis. Their markers for metabolic disease risks may also be elevated.
Small,
dense LDLs carry less cholesterol than large, buoyant LDLs, so a person
can have a normal LDL cholesterol level but a pattern B cholesterol
profile. However, lipidologist professor Carol Kirkpatrick, head
of the Wellness Center at Idaho State University, highlighted that for
most people, overall LDL particle number is more relevant than LDL size.
What we know now is that, yes, [small dense LDLs] may be important, but
it really ends up being a red flag for people who have metabolic
dysfunction.
Some studies have found that large LDLs have a neutral effect on atherosclerosis, though other scientists disagree. "We
know that statins, for instance, lower cardiovascular risk, and statins
preferentially reduce larger LDL particles," said professor Kevin Maki
of Indiana University, whose interest is in preventing and managing
cardiometabolic disease. However, the statin and LDL link has also been
challenged.
"It's
really unclear if the benefit of statins is because it lowers LDL,"
cardiologist Dr. Robert Dubroff states. "There are other drugs that can
lower LDL, and many of them have been tested in well-conducted
randomized trials and shown no benefit.” Dr. Dubroff indicated that
there are interventions that lower cardiovascular risk without lowering
LDL.
History
People
didn’t think critically about the fat that our ancestors had used for
thousands of years, we have eaten saturated fat, cooked with tallow,
cooked with lard, all these solid and saturated fats had been a staple
of the human diet for 100’s of generations, and they hadn’t caused heart
attacks until now. Seems obvious to us now, but it wasn’t then.
Cholesterol
has been the bogey man for several generations, it was supposedly going
to kill you either by Heart disease or a stroke, and this has been
proven to absolutely and positively untrue.
To
tell the origin of our story, I’ll end to go right back to the
beginning. How it came to be that cholesterol was originally thought of
as the baddie.
I’ll
begin over 120 years ago in 1901 when a German chemist was commissioned
by the German Navy to create a synthetic lubricant for diesel engines
in submarines. Hydrogenation was perfected in 1901 and patented in 1903
by Wilhelm Normann. He introduced the hydrogenation of fats, creating
what later became known as trans-fats.
His
product only had a very small market, as Germany only had about 100
submarines, so he sold his patent in 1908, the patent was bought by
Joseph Crosfield & Sons Ltd. . A company that had begun in 1814 as
Joseph Crosfield's soapery was established on the north bank of a loop
of the river Mersey in an area known as Bank Quay, near to urban
Warrington. From the autumn of 1909 hardened fat was being successfully
produced in what in a large scale plant in Warrington.
(In
1911 the company was purchased by Brunner, Mond & Company and 1919
it was absorbed into Lever Brothers, and 10 years later became a
subsidiary of Unilever.)
Joseph
Crosfield and Sons acquired Normann's patent ostensibly for use in the
production of soap. Their chief chemist, Edwin C. Kayser, was hired by
Procter & Gamble's business manager, John Burchenal, and they
patented two processes to hydrogenate cottonseed oil. Although their
initial intent was to completely harden oils for use as raw material for
making soap, these processes ensured that the fat would remain solid at
normal storage temperatures and could find use in the food industry.
Procter
& Gamble called the product Crisco, a modification of the phrase
"crystallized cottonseed oil". They used advertising techniques that
encouraged consumers not to be concerned about ingredients but to trust
in a reliable brand. Further success came from the marketing technique
of giving away free cookbooks in which every recipe called for Crisco.
Crisco vegetable oil was introduced in 1960. In 1976, Procter &
Gamble introduced sunflower oil under the trade name Puritan Oil, which
was marketed as a lower-cholesterol alternative.
Proctor
and Gamble who owned then owned the patent, and named the product
‘Crisco’. They commissioned the American Heart Association to say that
these trans fats were healthy, and natural fat contained a bogeyman
called cholesterol.
Proctor
and Gamble began to run adverts which said that butter and cream and
lard was an unhealthy way of cooking food, it contained something called
cholesterol. The used extensive ad campaigns and sold it as a healthier
way to cook, and also portrayed the use of animal fats which had been
used for centuries as ‘common’. This next bit is a little sexist, they
targeted housewives and made them feel less than ideal if they cooked
with historic animal fat and not Crisco.
1950’s
Heart
disease was beginning to kill people in large numbers.. the President
of America had a heart attack in 1955 and was out of action for 10 days,
this was a cause of Great concern to everyone, men were dying and from
something that hadn’t affected their parents. And no one understood why
this was happening. People dying in their prime..!
Could
it be caused by your personality type, Driven people didn’t really
relax and the stress was killing them?, could it be a vitamin
deficiency?, perhaps it was the fumes from car engines. Maybe cigarette
smoke?
