E-Mail Edition Volume 14 Number 5 |
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Published Winter, 2017 Published by Piccadilly Books, Ltd., www.piccadillybooks.com. Bruce Fife, N.D., Publisher, www.coconutresearchcenter.org |
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Content
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Nonprofit Organizations and Conflict of Interest
The dietary advice from national health organizations that should be
looking out for our best interests are often the ones that are causing
us the greatest harm.
Nonprofit health organizations are generally formed to increase public
awareness and promote and fund research. Their marketing campaigns give
the impression that everything they do is for your benefit. Of course,
running these organizations takes money and they depend heavily on
donations from the public as well as from industries and the government.
Much of their focus is on fundraising. One of the major expenses
incurred by these organizations is the salaries, bonuses, and perks paid
to their directors and officers. The more money these organizations rake
in, the bigger the payout to those in charge. This has, unfortunately,
influenced the policies of these organizations, with an interest more on
profit than on public health. Instead of looking out for you, they are
concerned more with their financial security. Consequently, companies
that are heavy donors can have a great deal of influence in the
organizations’ policies. The pharmaceutical, biotech, and food
industries take advantage of this and are among the major benefactors of
these organizations. For this reason, you need to view health
recommendations from these organizations with some degree of skepticism.
According to the authors of the AHA article we should stop using coconut
oil and other saturated fats and cook our foods in canola, corn,
soybean, or olive oils and it is perfectly healthy to deep fry your
foods in these oils. This statement goes contrary to many studies that
have clearly shown that these vegetable oils degrade quickly forming
harmful free radicals that promote inflammation and premature aging.
Keep in mind that the AHA is the same organization that for years told
us to eat margarine and partially hydrogenated vegetable oils, which are
loaded with trans fats, calling them “more heart-healthy” than saturated
fats. We now know that trans fats promote heart disease more than any
other type of fat. They are so harmful that the FDA is set to ban trans
fats completely by 2018.7 |
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You may have noticed the “American Heart Association Heart Check” seal of approval on hundreds of packaged foods at the grocery store. Food manufacturers pay thousands of dollars (up to $7,500 per product) annually for the AHA’s endorsement. These products are supposedly approved by the AHA as heart healthy food choices. However, among them are some of the most unhealthy foods you could choose, such cold breakfast cereals (e.g., Trix, Cocoa Puffs, Lucky Charms, French Toast Crunch, etc.), Prego Heart Smart sauces, candied yams, and processed lunch meats, which are loaded with sugar as well as trans fats, MSG, preservatives, and other questionable ingredients. Although the AHA no longer recommends partially hydrogenated vegetable oils (the source of trans fats), |
The American Heart Association Heart
Check seal of approval. |
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such as margarine, they still, however, give their seal of approval to
products containing trans fats. To call sugary breakfast cereals heart
healthy is a stretch of the imagination, especially since sugar is now
recognized as a major cause of heart disease.8 The Heart
Check seal brings in millions of dollars in revenue to the AHA. It
provides a way for food manufacturer’s to funnel money to the AHA
without looking like they are buying favors. |
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The American Heart Association promotes these products as health
foods.
The AHA considers Lucky Charms to be a healthy breakfast,
primarily because it is low in saturated fat and cholesterol. It looks
more like candy.
Look at the ingredient label. Not much real nutrition here. It is
mostly sugar. Of the first seven ingredients, three are sugars and
three are refined starches, which are quickly turned into sugar as
soon as they are consumed. Note that there are 10 grams of sugar in ¾
cup of cereal, which is about half a bowl. A typical serving (1 bowl)
supplies 20 grams of sugar. That’s equivalent to 5 tablespoons of
sugar along with 5 grams of starch and a hefty dose of artificial
colors, flavors, and preservatives!
The AHA would rather have you eat Trix
breakfast cereal than real food like coconuts.
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In addition, to the money they get from their Heart Check seal of
approval, they accept millions of dollars a year in donations from
such companies as Kellogg’s, PepsiCo, Nestle, Mars, Kraft, and
Domino’s Pizza. When you think of sources of nutritious foods, these
brands come in at the bottom of the pack.
References
1. Chowdhury, R., et al. Association of dietary, circulating, and
supplement fatty acids with coronary risk: a systematic review and
meta-analysis. Ann Intern Med 2014;160;398-406.
