E-Mail Edition Volume 14 Number 5
Published Winter, 2017
Published by Piccadilly Books, Ltd., www.piccadillybooks.com.
Bruce Fife, N.D., Publisher, www.coconutresearchcenter.org
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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.
The cholesterol hypothesis of heart disease states that the higher your
blood cholesterol, the greater your risk of cardiovascular disease. Some
proponents of this hypothesis have even gone so far as to claim that
high cholesterol not only increases the risk, but actually causes
cardiovascular disease. The cholesterol hypothesis was initially
proposed in the 1950s, and although it has been generally accepted, it
has never been proven.
Saturated fats have been criticized for decades as unhealthy because, in
general, they tend to increase blood cholesterol, which according to the
cholesterol hypothesis increases heart disease risk. The most common
argument against the use of coconut oil is that it is predominately a
saturated fat and; therefore, is said to have all of the adverse effects
associated with saturated fats.
However, in recent years a number of studies, including meta-analysis
studies that use the data from all appropriate previous studies, have
been published that exonerate saturated fats from any wrongdoing.1-4
These studies have shown that saturated fats do not increase the
risk of heart disease any more than other fats. In fact, some studies
have shown that saturated fats in comparison to polyunsaturated fats
actually reduce the risk of stroke—one of the major consequences of
Despite these new studies, some people are so entrenched by years of
warnings about the danger of saturated fats, that they find it hard to
accept. Many people have built their careers around the now outdated
cholesterol hypothesis of heart disease and are not willing to admit
they were wrong. Doctors, government officials, and educators who
receive funding from the drug industry ignore these studies and continue
to promote the cholesterol hypothesis and demonize saturated fats and
cholesterol as major threats to our health.
The food and drug industries use the cholesterol hypothesis as
justification for promoting certain products. The statin
cholesterol-lowering drugs, for example, are the most profitable drugs
of all time, earning the makers billions of dollars annually. Food
companies use this concept as a means to sell vegetable oils,
shortenings, and low-fat products as healthy alternatives to saturated
fat and cholesterol containing products.
Now that saturated fat and cholesterol have been shown not to promote
cardiovascular disease, these anti-saturated fat proponents are at a
great disadvantage, and they know it. They cannot win an argument based
on the available studies, although they may still try by using old,
In order to deceive the public and the healthcare community, the
pharmaceutical industry and its allies have taken a different approach.
Instead of using studies as their primary form of proof, they use the
“official” statements from organizations such as The American Heart
Association (AHA), The American Diabetes Association (ADA), The American
Cancer Society (ACS), and others. The assumption is that any statement
coming from these organizations must be accurate because it represents
the position or consensus of the members of these organizations, which
usually consists of physicians, researchers, and educators. Therefore,
it is assumed that any statement from these organizations represents the
most scientifically accurate position on the topic no matter how many
studies you can cite to the contrary, the organization’s position trumps
So, to back their position that saturated fats are harmful, they cite
the position of the AHA, ADA, ACS, and others. If they can get two or
three different organizations saying the same thing, their argument is
all that much more authoritative and unquestionable.
This may sound reasonable; however, there is one major flaw. These
organizations are notoriously biased towards their benefactors—the
businesses and industries that provide the majority of their funding.
Their positions are not based on science but rather on money (i.e.,
Recently the American Heart Association (AHA) published a report in the
journal Circulation that
basically gives the AHA’s position on saturated fats.6 The
authors call their report “A Presidential Advisory from the American
Heart Association.” The word “Presidential” is used as a means to make
the report appear to be more authoritative than it really is. In brief,
the article stated that saturated fats raise blood cholesterol, and high
cholesterol promotes heart disease. Therefore, they advise against the
use of saturated fats, including coconut oil, and recommend the use of
polyunsaturated vegetables oils as a healthier alternative. All of the
evidence given for their position was based on old, questionable
studies. None of the newer studies that superseded the older studies
were used. Also missing was the role sugar plays in cardiovascular
The AHA statement wasn’t anything new, it only
reiterated the AHA’s longstanding promotion of the cholesterol
hypothesis and the use of its backers products—cholesterol-lowering
drugs and polyunsaturated vegetable oils.
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
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.
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.
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.
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.
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.
Coke and Pepsi Influence the
Policies of Nonprofit Organizations
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.
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.
1. Aaron, DG, and Siegel, MB. Sponsorship of national health organizations by two major soda companies. AJPM 2017;52:20-30.
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.
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.
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
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.
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
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.
* The oleochemical industry uses fatty acids from vegetable and animal fats for various applications, such as polymers, surfactants, paints, coatings, engine lubricants, and others.
Figure 1. Chemical structure of saturated fatty acids and their % composition in coconut oil (Codex, 2015).
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.†
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
† 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).
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.
Figure 2. Fatty acid composition of various lipids: vegetable oils, animal fat, and human storage and structural lipids.
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
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 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).
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.
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.
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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