DrG's Medisense Feature Article
19042-Good_Egg
Good or Bad Egg
by Ann Gerhardt, MD
April 2019
Print Version
Bottom Line at the Top: Eggs are
a great source of nutrition and
deliver few calories. Though eggs’ cholesterol may
raise blood cholesterol levels of those who eat them, this
doesn’t occur in a sizable portion of the
population.
Eggs got a bad rap many years ago, when Ancel Keys’ studies
first linked diet, cholesterol and heart disease. Because egg
yolks contain a lot of cholesterol, the medical profession rapidly
vilified them. People in the know switched to egg white
omelettes, since all the cholesterol is in the yolks.
Umpteen studies attempted to define the number of eggs possible to eat
each week without losing cholesterol control. Some studies,
however, didn’t find an association of egg consumption with
either cholesterol levels or cardiovascular disease (CVD)
1.
Study after study of (usually) men of various ages found differing
results, especially in cases in which there was no control of the
entire diet. In a well-controlled study of healthy 18-19
year-old South African men, three, seven or fourteen eggs per week had
no effect on cholesterol levels
2.
Scientists veered away from the dietary cholesterol focus, leaving
behind an assumption that we should all limit dietary
cholesterol. Research moved on to dietary saturated
fat’s major contribution to CVD.
This was good news for seniors, for whom eggs are an easily-prepared
and inexpensive protein option. Eggs are a rich source of
nutrition, providing protein (about 7 grams
per egg), lutein, xeaxanthine, iodine, selenium, molybdenum, choline,
biotin and vitamins A, B2, B5, B12, folate, E & D.
Lutein and xeaxanthine are carotenoids that protect against macular
degeneration blindness.
As early as the 1970s, we knew that our livers make cholesterol when we
don’t consume it, since it is essential for building the
body’s cells and hormones. The more
cholesterol we eat, the less the liver makes, and vice versa.
At least that’s the way it’s supposed to work, but
physiology is neither simple nor uniform.
For a sizable number of people, eating high cholesterol foods does not
turn off the liver’s cholesterol
synthesis. Extra dietary cholesterol bumps up their
total and LDL-cholesterol, putting them at risk for CVD.
People whose cholesterol level paralleled their dietary cholesterol
were called hyper-responders, as opposed to those whose egg intake had
no effect on the cholesterol level
3. I saw
hyper-response
first-hand in a young man with cholesterol levels in the 250-300 mg/dl
range (even while on medication), whose egg consumption of a dozen
daily at Easter time transiently catapulted his cholesterol over 500
mg/dl. Unfortunately, we can’t predict which people
are hyper- and hypo-responders.
The Kuopio Ischaemic Heart Disease risk factor study
4,
observed the
risk of Finnish middle-aged men developing diabetes over a 20-year
time-span. Those who ate about 7 eggs per week were 38% less
likely to become diabetic than those who ate fewer
eggs. It’s unclear why eggs would prevent
diabetes, unless eggs contain unidentified protective bio-active
compounds, or people who eat more eggs eat less of something else, like
perhaps gooey pastries.
The Kuopio study also noted that those who ate more cholesterol did not
have higher blood cholesterol levels. The Australian Diabetes
and Egg study also found no impact on blood cholesterol, in spite of
greater total dietary cholesterol ingestion by men who ate more
eggs
5.
It seems that non-American studies show less of a dietary to blood
cholesterol link. Scientists might do better to figure out
why Americans fare worse with eggs.
Recent upset: A March 2019 Journal of the American Medical
Association article lays blame for diet-induced CVD and all-cause death
on eggs and dietary cholesterol
6. The authors pooled
data
from 6 prior American studies of racially and ethnically diverse
populations, using five different diet analysis methods. They
applied some assumptions and extensive statistical manipulation to put
those studies’ data in a consistent format and analyze the
various diet factors and confounders using a number of
models. Total animal protein and cholesterol from all sources
were significant co-culprits.
They concluded that someone eating 600 mg cholesterol per day incurred
a 37% increased risk of CVD and death. That’s an average
risk, comprised of people who didn’t die and those who
did. Extrapolating averages of dietary consumption and health
to individuals ignores the fact that each subject contributed a data
point falling anywhere from far below to far above the
mean. Conclusions based on averages don’t
apply to outliers, so they don’t necessarily apply to you.
Should this one study negate the preceding body of work, which was
extensive and convincing enough for the American College of Cardiology
and American Heart Association’s 2014 Lifestyle Guidelines
and the 2015-2020 Dietary Guidelines for Americans to minimize dietary
cholesterol’s impact on CVD. Is this study truly
superior?
The investigators or all six groups collected diet data using
self-reported food frequency questionnaires at the beginning of the
study, then observed their subjects’ health outcomes for up
to 31 years. The nutrition community recognizes that these
questionnaires are inherently flawed, since people under-report foods
they believe to be unhealthy and have imperfect memories for what they
eat. Plus, dietary intake at one point in time
doesn’t truly represent what people consistently eat for the
next 31 years: Some folk change their diet over time in
response to public health recommendations, some choose whatever is on
sale at Costco and others zig-zag from one foodie fad to another.
A study of 29,615 people is a lot, but this was no
‘study’ in a scientific sense. It merely
pooled data from others who had just watched these people.
There was no randomized, controlled trial, and as such it cannot
establish cause and effect. A lot of people who ate eggs
didn’t suffer from CVD and die, and vice versa.
Public health agencies lump together data to issue guidelines for
desirable diets and lifestyles. Those decrees morph over
time, depending on new data. On the other hand, current
medical thinking advises us to move to “individualized
medicine.” We are hyper- or hypo-responders to
dietary cholesterol and we have widely varying risks of CVD, cancer,
diabetes, malnutrition and macular degeneration.
Some have access to varied diets, money to pay for them and the
wherewithal to prepare them, and some don’t.
To truly practice personalized care, we should consider an
individual’s circumstances and risks and advise
accordingly. We could even
‘test’ the egg hypothesis with the Easter Egg test
my patient did: Do one blood lipid panel on a
cholesterol-restricted diet and another at least a month after
dramatically increasing plain egg consumption, while keeping all other
dietary content, exercise, stress levels, sleep, alcohol consumption,
tobacco use and weight absolutely the same. If levels soar,
temper egg intake. If not, do you prefer over-easy or
scrambled?
References
1) Dawber TR, et al. Am J Clin
Nutr 1982;36:617-25
2) Vorster HS et al. Am J Clin
Nutr 1992;55:400
3) Beynen AC & Katan M.
Atherosclerosis 1985;57:19-31
4) Salonen JT, et al. Ann Med
1989;21:227-9
5) Fuller NR, et al. Am J Clin Nutr
2018;107:921-31
6) Zhong VW et al. JAMA
2019;321:1081-98