These could be viable hypothesis..
But one other hypothesis was suggested by a pathologist from The University of Minnesota Mr Ancel Keys. (Boo-Hiss)
Ancel
Keys was considered a very aggressive man, an arrogant bully, even by
his friends, he was a forceful man, he would happily argue his opinion.
He came up with what became known as his Heart Diet Hypotheses.
And
his idea what that you would eat saturated fat and cholesterol your
diet, eggs cheese dairy meat etc, and this would lead to you having
elevated cholesterol in your blood, and this would somehow clog up your
arteries. And you would have a heart attack. This is still how some
people see fat even now.
1960
The
American Heart Association. At the time, this was the only public
health group that was dealing with Heart disease, and everyone was
following their advice, it was a simpler time and people still believed
public bodies acted in the best interest of the public.
The
American heart association would like to tell people what to do, but
there was no data. So Ancel wangled himself onto the nutrition committee
of the newly formed American Heart Association
1961
With
not much more data available, He was able to get his recommendation
published called Dietary Fat and its Relation to Heart Attacks and
strokes. His idea was that you needed to restrict your dietary fat and
Cholesterol in order to prevent heart disease. This was the first advice
anywhere in the world. No other advice was available, and despite this
being complete wrong; the idea stuck.
The advice became institutionalised, repeat something often enough, and becomes considered fact.
It
was a very simple idea, it was easy to understand, and easy to
visualise. Cut out animal foods, replace butter, replace it with
margarine, replace the saturated fat with unsaturated fat and you won’t
die.
The
world breathed a sigh of relief, we had an answer to the problem, it
was fairly simple to grasp, it sounds logical, and it isn’t really an
inconvenience.
People
didn’t think critically about the fat that our ancestors had used for
thousands of years, we have eaten saturated fat, cooked with tallow,
cooked with lard, all these solid and saturated fats had been a staple
of the human diet for 100’s of generations, and they hadn’t caused heart
attacks until now. Seems obvious to us now, but it wasn’t the truth.
In parallel to the above, Here’s a little history on rapeseed oil:
During
WWII, rapeseed oil was grown widely in Canada to be used on naval ships
as a lubricant. When the war ended, there was so much farmland in
Canada already dedicated to growing rapeseed that they wanted to find
other uses for it so they could continue selling it for a profit.
The
problem with rapeseed oil: It’s such a terribly foul-tasting and
rancid-smelling oil that it isn’t fit for human consumption.
So
they spent the next few decades until the 1970’s working out a way to
make it edible. That process requires heavy refining, bleaching and
deodorising using harsh chemicals (as far from “natural” as it gets) to
finally yield the neutral-tasting, odourless oil that now sits on
supermarket shelves and has the masses believing it is good for the
heart. Rapeseed oil is sold in the US and Canada as Canola oil.
(Canadian Oil Low Acid)
Fast
forward to today: Almost all processed and pre-packaged foods –
everything from crisps and breakfast cereal to canned soups and salad
dressings – are made with ‘seed oils’; sunflower, rapeseed, canola,
cottonseed, soybean/vegetable or corn oil.
Why?
Because they’re cheap to produce. And because many people are still in
this mindset that cooking oils are somehow better for you than natural
saturated fats like tallow or butter.
With
the enormous variety of cooking oils available on the grocery store
shelves it can be very frustrating and confusing to decide which ones
are the most healthy and how to properly use them. There are many
differing opinions out there about which oils are good or bad, but many
of the opinions are just that – opinion. And often they’re completely
misinformed.
Scientific
research has been clouded and falls into two camps; research that has
been bought and paid for by the companies that sell seed oils, and the
research with little or no vested interest.
We shall only look at the ‘no vested interest’ information.
Of primary importance is which oils are stable when heated and thus don’t oxidise (ie, carcinogenic) or go rancid easily.
Oxidation
and/or rancidity can take an otherwise healthy oil and turn it into a
free radical laced toxic swill that you really do not want to ingest.
Of equal importance is the oil’s fatty acid profile, which has a huge impact on its health benefits, or lack thereof.
I
have the majority list of most edible oils that are commonly available
for purchase, which ones to use, what to use them for and which ones to
avoid altogether. I could discuss the basic biochemistry of the
different groups of fatty acids they contain. This is important to
understanding why certain oils should be used and others avoided.
Of
particular importance is the degree of saturation of each fatty acid.
The more saturated a fat is the less prone it is to becoming oxidised
from light and heat exposure, the less likely it is to go rancid, and
therefore the more suitable it is for cooking involving heat.
The
less saturated they are the more prone they are to breakdown with light
and In these cases extra precaution needs to be taken – and certain
types of oils are best avoided altogether.