2 .Ramsden, CE and Zamora, D. Use of dietary linoleic acid for
secondary prevention of coronary heart disease and death: evaluation
of recovered data from the Sydney Diet Heart Study and updated
meta-analysis. BMJ 2013;346:e8707.
3. Micha, R and Mozaffarian, D. Saturated fat and cardiometabolic risk
factors, coronary heart disease, stroke and diabetes: a fresh look at
the evidence. Lipids 2010;45:893-905.
4. Siri-Tarino, PW, et al. Meta-analysis of prospective cohort studies
evaluating the association of saturated fat with cardiovascular
disease. Am J Clin Nutr 2010;91:535-546.
5. Gillman, MW, et al. Inverse association of dietary fat with
development of ischemic stroke in men. JAMA 1997;278:2145-2150.
6. Dietary fats and cardiovascular disease. Circulation
2017;135:00-00. 7.https://www.fda.gov/food/ingredientspackaginglabeling/
foodadditivesingredients/ ucm449162.htm.
8.
https://www.health.harvard.edu/blog/eating-too-much-added-sugar-increases-the-risk-of-dying-with-heart-disease-201402067021.
9.
http://www.newsweek.com/should-kids-take-statins-fight-cholesterol-92925.
10. http://time.com/120958/who-really-needs-to-take-a-statin/.
11.
http://unitehere.org/wp-content/uploads/AHA-Industry-Contribs_FINAL.pdf.
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Coke and Pepsi Influence the
Policies of Nonprofit Organizations
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Big businesses like Coca-Cola and PepsiCo give
millions of dollars to health organizations in an effort to appear that
they are socially responsible corporate citizens, but then turn around
and lobby vigorously against public health measures that would better
our health. This is not just a public relations gimmick; it is a part of
their marketing strategy. Many health organizations that originally
supported public health measures to reduce Americans’ soda intake,
suddenly changed their minds once they began receiving “donations” from
these industries. Over a five year period Coca-Cola, PepsiCo, and the
American Beverage Association have given millions of dollars to nearly
100 prominent health organizations. |
Storyblocks.com |
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These findings
are revealed
in a study published by the
American Journal of Preventive Medicine. The study documents the
beverage industry’s deep financial ties to the health community as part
of a strategy to silence health critics and gain unlikely allies against
soda regulations.
The study’s authors, Michael Siegel, a professor at
the Boston University school of public health, and Daniel Aaron, a
student at Boston University’s medical school, scoured public records
including news releases, newspaper databases, lobbying reports, the
medical literature and information released by the beverage giants
themselves. While some of the incidents cited in the study have been
reported by the media, this report is the first to take a comprehensive
look at the beverage industry’s strategy of donating to health
organizations while at the same time lobbying against public health
measures. The study tracked industry donations and lobbying spending
from 2011 through 2015, at a time when many cities were considering
imposing soda taxes or other regulations to combat obesity and diabetes.
“We wanted
to look at what these companies really stand for,” said Aaron, the
study’s co-author. “And it looks like they are not helping public health
at all — in fact, they’re opposing it almost across the board, which
calls these sponsorships into question.”
Aaron said that the industry donations create
“clear-cut conflicts of interest” for the health groups that accepted
them. The report found a number of instances in which influential health
organizations accepted beverage industry donations and then suddenly
backed away from supporting soda taxes or remained noticeably silent
about the initiatives.
In one instance cited in the study, the nonprofit
group Save the Children, which had actively supported soda tax campaigns
in several states, abruptly withdrew its support in 2010.
The group was
a leader in the push to tax sweetened soft drinks
as a way to combat childhood obesity and supported soda tax campaigns in
several states. However, in 2010 it accepted a $5 million grant from
Pepsi and was actively seeking an equally lucrative grant from Coke to
“help pay for its health and education programs for children”.
Save the Children surprised activists around the
country when it announced that it would no longer support efforts to tax
soft drinks. Carolyn Miles, the chief operating office of the
organization, said there was no connection between the group’s
about-face on soda taxes and the grants from Coke and Pepsi, both of
which fiercely opposed the soda taxes. Miles said that after taking part
in campaigns against soda taxes, they reviewed the issue and decided it
was too controversial to continue and that their decision was unrelated
to any corporate support they had received.2
Decisions like this make one wonder if these
nonprofit organizations are interested more in profit than in their
proclaimed cause. It appears that the cause really doesn’t matter that
much, it is simply a means, an excuse, to raise money to enrich
themselves.
