This
week, I released the third part of my
cholesterol series. I discussed how cholesterol may not be the bad guy it’s “cracked
up” to be. Specifically, although certain drugs may be effective in reducing
the numbers, it doesn’t necessarily translate to better overall mortality
outcomes. This means, lower cholesterol numbers don’t always lead to lower
death rates making other factors important to consider. (See my homepage for
details and a video link on seven factors to consider if one has high
cholesterol.)
Another
big topic when discussing cholesterol is the role of egg consumption and cardiovascular
risk. Eggs are a source of cholesterol, so many believe that if you eat cholesterol,
your cholesterol goes up. That’s bad, right?
An
Exaggeration…It’s Shocking!
Here’s
a great summary of how previous reports on a diet rich in saturated fat and cholesterol
may not have the link to high serum cholesterol
and cardiovascular risk factors that you have been lead to believe:
For many
years, both the medical community and the general public have incorrectly
associated eggs with high serum cholesterol and being deleterious to health,
even though cholesterol is an essential component of cells and organisms. It is
now acknowledged that the original studies purporting to show a linear relation
between cholesterol intake and coronary heart disease (CHD) may have contained
fundamental study design flaws, including conflated cholesterol and saturated
fat consumption rates and inaccurately assessed actual dietary intake of fats
by study subjects. Newer and more accurate trials, such as that conducted by
Frank B. Hu of the Harvard School of Public Health (1999), have shown that
consumption of up to seven eggs per week is harmonious with a healthful diet,
except in male patients with diabetes for whom an association in higher egg
intake and CHD was shown. The degree to which serum cholesterol is increased by
dietary cholesterol depends upon whether the individual’s cholesterol synthesis
is stimulated or down-regulated by such increased intake, and the extent to
which each of these phenomena occurs varies from person to person. Several
recent studies have shed additional light on the specific interplay between
dietary cholesterol and cardiovascular health risk. It is evident that the
dynamics of cholesterol homeostasis, and of development of CHD, are extremely
complex and multifactorial. In summary, the earlier purported adverse
relationship between dietary cholesterol and heart disease risk was likely
largely over-exaggerated. (1)
The Tale of
the Hyper-responders-Who Cares In This Case?
The
following abstract explains how, in 30% of the population eating eggs may
increase both low-density lipoproteins and high-density lipoprotein. However,
who cares?! As the following except reported, it may be the “good-bad-cholesterol”
that is fluffy and less plaque-promoting anyway:
It is also
important to note that 70% of the population experiences a mild increase or no
alterations in plasma cholesterol concentrations when challenged with high
amounts of dietary cholesterol (hyporesponders). Egg intake has been shown to
promote the formation of large LDL, in addition to shifting individuals from
the LDL pattern B to pattern A, which is less atherogenic. Eggs are also good
sources of antioxidants known to protect the eye; therefore, increased plasma
concentrations of lutein and zeaxanthin in individuals consuming eggs are also
of interest, especially in those populations susceptible to developing macular
degeneration and eye cataracts.
SUMMARY: For these reasons, dietary recommendations aimed at restricting
egg consumption should not be generalized to include all individuals. We need
to acknowledge that diverse healthy populations experience no risk in
developing coronary heart disease by increasing their intake of cholesterol
but, in contrast, they may have multiple beneficial effects by the inclusion of
eggs in their regular diet. (2)
A
more recent paper which summarized presentations given at the 2011 Experimental
Biology meetings about the latest research and a paleoanthropological
perspective pertaining to the relationship between dietary cholesterol intake and
cardiovascular disease risk, further supported this connection.They reported that the United States
may be a bit more “reactive” to cholesterol than other countries:
It is
evident that the recommendations are less stringent than those made in the
United States (50). In fact, as noted, some countries have no recommendations
for dietary cholesterol. The European Union, Korea, India, Canada, and New
Zealand, among other countries, do not have a recommendation for cholesterol
intake in their dietary guidelines, based on several lines of evidence
including 1) the lack of effect of egg intake and CHD risk; 2) the consistent
increases observed in HDL-C under numerous dietary interventions that include
dietary cholesterol; 3) the formation of less atherogenic or protective
lipoproteins with egg consumption; and 4) the additional benefits of eggs for
memory and protection against macular degeneration. (3)
Why Did Some
Studies Report A Link to a Cholesterol-Rich Diet and Bad Outcomes?
