summarize: The balance of our diet is composed of fat—or rather fats, plural. Fat is
essential, but too much can be problematic both in terms of total energy
intake and also metabolically. It should be relatively straightforward, but
dietary fat has a sordid past that also creates a lot of confusion.
Fats have long had a bad rap, on two counts: their high caloric content
(9 kcal/g) and their role in raising LDL cholesterol and thus heart disease
risk. Like carbohydrates, fats are often labeled “good” or “bad” on the basis
of one’s tribal or political stripes; in actuality, of course, it’s not that black
and white. Fats have an important place in any diet, and therefore it’s
important to understand them.
While carbohydrates are primarily a source of fuel and amino acids are
primarily building blocks, fats are both. They are very efficient fuel for
oxidation (think: slow-burning logs) and also the building blocks for many of
our hormones (in the form of cholesterol) and cell membranes. Eating the
right mix of fats can help maintain metabolic balance, but it is also important
for the health of our brain, much of which is composed of fatty acids. On a
practical level, dietary fat also tends to leave one feeling more satiated than
many types of carbohydrates, especially when combined with protein.
There are (broadly) three types of fats: saturated fatty acids (SFA),
monounsaturated fatty acids (MUFA), and polyunsaturated fatty acids
(PUFA).
[*9] The differences between these have to do with differences in
their chemical structure; a “saturated” fat simply has more hydrogen atoms
attached to its carbon chain.
[*10] Within PUFA, we make one more important
distinction, which is to separate the omega-6 from the omega-3 variants (also
a chemical distinction having to do with the position of the first double bond).
We can further subdivide omega-3 PUFA into marine (EPA, DHA) and
nonmarine sources (ALA). Salmon and other oil-rich seafood provide the
former, nuts and flaxseed the latter.
The key thing to remember—and somehow this is almost always
overlooked—is that virtually no food belongs to just one group of fats. Olive
oil and safflower oil might be as close as you can get to a pure
monounsaturated fat, while palm and coconut oil might be as close as you can
get to a pure saturated fat, but all foods that contain fats typically contain all
three categories of fat: PUFA, MUFA, and SFA. Even a ribeye steak contains
a lot of monounsaturated fats.
So it’s not really possible or feasible to try to eliminate certain categories
of fatty acids from the diet entirely; instead, we try to tweak the ratios. The
default fat state of most of my patients (i.e., their baseline fat consumption
when they come to me) works out to about 30–40 percent each of MUFA
and SFA, and 20–30 percent PUFA—and within that PUFA group, they are
generally consuming about six to ten times more omega-6 than omega-3s and
usually scant amounts of EPA and DHA.
From our empirical observations and what I consider the most relevant
literature, which is less than perfect, we try to boost MUFA closer to 50–55
percent, while cutting SFA down to 15–20 percent and adjusting total PUFA
to fill the gap. We also boost EPA and DHA, those fatty acids that are likely
important to brain and cardiovascular health, with marine fat sources and/or
supplementation. We titrate the level of EPA and DHA in our patients’ diets
by measuring the amount of each found in the membranes of their red blood
cells (RBC), using a specialized but readily available blood test.
[*11] Our
target depends on a person’s APOE genotype and other risk factors for
neurodegenerative and cardiovascular disease, but for most patients the range
we look for is between 8 and 12 percent of RBC membrane composed of
EPA and DHA.
Putting all these changes into practice typically means eating more olive
oil and avocados and nuts, cutting back on (but not necessarily eliminating)
things like butter and lard, and reducing the omega-6-rich corn, soybean, and
sunflower oils—while also looking for ways to increase high-omega-3 marine
PUFAs from sources such as salmon and anchovies.
[*12]
But once again, this is where the SAD, our modern food environment,
comes in to complicate things. A hundred years ago, our ancestors would
have gotten all their fat from animals, in the form of butter, lard, and tallow,
and/or fruits, such as olives, coconuts, and avocados. They would have done
so mostly by consuming these foods in their relatively natural state, and
achieving a reasonable balance of fatty acids would have come fairly easily.
Over the course of the twentieth century, advances in food-processing
technology enabled us to chemically and mechanically extract oil from
vegetables and seeds that otherwise would have been impossible to get. These
new technologies suddenly allowed vast quantities of oils high in
polyunsaturated fats, such as corn and cottonseed oil (aka linoleic acid, a
PUFA), to flood into the food supply. Our per capita consumption of soybean
oil, for example, has increased over a thousand-fold since 1909; meanwhile,
studies have found that levels of linoleic acid found in human fat tissue have
also increased, by 136 percent over the last half century.