When New York proposed a ban on extra-large sodas
in 2012, the Academy of Nutrition and Dietetics encouraged consumers to
be aware of how all beverages fit into their healthful daily eating plan
and expressed its support for strategies designed to encourage people to
make healthful food choices.3 Soon thereafter the academy
accepted $875,000 in donations from Coke. That was enough to silence
them and the organization said no more on the issue.
All of the major health organizations that could
influence public opinion regarding the consumption of soft drinks and
sugar seem to receive donations from the beverage industry. The American
Diabetes Association accepted $140,000 from the Coke between 2012 and
2014. The American Heart Association received more than $400,000 from
the company between 2010 and 2015. And the National Institutes of Health
received nearly $2 million from them between 2010 and 2014. It is no
wonder why these organizations are not more vocal in warning consumers
about the dangers of over consuming sugar and sugary beverages.
From 2011 to 2015, Coke spent on average more than
$6 million per year lobbying against public health measures aimed at
curbing soda consumption. Pepsi spent about $3 million per year during
that period, and the American Beverage Association spent more than $1
million each year.
In 2009 alone, when the government proposed a
federal soda tax to curb obesity that would help finance health care
reform, Coke, Pepsi and the American Beverage Association spent a
combined $38 million lobbying against the measure, which ultimately
failed.
The growing awareness that sugary drinks are
unhealthy is troubling to the beverage industry. Over the past two
decades consumption of sugar sweetened sodas has dropped in the US by 25
percent. In 2015 Coke tried to change that perception by initiating a
campaign to convince people that sugar is not the cause of obesity, it
is consumers’ lack of willpower to control their calorie intake combined
with their lack of exercise that is the real problem. If you limit total
calorie intake, primarily by eating a low-fat diet, and burn off
calories by exercising more, it doesn’t matter what you eat. It’s all
about calories. You can enjoy all the sugary drinks you want without
fear. This strategy is not new, this idea has been promoted by all the
major health organizations for years. The only problem is that it
doesn’t work! You cannot exercise your way out of a bad diet.4-5
To provide the
scientific evidence to support their new campaign Coke paid for
scientific research to downplay the link between sugary drinks and
obesity. They commissioned scientists to advance their message in
medical journals, at conferences, and through social media. To help get
the word out, Coke even created their own nonprofit organization to push
their agenda called the Global Energy Balance Network.6 This
organization was set up to act as a third party, giving the appearance
it was independent of industry influence and control. Its only purpose
was to promote the argument that calorie intake and exercise are the
primary factors that contribute to obesity and diabetes, and that types
of foods (meaning sugar) are unimportant.
Professors and
researchers from respected universities were recruited to run the new
organization to give it academic and authoritative clout comparable to
the American Heart Association and other national health organizations.
The founding members of the new organization included James O. Hill, a
professor at the University of Colorado School of Medicine, Steven N.
Blair, a professor at the University of South Carolina, and Gregory A.
Hand, dean of the West Virginia University School of Public Health. Coke
donated $1.5 million to these people to start the organization.
The networks’
website, gebn.org, is registered to Coca-Cola, and the company is also
listed as the site’s administrator. The organization’s president, James
O. Hill explains that Coke offered to do these things because the
network’s members didn’t know how. But he was quick to state, “They’re
not running the show. We’re running the show.” Of course he would say
that or the whole credibility of the organization would be ruined.
The Global
Energy Balance Network isn’t the only health organization that has been
established through industry’s backing, there are others, but they work
hard to hide their affiliations. Once the network’s connection with Coke
became public the backlash from impartial scientists was so great the
organization lost its credibility. Many other researchers stepped
forward to denounce the organization as simply a front to promote Coke’s
agenda. Embarrassed that the fraud had been exposed, Coke pulled its
funding and the network disappeared.
From 2010 to
2015 Coke spent more than $120 million on academic research and
partnerships with health organizations in an attempt to shape public
opinion, divert attention away from the real causes of obesity and
diabetes, create confusion among academics, and influence public policy
makers.7
What is really
troubling is that Coke isn’t the only company that is doing this. Pepsi,
Mars, Nestle, Kraft, and other major food companies as well as
pharmaceutical and biotech companies are all doing the same thing, some
of them laying out even more money to influence research and public and
medical opinion. By accepting funding from these companies, health
organizations are inadvertently becoming participants in their
marketing plans.