So,
if this is true, why have we been bombarded with the media telling us to watch
our cholesterol intake? It may have been from some biased information. A 2005
study suggested that previous links to coronary heart disease and cholesterol
intake didn’t account for other factors in the diet that lead to poor health:
As early as
at the beginning of the last century, animal studies have pointed to a causal
role of dietary cholesterol in atherogenesis. In humans, however, most
observational studies have not provided convincing evidence for an impact of
cholesterol intake on coronary heart disease (CHD). Rather, these studies have
consistently established a close association between a certain eating pattern
and the risk of CHD. This eating pattern has usually been characterized by a
high intake of total fat, saturated fatty acids (SFA) and cholesterol, and a
low intake of fiber and polyunsaturated fatty acids (PUFA). In typical western
diets the amounts of total fat, SFA, and cholesterol are strongly correlated
with each other, while they are negatively related to the intake of fiber and
PUFA. Thus, it has not been possible to determine whether the association
between the above mentioned eating pattern and CHD is due to the high
consumption of SFA, cholesterol, both, or an insufficient supply of one or more
protective factors such as fiber or PUFA. As the consumption of eggs leads to a
high intake of cholesterol without necessarily resulting in high uptake levels
of SFA and total fat, several groups have tried to elucidate the effect of
cholesterol by investigating the relationship between the consumption of eggs
and the development of CHD. Based on these studies, the association between
dietary cholesterol and CHD risk is, if anything, minor in nature. This is
consistent with the finding that an increase in dietary cholesterol intake
results in only a minimal increase in the total/high-density lipoprotein
cholesterol ratio. Taken together these studies suggest that the association
between dietary cholesterol and CHD is small, as most subjects can effectively
adapt to higher levels of cholesterol intake. Nevertheless, lowering dietary
cholesterol content might reduce the risk of CHD considerably in a subgroup of
individuals who are highly responsive to changes in cholesterol intake.(4)
What About
the Risk OF NOT Eating Eggs?
This
abstract explores the detrimental effects of not including eggs, which include
the negative impact on cognitive health:
In the
1960s, the thesis that dietary cholesterol contributes to blood cholesterol and
heart disease risk was a rational conclusion based on the available science at
that time. Fifty years later the research evidence no longer supports this
hypothesis yet changing the dietary recommendation to limit dietary cholesterol
has been a slow and at times contentious process. The preponderance of the
clinical and epidemiological data accumulated since the original dietary
cholesterol restrictions were formulated indicate that: (1) dietary cholesterol
has a small effect on the plasma cholesterol levels with an increase in the
cholesterol content of the LDL particle and an increase in HDL cholesterol,
with little effect on the LDL:HDL ratio, a significant indicator of heart
disease risk, and (2) the lack of a significant relationship between
cholesterol intake and heart disease incidence reported from numerous
epidemiological surveys. Over the last decade, many countries and health
promotion groups have modified their dietary recommendations to reflect the
current evidence and to address a now recognised negative consequence of
ineffective dietary cholesterol restrictions (such as inadequate choline
intake). In contrast, health promotion groups in some countries appear to
suffer from cognitive dissonance and continue to promote an outdated and
potentially hazardous dietary recommendation based on an invalidated
hypothesis. This review evaluates the evidence for and against dietary
cholesterol restrictions and the potential consequences of such restrictions. (5)
So, What’s
the Take Home (On Eggs)?
1.
For most people, eating eggs could actually be beneficial for increasing “happier
and fluffier LDL” cholesterol, especially if not overdone.
2.
Eat organic, cage-free eggs or you could be getting inflammatory ratios of
unhealthy fats and exposure to pesticides and hormones that COULD raise
inflammation in your body and stress your heart.
3.
Test your numbers to look for true risk and other potential causes:
·A complete lipid panel that assesses for lipid particle size,
insulin resistance score, and inflammatory enzymes associated with cardiovascular
risk
- Genetic profiles, such as
ApoAE gene variations to assess if statins would be helpful based on one’s
ability to clear lipids - Inflammatory and nutritional
markers such as fibrinogen, homocysteine, hsCRP, and ferritin - Heavy metal burden
- Testosterone, thyroid, and
hormonal balance, including cortisol - Liver and kidney function
4.
Eat an organic, whole-food diet rich in fiber and plant foods containing
protective phytonutrients.
5.
Have fun with friends. Social isolation is a major risk factor for
cardiovascular mortality- the literal mind-body connection. (6-7)
So…gotta love the incredible, edible egg!
References:
(1) Dietary cholesterol and the risk of
cardiovascular disease in patients: a review of the Harvard Egg Study and other
data. Int J Clin Pract Suppl. 2009
Oct;(163):1-8, 28-36. doi: 10.1111/j.1742-1241.2009.02136.x.
(2) Dietary cholesterol provided by eggs and plasma
lipoproteins in healthy populations. Curr
Opin Clin Nutr Metab Care. 2006 Jan;9(1):8-12. PMID:16340654
(3) Exploring the Factors That Affect Blood
Cholesterol and Heart Disease Risk: Is Dietary Cholesterol as Bad for You as
History Leads Us to Believe? Adv Nutr.
Sep 2012; 3(5): 711-717. doi: 10.3945/an.111.001321
(4) Dietary cholesterol, atherosclerosis and
coronary heart disease. Handb Exp Pharmacol.
2005;(170):195-213.
(5)
Dietary cholesterol, heart disease risk and cognitive dissonance. Proc Nutr
Soc. 2014 May;73(2):161-6. doi: 10.1017/S0029665113003844. Epub 2014 Jan 9.
(6)
Erica C. Leifheit-Limson, et al. The
Role of Social Support in Health Status and Depressive Symptoms After Acute
Myocardial Infarction: Evidence for a Stronger Relationship Among Women. Circulation:
Cardiovascular Quality and Outcomes. 2010; 3: 143-150.
(7) Dean Ornish , MD. Love and Survival: The
Scientific Basis for the Healing Power of Intimacy. Harper Collins. New
York:NY. 1998.