This industrial fat revolution also helped create trans fats, listed on
ingredient labels as “partially hydrogenated vegetable oils” (think: margarine),
which in turn helped enable the proliferation of the SAD, in part because they
allowed foods to remain shelf stable for longer periods. But trans fats also
contributed to atherosclerosis (by raising apoB) and have been banned by the
FDA.
It is tempting to indict this massive proliferation of soybean and other
seed oils as the dietary bad guy responsible for our obesity and metabolic
syndrome epidemic. Anything that goes up by a thousand-fold in the same
few decades in which our health goes to hell in a handbasket can’t be good,
right? Even just a few years ago, I used to think this was the case. But the
closer and closer I look at the data, the less and less sure I am that we can say
much in this regard.
In fact, the most comprehensive review of this topic, Polyunsaturated
Fatty Acids for the Primary and Secondary Prevention of Cardiovascular
Disease, published by the Cochrane Collaboration in 2018—a 422-page
summation of all relevant literature from forty-nine studies, randomizing over
twenty-four thousand patients—drew the following conclusion: “Increasing
PUFA probably makes little or no difference (neither benefit nor harm) to our
risk of death, and may make little or no difference to our risk of dying from
cardiovascular disease. However, increasing PUFA probably slightly reduces
our risk of heart disease events and of combined heart and stroke events
(moderate-quality evidence).”
Slight advantage to increasing PUFA, noted. A more recent publication by
the Cochrane Collaboration, published in 2020 as a 287-page treatise titled
Reduction in Saturated Fat Intake for Cardiovascular Disease, looked at
fifteen RCTs in over fifty-six thousand patients and found, among other
things, that “reducing dietary saturated fat reduced the risk of combined
cardiovascular events by 17%.” Interesting. But the same review also found
“little or no effect of reducing saturated fat on all-cause mortality or
cardiovascular mortality.” Furthermore, “There was little or no effect on
cancer mortality, cancer diagnoses, diabetes diagnosis, HDL cholesterol,
serum triglycerides or blood pressure, and small reductions in weight, serum
total cholesterol, LDL cholesterol and BMI.”
Slight disadvantage to saturated fats, but no observed effect on mortality.
Last, yet another recent review, published in late 2020, titled Total Dietary
Fat Intake, Fat Quality, and Health Outcomes: A Scoping Review of Systematic
Reviews of Prospective Studies, examined fifty-nine systematic reviews of
RCTs or prospective cohort studies and found “mainly no association of total
fat, monounsaturated fatty acid (MUFA), polyunsaturated fatty acid (PUFA),
and saturated fatty acid (SFA) with risk of chronic diseases.”
I could go on, but I think you get the point. The data are very unclear on
this question, at least at the population level. As we discussed in the
introduction to Medicine 3.0 and earlier in this chapter, any hope of using
broad insights from evidence-based medicine is bound to fail when it comes
to nutrition, because such population-level data cannot provide much value at
the individual level when the effect sizes are so small, as they clearly are here.
All Medicine 2.0 has to offer is broad contours: MUFA seems to be the
“best” fat of the bunch (based on PREDIMED and the Lyon Heart study),
and after that the meta-analyses suggest PUFA has a slight advantage over
SFA. But beyond that, we are on our own.
Medicine 3.0 asks, what is the “best” mix of fats for our patient? I use an
expanded lipid panel to keep track of how changes in fatty acid consumption
may affect my patients’ cholesterol synthesis and reabsorption, and their
overall lipid and inflammatory response. Subtle changes in fat intake,
particularly of saturated fats, can make a significant difference in lipid levels
in some people, as I have learned over and over again—but not in others.
Some people (like me)
[*13] can consume saturated fats with near impunity,
while others can hardly even look at a slice of bacon without their apoB
number jumping to the 90th percentile.
Medicine 2.0 says this proves that nobody should eat saturated fats,
period. Medicine 3.0 takes these data and says, “While it is obviously not
good that our patient’s apoB has gone up this much, it now presents us with a
choice: Should we consider medication to lower their apoB, or reduce their
intake of saturated fats? Or both?” There is no obvious or uniform answer
here, and addressing this not-too-uncommon situation comes down to a
judgment call.
In the final analysis, I tell my patients that on the basis of the least bad,
least ambiguous data available, MUFAs are probably the fat that should make
up most of our dietary fat mix, which means extra virgin olive oil and high-
MUFA vegetable oils. After that, it’s kind of a toss-up, and the actual ratio of
SFA and PUFA probably comes down to individual factors such as lipid
response and measured inflammation. Finally, unless they are eating a lot of
fatty fish, filling their coffers with marine omega-3 PUFA, they almost always
need to take EPA and DHA supplements in capsule or oil form.