References
1. Aaron, DG, and Siegel, MB. Sponsorship of national health
organizations by two major soda companies. AJPM 2017;52:20-30.
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Study Says It’s Inflammation, Not Cholesterol, that Causes Heart Disease
For years blood cholesterol levels were used as
the primary indicator of heart disease risk. The belief was that the
higher your cholesterol levels, the more likely it is for the
cholesterol to attach itself to the artery walls, blocking the artery
and causing atherosclerosis, leading to a heart attack or stroke. For
this reason, much effort has been spent on reducing cholesterol levels
through diet and drug therapies. Despite success in reducing blood
cholesterol, heart attacks and strokes are still among our greatest
health concerns. Reference 1. Ridker, PM, et al. Antiinflammatory therapy
with canakinumab for atherosclerotic disease. N Engl J Med
2017;377:1119-1131. 2. Zakaric, ZA, et al. In vivo antinociceptive
and anti-inflammatory activities of dried and fermented processed virgin
coconut oil. Med Princ Pract 2011;20:231-236. 3. Intahphuak, S., et al. Anti-inflammatory,
analgesic, and antipyretic activities of virgin coconut oil. Pharm Biol
2010;48:151-157 4. Kain, V, et al. Excess omega-6 fatty acids
influx in aging drives metabolic dysregulation, electrocardiographic
alterations and low-grad chronic inflammation. Am J Physiol Heart Circ
Physiol 2017 Oct 6:ajpheart.00297.2017. 5. Neuhofer, A, et al. An accelerated mouse model for atherosclerosis and adopose tissue inflammation. Cardiovasc Diabetol 2014 Jan 17;13:23.
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A Half-Truth is
Not the Whole Truth: The AHA Position on Saturated Fat
Dr. Fabian M. Dayrit
Professor, Ateneo de Manila University, Philippines
Chairman, Scientific Advisory Committee for Health, Asian and Pacific
Coconut Community
Abstract
This second in this series of papers will present the biases in
the American Heart Association’s, (AHA) 2017 Presidential Advisory with
respect to saturated fat. Although important differences in the
metabolic properties of specific SFA have been known since the 1960s,
the AHA still considers all SFA as one group having the same properties.
There is abundant research available that supports the designation of C6
to C12 fatty acids as medium-chain fatty acids (MCFA). This is
particularly relevant to coconut oil, which is made up of about 65%
MCFA. Ignoring the evidence, AHA simply labels coconut oil as SFA. The
AHA promotes half-truths, not the whole truth. |
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Abbreviations: AHA: American Heart Association; CHD: coronary heart disease; CVD: cardiovascular disease; HDL: high-density lipoprotein; LCFA: long-chain fatty acid; LDL: low-density lipoprotein; MCFA: medium-chain fatty acid; MCT: medium-chain triglyceride; oxLDL: oxidized low-density lipoprotein; PUFA: polyunsaturated fatty acid; oxLDL: oxidized low-density lipoprotein;
SFA: saturated fatty acid
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Introduction On June 16, 2017,
the American Heart Association issued its AHA Presidential Advisory
which repeated its recommendation to “shift from saturated to
unsaturated fats” (Sacks et al., 2017). While this advisory did not
present any new data, it provided a re-analysis of old data which
selectively rejected some studies which it claims did not satisfy
“rigorous criteria for causality,” while reinforcing those which were
favorable to its conclusions.
The first paper in this series (Dayrit,
2017) showed that the scientific basis upon which the AHA made its
recommendations is flawed and the
Dietary Guidelines for Americans,
which has been recommending a low-saturated fat diet for 35 years, has
made Americans obese even as heart disease – the supposed concern of the
AHA – has remained the top health problem. This second article will focus on “saturated
fatty acids,” the fat that AHA wants us to minimize. This article will
analyze the 2017 AHA Presidential Advisory and provide counter evidence
from the scientific literature, including clinical studies, to show that
much of the confusion that we have today regarding the role of these
fats in a healthy diet stems from the selective use of scientific
information regarding saturated fat. The 2017 AHA Presidential Advisory
provided only half the truth on saturated fat.
