When my daughter was still in kindergarten, her pediatrician told us that her blood cholesterol was high, that she probably had a congenital predisposition to high cholesterol, and that we should begin early to modify her diet to moderate her risk of hert disease later in life.
Now my daughter is 28 and she asked me last week if she should be eating less chocolate and coconut to protect her long-term health. I knew enough to know that the answer to her question was a subject of deep controversy, and I didn’t know where I stood on the subject.
In my daughter’s honor, I am devoting this week and next to researching cholesterol and will report the results here. Here are some questions I set out to answer. (Please post comments suggesting your own).
- If your cholesterol is high because of diet, does this lead to increased risk of heart disease?
- If your cholesterol is high because of your genes, not diet, does this lead to an increased risk of heart disease?
- Does consumption of saturated fats lead to higher levels of blood cholesterol?
These questions are elementary and the legitimacy of watching and treating blood cholesterol levels depends on the answers. Assuming there is reason for “yes”, there are further questions:
- What foods contribute to high/low cholesterol levels?
- Are there supplements that help to lower cholesterol? If so, what is their effect on overall mortality risk?
- How does treatment with statins compare to treatment with diet and supplements?
It has been standard practice among doctors for the last 50 years at least to treat serum cholesterol levels as a risk factor for heart disease, and to assume that there is a causal connection. Half of Americans over 65 are taking prescription statin drugs (and ⅙ of people between 45 and 65) [ref]. It’s clear that statins lower cholesterol in the blood, but whether the drugs lower risk of heart disease is less clear, and there may be no benefit at all for overall mortality rate [ref].
The above questions are difficult because there is such a deep division of opinion in the medical community. The mainstream view, which has the best data and the best studies behind it, is also suspect, in my mind, because so much of the science has been funded by the pharmaceutical industry. Statin drugs are a $35 billion dollar industry in America, growing rapidly, and I have seen an estimate as high as $200 billion per year worldwide.
Differences in evaluations of statin drugs are stark
Here is a semi-popular report published by Harvard Medical School health blog. Peter Wehrwein notes that statin use is rising rapidly and heart disease deaths are falling rapidly.
A meta-analysis published in Journal of the American Medical Assoc (1997) concluded: “This overview of all published randomized trials of statin drugs demonstrates large reductions in cholesterol and clear evidence of benefit on stroke and total mortality. There was, as expected, a large and significant decrease in cardio-vascular mortality, but there was no significant evidence for any increases in either non-CV deaths or cancer incidence.”
A nutrition conference in Copenhagen (2010) produced the take-home message that every time an individual replaces 1% of the saturated fats in his diet with poly-unsaturated fats, his blood cholesterol decreases enough to afford a 2 to 3% reduction in risk of heart attack.
On the other side, here is the conclusion of a meta-study (2010) also published in the JAMA, pulling together results from 11 different studies over 40 years: “This literature-based meta-analysis did not find evidence for the benefit of statin therapy on all-cause mortality in a high-risk primary prevention set-up.” Dr Fred Kummerow, author of Cholesterol is not the Culprit, was featured by Dr Mercola this week. “Over the past 60 years, his research has repeatedly demonstrated that there’s NO correlation between high cholesterol and plaque formation that leads to heart disease Dr. Kummerow’s work shows that it’s not cholesterol that causes heart disease; rather it’s the trans fats and oxidized cholesterol that are to blame.”
Opposition to the standard hypothesis (saturated fats => High LDL => Stroke and heart attack) is not limited to the “natural medicine” community. It is broad and varied, some of it well-rooted in standard methodology of biochemistry and epidemiology.
“A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.” (2010)
I know of no other place in standard medical practice where the gulf between credible, opposing viewpoints is so vast. I will continue to read, and next week promise to report what I can about why the disagreements are so deep and the contradictions so stark.
Petroleum oils are simply chains of carbon atoms surrounded by hydrogen. Each C can make 4 bonds, so most of the C’s in the middle attach to one C on each side and two more H’s.
Organic oils and fats are “fatty acids”, which means that they differ from the simple chains by the addition of an “acid group” on the end. An acid group has two extra oxygen atoms, and is written COOH.
These are all saturated fats, meaning “as much hydrogen as the carbons can hold”. This makes more sense when we define an unsaturated fat as one that has double-bonded carbon atoms. Some C’s instead of being attached to 2 C’s and 2 H’s have only 1 H. They still have 4 bonds total, so they devote an extra bond to each other – a “double bond” between C’s.
Double bonds are more chemically reactive. It is easier to break the chain at a double bond than at another place along the chain where there are only single bonds, and so fats with double bonds are more easily oxidized during cooking than saturated fats. Unsaturated fats have a lower melting point, and are likely to be liquid at room temperature.
Omega 6 and omega 3: These designations refer to the location of the double bond. Omega 3 means that the 3rd bond is double, counting from the tail end, or omega end of the chain. (The COOH is the head or “alpha” end; the opposite end of the chain is the tail or “omega” end.)
Trans fat: Here’s a curious and useful fact from chemistry: the atoms in a molecule are always vibrating, wiggling and bouncing around. Part of this is rotation around each bond. Single bonds can rotate freely. But double bonds cannot rotate. This means that the double bonds create the possibility of two different forms of a molecule. The part of the chain on the right and the rest of the chain on the left of the double bond can be on the same side, creating a bent, V-shaped chain. This is the “cis” form. Or the two parts of the chain can be on opposite sides, so the double bond appears as just a kink in the chain, but not a bend. This is the “trans” form.
In nature, one finds mostly “cis” fats. Trans fats are mostly manufactured in food processing
This is a double bond in the “trans” configuration. There is no bend in the chain.
Trans fats have a little kink in the chain, but the chain is basically straight. “Cis” fats are V-shaped molecules with a bend in the middle.
Cholesterol is an essential, multi-purpose chemical, manufactured and used by every animal species and every cell within the animal. Cholesterol gives cell membranes their pliability, and it is also used as a raw material for synthesis of hormones within a cell.
The molecular structure is much more complicated than the fatty acids described above. It contains four linked rings of carbon atoms, and one OH group in the lower left corner, making it technically an alcohol.
Since cholesterol has very limited solubility in water, it is carried around in the blood by lipoprotein molecules that attach onto the cholesterol molecule at one end and dissolve in water at the other end. High density lipoproteins (HDL) are called “good cholesterol”, and low density lipoproteins (LDL) are called “bad cholesterol”, but whether this blood constituent is actually related to risk of heart disease remains in dispute.
This post originally appeared in Josh’s blog here: http://joshmitteldorf.scienceblog.com/2014/05/14/cholesterol-a-medical-controversy-i-background/