But to save you half an hour..
Organic grass-fed Tallow, Organic grass-fed Butter, and if you are a vegetarian, Coconut Oil.
If
you fancy olive oil, make sure it isn't mass produced from a
supermarket, but single estate, date of harvest given etc. don’t cook
with it.
The
reason is simple, it’s a high value item and most olive oil that are
sold in the supermarkets have been adulterated with seed oils. There is
more olive oil sold globally than could possibly be created from the
amount of Olive trees on the planet.
Boring bit about statins.
In
1971, Akira Endo, a Japanese biochemist working for the pharmaceutical
company Sankyo, began to investigate cholesterol. Research had already
shown cholesterol is mostly manufactured by the body in the liver with
the enzyme HMG-CoA reductase. The first agent Endo and his team
identified was mevastatin (ML-236B), a molecule produced by the fungus
Penicillium citrinum.
A
British group isolated the same compound from Penicillium
brevicompactum, named it compactin, and published their report in 1976.
The British group mentions antifungal properties, with no mention of
HMG-CoA reductase inhibition. Mevastatin was never marketed, because of
its adverse effects of tumors, muscle deterioration, and sometimes
death in laboratory dogs.
Cholesterol
researcher Daniel Steinberg writes that while the Coronary Primary
Prevention Trial of 1984 demonstrated cholesterol lowering could
significantly reduce the risk of heart attacks and angina, physicians,
including cardiologists, remained largely unconvinced.
Never
one to ignore a new profitable drug, P. Roy Vagelos, chief scientist
and later CEO of Merck & Co, was interested, and made several trips
to Japan starting in 1975. By 1978, Merck had isolated lovastatin
(mevinolin, MK803) from the fungus Aspergillus terreus, first marketed
in 1987 as Mevacor.[11]
In
the 1990s, as a result of public campaigns, people in the United States
became familiar with their cholesterol numbers and the difference
between HDL and LDL cholesterol, and various pharmaceutical companies
began producing their own statins, such as pravastatin (Pravachol),
manufactured by Sankyo and Bristol-Myers Squibb. I
n
April 1994, the results of a Merck-sponsored study, the Scandinavian
Simvastatin Survival Study, were announced. Researchers tested
simvastatin, later sold by Merck as Zocor, on 4,444 patients with high
cholesterol and heart disease. After five years, the study concluded the
patients saw a 35% reduction in their cholesterol, and their chances of
dying of a heart attack were reduced by 42%.[11][180] In 1995, Zocor
and Mevacor both made Merck over US$1 billion.[11]
This is where statistics are used to convince non mathematicians that black is orange.
Link
to lancet study. Randomised trial of cholesterol lowering in 4444
patients with coronary heart disease: the Scandinavian Simvastatin
Survival Study (4S) - The Lancet
All
trial candidates actually had coronary heart disease (CHD). This is
the actual paper, and I’ll translate at the end of each paragraph
4444
patients with angina pectoris or previous myocardial infarction and
serum cholesterol 5·5-8·0 mmol/L on a lipid-lowering diet were
randomised to double-blind treatment with simvastatin or placebo. 4444
people who had heart disease with what used to be a normal, level of
cholesterol.
Over
the 5·4 years median follow-up period, simvastatin produced mean
changes in total cholesterol, low-density-lipoprotein cholesterol, and
high-density-lipoprotein cholesterol of -25%, -35%, and +8%,
respectively, with few adverse effects. 256 patients (12%) in the
placebo group died, compared with 182 (8%) in the simvastatin group.
The
relative risk of death in the simvastatin group was 0·70 (95% Cl
0·58-0·85, p=0·0003). The 6-year· probabilities of survival in the
placebo and simvastatin groups were 87·6% and 91·3%, respectively. There
were 189 coronary deaths in the placebo group and 111 in the
simvastatin group (relative risk 0·58, 95% Cl 0·46-0·73), while
noncardiovascular causes accounted for 49 and 46 deaths, respectively.
622 patients (28%) in the placebo group and 431 (19%) in the simvastatin
group had one or more major coronary events. The relative risk was 0·66
4444 people with heart disease/Angina/or had already had a heart attack.
189 untreated people died of heart attack
49 untreated people just died
622 untreated people had a heart attack and didn’t die
860 untreated people died in total
111 treated people died of heart attack
46 treated people just died
431 treated people had a heart attack and didn’t die
588 treated people died in total
The
hidden information is that less than 5000 people were studied in this
single trial. 20 such trials may have been conducted on behalf of the
same company. 19 studies with vastly different results may have remained
unpublished. After all, these studies are paid for by the drug
manufacturer. In this case Merck.