SFA, MCFA and LCFA Saturated fatty
acids (SFAs) generally refer to the following linear carboxylic acids:
caproic (C5H11CO2H, C6), caprylic (C7H15CO2H, C8), capric (C9H19CO2H,
C10), lauric (C11H23CO2H, C12), myristic (C13H27CO2H, C14), palmitic
(C15H31CO2H, C16:0), and stearic (C17H35CO2H; C18:0). SFAs share the
same structural features, but differ in their molecular size. Figure 1
shows their chemical structure and their % composition in coconut oil.
Because of the apparent similarity in their chemical structures, SFAs
are often assumed to possess the same biochemical and physiological
properties. This is not true. Coconut oil is an
important chemical feedstock for the oleochemical industry*.
It is hydrolyzed and separated into its individual fatty acids. Lauric
acid (C12), the main component of coconut oil, has the highest
commercial value and is used in the manufacture of various surfactants.
There was a need to find applications for the other fatty acids. In the
1960s, a new synthetic group of fats was developed – “medium-chain
triglyceride” (MCT) – which was made up mainly of C8 and C10. This
commercial mixture was later called “MCT oil” and the main component
fatty acids, C8 and C10, were called “medium-chain fatty acids” (MCFA).
Initial feeding studies on rats showed that MCT oil was non-toxic and
did not lead to weight gain compared with lard (Senior, 1968). Human
clinical trials later showed that MCT oil was useful for patients with
lipid disorders and for weight loss and it became commercially available
in the mid-1960s (Harkins & Sarett, 1968). Since then, MCT oil has been
widely used in clinical practice as a special dietary oil and has been
classified by the US FDA as GRAS (generally recognized as safe) (FDA,
2012). Because of its wide commercial availability and safety, medical
researchers use MCT oil in their research. Consequently, most medical
researchers consider MCFA to include C8 and C10 only; by exclusion, they
use the term “long-chain” fatty acids (LCFA) to mean the longer SFAs,
C12 and longer.
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*
The oleochemical industry uses fatty acids from vegetable and animal
fats for various applications, such as polymers, surfactants, paints,
coatings, engine lubricants, and others. |
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Figure 1. Chemical structure of
saturated fatty acids and their % composition in coconut oil (Codex,
2015). |
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This historical account clearly shows that the
classification of MCFA as C8 and C10 was based on the commercial
availability of MCT oil and not on scientific considerations, and its
wide use in clinical research reinforced this. However, based on
biochemical and physiological properties, the classification of MCFA
should include the fatty acids from C6 to C12.† Numerous
researchers consider MCFAs to include the fatty acids from C6 to C12
based on their metabolic properties (Bach & Babayan, 1982; St. Onge &
Jones, 2002; McCarty & DiNicolantonio, 2016; Schonfeld & Wojtczak, 2016;
TMIC, 2017). MCFAs possess special properties that differentiate them
from LCFAs. This section will highlight some of the special
characteristics of MCFAs in general, and C12 in particular, will show
why using only the single category of “saturated fatty acid” is a
half-truth.
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† It is relevant to
mention here that commercial products with a composition that includes
C6 to C12 are now available for special dietary purposes, such as a
ketone diet (see later). |
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SFAs in
various fats and oils All biological organisms and cells utilize
different fatty acids to produce lipids that are characteristic of the
organism and cell type to fulfill its structural or functional
requirements. The fatty acid profiles of the various vegetable oils are
characteristic of the plant source (Codex, 2015). Coconut oil has a
characteristic fatty acid profile that differs from other vegetable oils
in terms of its fatty acid profile: almost 50% is C12, about 65% is C6
to C12, and 92% is saturated. In contrast, the fatty acid profiles of
all other vegetable oils start mainly with C16 and contain a significant
proportion of unsaturated fatty acids. For example, soybean oil and corn
oil both contain over 50% C18:2 (linoleic acid, an omega-6 fatty acid)
and over 80% total unsaturated fat. Even animal fats, such as beef fat
and lard, contain a substantial amount of unsaturated fat. For example,
both beef fat and lard contain about 60% total unsaturated fatty acids
even though these are often referred to as “saturated fat”. Clearly, the
fatty acid composition of coconut oil is very different from those of
animal fats, including butter (Figure 2).
Another feature
that sets the group of MCFAs (C6 to C12) apart is that they are not
generally present in human abdominal fat and liver fat, and they are not
constituents of serum lipids, whether as triglycerides or phospholipids.
Analysis of fats in the liver using mass spectral imaging analysis did
not detect any MCFA; the smallest fatty acid found was C14 (Debois et
al., 2009). This is consistent with the claims that MCFAs (C6 to C12)
comprise a separate category from LCFA and that the use of “SFA” as a
common label for this group is incomplete. |
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Figure 2. Fatty acid composition of
various lipids: vegetable oils, animal fat, and human storage and
structural lipids. |
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Another distinguishing characteristic of the
group of MCFA (C6 to C12) is that they are rarely found attached to
cholesterol as fatty acid ester derivatives. Plasma cholesterol is
attached to long chain saturated and unsaturated fatty acid esters, in
particular C16:0, C18:0, C18:1, C18:2, and C20:4 (AOCS, 2014). That is,
LCFA and PUFA are involved with the circulation of cholesterol around
the blood stream and cholesterol deposited in arterial plaques, not
MCFA.
Metabolic properties of SFAs The metabolic
properties of the various SFAs clearly show differences between MCFA and
LCFA. Here, we describe three major steps: first, lipase hydrolysis to
release the free fatty acid; second, transport of the free fatty acid
across the membrane to enter the cell; and third, mitochondrial
oxidation to produce energy. The first step
involves the release of fatty acids from the triglyceride, a process
called hydrolysis. In a study of various triglycerides using rat
pancreatic lipase, C12 was found to be released most rapidly, followed
by C4 (butyrate) (Mattson & Volpenhein, 1969). The second
limiting step in the metabolism of SFAs is the rate at which it can
cross the membranes of cells where they can be metabolized. MCFA can
cross the membrane rapidly while LCFA and PUFA require carnitine
(Bremer, 1983; Schafer et al., 1997; Hamilton, 1998). The third step is
fatty acid oxidation. In human liver mitochondria, C12 is more rapidly
and completely oxidized compared with C18 (DeLany et al., 2000). This is
one reason why coconut oil is not fattening and is better for metabolic
energy than other vegetable oils. Thus, a detailed
accounting of the steps in the metabolism of SFAs shows that their
properties and behavior are not the same. MCFA (C6 to C12) are clearly
different from LCFA (C14 and longer).
Ketogenesis Ketogenesis
refers to the production of ketone bodies (KBs) – beta-hydroxybutyrate
(BHB), acetoacetate (Acac) and acetone – from the metabolism of fat
mainly in the liver. Ketone bodies are energy-rich molecules that are
released by the liver into circulation to be used by other tissues and
organs, such as the heart, brain and muscles (Krebs, 1970; Liu, 2008).
This is the basis for the ketogenic diet. There are three
ways of inducing ketogenesis: first, by ingestion of MCFAs; second, by
taking a very high-fat diet (greater than 80%) using on a long-chain
vegetable oil, such as corn oil or soybean oil (Akkaoui 2009); and
third, by fasting. Upon ingestion
and entering the small intestine, fatty acids are channeled either to
the portal vein going directly to the liver, or are repackaged into
other lipid bodies (called chylomicrons) to enter the bloodstream. MCFAs
pass directly through the portal vein to the liver where they are
converted into ketone bodies. Thus, MCFAs provide the most convenient
and rapid way of producing ketone bodies. LCFAs and PUFAs are packaged
into chylomicrons and are bound to cholesterol and circulate around the
bloodstream after which they are deposited in the liver (Bach & Babayan,
1982).
The unique properties of C12 C12 has special
properties that are not shared even by other MCFAs: its distribution in
the small intestine is variable; and it has strong antimicrobial
properties.
Distribution in intestine
C12 is unique because
its distribution between the portal vein and lymphatic system depends on
the feeding condition (You et al., 2008). Under normal conditions, most
of the C12 is channeled to the portal vein. However, a concentrated
injection of C12 has been shown to distribute about half to the portal
vein and half to the lymphatic system (Sigalet et al., 1997). Ingestion
of C12 together with proteins may direct more C12 to the lymphatic
system (Schonfeld & Wojtczak, 2016)
(Figure 3). This special behavior of C12 was foretold as early as the
1950s, when some researchers suggested the additional categories of
“intermediate-chain fatty acids” (Schon et al., 1955; Goransson, 1965;
Knox et al., 2000), and “transition fatty acid” (You et al., 2008). |
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Figure 3. Hydrolysis of triglycerides
and distribution of various fatty acids between the portal vein and
bloodstream. Depending on the dietary condition, C12 can be distributed
to both in varying amounts. |
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Antimicrobial properties C12 is recognized
as the most effective antimicrobial fatty acid. C12 and its
monoglyceride, monolaurin, have significant antimicrobial activity
against gram positive bacteria and a number of fungi and viruses.
Considering its antimicrobial property, it is an important property that
some C12 can enter the bloodstream to provide antimicrobial protection.
Because C12 and monolaurin are non-toxic and inexpensive, many food and
cosmetic products use these compounds as antimicrobial agents.
Interestingly, some antimicrobial natural products have been discovered
that have a C12 group attached. Other MCFAs, C8 and C10, have limited
antimicrobial activity; LCFAs have very little, if any, antimicrobial
activity (Dayrit, 2015). To summarize the discussion thus far: MCFA (C6
to C12) have very different biochemical and physiological properties
from LCFA (C14 to C18). However, not once did the 2017 AHA Presidential
Advisory refer to the existence of MCFA and LCFA and simply used the
general category of SFA. This is not scientifically justifiable,
and for a scientific society like the AHA, this is inexcusable.
“Saturated fat” and “animal fat” in the scientific literature The vast majority
of epidemiological studies, starting from Ancel Keys (1957) to the
present, have failed to distinguish MCFA and LCFA and make their
conclusions using the gross category of SFA. Unlike PUFAs, which are
differentiated as omega-6 and omega-3, most epidemiologists, except
those who study coconut oil in the diet, ignore the differences between
MCFA and LCFA. In fact, most doctors and nutritionists commit the error
of lumping animal fats and coconut oil into one category. Is it any
wonder then that the wrong dietary advice has been made for coconut oil
and C12? There are,
however, a few papers that have specifically addressed C12. In 2003,
Mensink and co-workers combined the results of 60 controlled trials into
a single analysis (called a meta-analysis) and calculated the effects of
the amount and type of fat on the ratio of total cholesterol to HDL
(high-density lipoprotein), as well as to lipids. They reported that C12
increased HDL so that the net effect was to decrease the ratio of total
cholesterol to HDL, a beneficial result. On the other hand, the LCFAs
C14 and C16:0 had little effect on the ratio, while C18:0 reduced the
ratio slightly. This is certainly a favorable result for C12.
Interestingly,
the 2017 AHA Presidential Advisory also disposed of the beneficial
properties of HDL without adequate proof, proclaiming that now CHD would
be all about LDL: "...changes in HDL-cholesterol caused by diet or drug
treatments can no longer be directly linked to changes in CVD, and
therefore, the LDL-cholesterol-raising effect should be considered on
its own." Since HDL is
generally considered a standard lipid indicator, it is incumbent upon
the AHA to provide definitive evidence to support its claim that HDL is
now useless as a predictor of CHD. Today, several types of LDL particles are
known. LDL particles can be small and dense LDL (sdLDL) or large and
buoyant (lbLDL). sdLDL is more susceptible to oxidation producing
oxidized LDL (oxLDL). Thus sdLDL is more atherogenic and has been shown
to be a strong predictor of CHD, while large buoyant LDL is not
(Toft-Petersen et al., 2011; Hoogeveen et al., 2014). In a 10-year
study in Finland on 1,250 subjects, the various types of lipoproteins –
LDL, HDL, and oxLDL – were measured. The study concluded that oxLDL, in
proportion to LDL and HDL, was a strong risk factor of all-cause
mortality independent of confounding factors (Linna et al., 2012).
Furthermore, it has also been reported that the ratio of triglyceride to
HDL is also a predictor for coronary disease (da Luz et al., 2008). If
this is the case, HDL should remain an important lipid parameter,
contrary to the AHA proclamation. In the case of
LDL, the absence of data on sdLDL and oxLDL in early studies involving
LDL measurements makes their conclusions questionable. Correlations
which have been made between LDL and CHD cannot therefore be considered
reliable.
Conclusion
The warnings against saturated fat started
with Ancel Keys. Keys never showed any appreciation for the physiologic
differences between medium-chain fat and long-chain fat. The AHA has
adopted this position to ignore the distinction between MCFA and LCFA
despite numerous advances in their science. Detailed comparison of the
fatty acid composition shows that coconut oil is very different from
animal fat and studies that assume that they are similar are therefore
in error. These may be one of the reasons why the Dietary Guidelines
have not worked. To this
conclusion, we can apply the warning that Benjamin Franklin once made:
“Half a truth is
often a great lie.”
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