Wissenschaftliche Hintergrundinformationen zur Ernährung mit Kokosfett

Hier finden Sie ganzheitliche und vollständige Informationen zum Kokosfett von einer der besten Gesundheits-Websites:
https://www.zentrum-der-gesundheit.de/tags,kokosoel.html

Kokosöl bringt dem Gehirn mehr Energie

Quelle: Zentrum der Gesundheit, aktualisiert: 04.07.2018

Steve Newport ist wohl das bekannteste Beispiel dafür, dass Kokosöl in der Lage ist die menschliche Gehirnfunktion zu verbessern und sogar die Symptome von Alzheimer zu lindern. Doch was passiert da genau in unserem Gehirn? Auch die Wissenschaft hat sich ausgiebig damit beschäftigt, was diese positiven Effekte des Kokosöls ausmachen könnte.

Inhaltsverzeichnis

  • Kokosöl bei Alzheimer
  • Energiemangel im Gehirn
  • Energiequelle Glukose
  • Hoher Blutzucker tötet Nerven
  • Alternative Energie fürs Gehirn
  • Besondere Fette im Kokosöl
  • Kokosöl liefert Ketone zur Energiegewinnung
  • Kokosöl und die Omega-3 Verfügbarkeit
  • Kokosöl gegen Plaque?
  • Wie viel Kokosöl ist gut für mich?
  • Weitere interessante Informationen zum Kokosöl

Kokosöl bei Alzheimer

Steve Newport hat es geschafft, mit Hilfe von Kokosöl gegen seine Alzheimer-Erkrankung anzukämpfen. Die tägliche Einnahme von Kokosöl führte dazu, dass sich seine schweren Symptome deutlich zurückbildeten. Scheinbar verleiht Kokosöl dem Gehirn neue Energie, wodurch seine Funktionsfähigkeit wieder aktiviert werden kann.
Die bemerkenswerte Geschichte von Steve Newport können Sie hier nachlesen.

Energiemangel im Gehirn

Das menschliche Gehirn benötigt permanent ausreichend Energie, um seine komplexen Aktivitäten verrichten zu können. Wird diese konstante Energieversorgung unterbrochen, beginnen die Gehirnzellen langsam abzusterben.
Kurzfristig kann die Unterversorgung des Gehirns zu Symptomen wie Kopfschmerzen, kognitiven Dysfunktionen und Müdigkeit führen. Leidet das Gehirn jedoch langfristig unter einem Energiemangel, können sich schwere neurodegenerative Erkrankungen einstellen. Zu den bekanntesten dieser Art zählen der Morbus Alzheimer und der Morbus Parkinson.

Energiequelle Glukose

Um einem Energiemangel entgegenzuwirken, ist unser Gehirn auf die ausreichende Versorgung mit Glukose angewiesen. Sie gelangt normalerweise über das Blut ins Gehirn und wird dort mit Hilfe eines speziellen Hormons, dem Insulin, in die Gehirnzellen geschleust, wo die dort ansässigen Mitochondrien die Glukose schliesslich in Energie umwandeln.
Dieser natürliche Ablauf funktioniert jedoch bei vielen neurodegenerativen Leiden nicht mehr, da die Nervenzellen in bestimmten Regionen des Gehirns bereits insulinresistent geworden sind. Das hat zur Folge, dass diese Hirnzellen nun nicht mehr in der Lage sind, die vorhandene Glukose aufzunehmen. Es kommt zu einem anhaltenden Energiemangel.

Hoher Blutzucker tötet Nerven

Insulinresistente Hirnzellen bergen darüber hinaus noch eine weitere Gefahr, denn die nicht aufgenommene Glukose verbleibt im Gehirn und erhöht dort den Blutzuckerspiegel. Ein hoher Blutzucker-Wert wirkt jedoch toxisch auf die Nerven, da sich der Blutzucker mit bestimmten Proteinmolekülen verbindet und so genannte Advanced Glycation End-Products (AGEs) bilden kann.
Diese AGEs erhöhen auf dramatische Weise den oxidativen Stress im Körper, was zur Bildung freier Radikale führt, die das Nervengewerbe angreifen und beschädigen.
Auf diese Weise wird das Absterben von Zellen im Gehirn enorm begünstigt. [Quelle 1 ; Quelle 2]

Alternative Energie fürs Gehirn

Würde es nun gelingen, den unterversorgten Zellen wieder ausreichend Energie zuzuführen, könnte das Problem behoben und ihr Absterben verhindert werden. Je nach Stadium der Erkrankung würde deren Verlauf zumindest deutlich verlangsamt. Im besten Fall könnte die Entwicklung der Erkrankung gar verhindert werden.
Doch hat das Gehirn überhaupt eine Chance, trotz insulinresistenter Zellen, an die überlebenswichtige Energie zu gelangen?
Die Antwort lautet: Ja, denn es gibt tatsächlich eine alternative Energiequelle für das Gehirn. Hierbei handelt es sich um spezielle Fettsäuren, die das Gehirn ebenso wie Glukose mit Energie versorgen können, ohne auf Insulinrezeptoren angewiesen zu sein.
Und genau diese Fettsäuren liefert das Kokosöl.

Besondere Fette im Kokosöl

Neben der Muttermilch ist Kokosöl die beste natürliche Quelle für so genannte mittelkettige Triglyzeride (MCTs). Und kein anderes Fett oder Öl liefert derart viele MCTs wie das Kokosöl.
MCTs weisen gegenüber anderen Fettsäuren einige Vorzüge auf.
Die Tatsache, dass sie vom Körper nicht auf dieselbe Weise verarbeitet werden wie die meisten Fette, die hauptsächlich langkettige Triglyzeride (LCTs) enthalten, beschreibt nur einen dieser Vorteile. Allerdings ist dieser im Zusammenhang mit der schnellen Energieversorgung des Gehirns von grosser Bedeutung.
Der normale Stoffwechsel der LCTs ist von Gallensalzen abhängig, die u. a. zur Fettverdauung von der Gallenblase ausgeschüttet werden. Nur mit Hilfe dieser Gallensalze und in Kombination mit fettspaltenden Enzymen können Fette aus langkettigen Fettsäuren
in einem aufwendigen Prozess abgebaut und verdaut werden. Es dauert somit eine Weile, bis diese Fettsäuren den Körperzellen Energie liefern können.
Die MCTs aus Kokosöl sind sehr viel leichter und schneller für den Körper verwertbar, denn sie umgehen den Gallenstoffwechsel und gelangen ohne Hilfe der Enzyme auf direktem Weg vom Dünndarm in die Leber. Hierzu müssen sie auch nicht erst an spezielle Eiweisse
gebunden werden, ohne die LCTs gar nicht erst im Blut transportiert werden könnten. Daher stehen die MCTs der Leber wesentlich schneller zur Verfügung.

Kokosöl liefert Ketone zur Energiegewinnung

In der Leber angekommen verwendet diese einen Teil der MCTs zur Deckung ihres eigenen Energiebedarfs. Den übrigen Teil wandelt die Leber in sogenannte Ketone (aus Fett gebildete Energielieferanten) um. Diese werden bei einem bestehenden Glukosemangel über das Blut direkt ins Gehirn transportiert.
Dort profitieren die unterversorgten, insulinresistenten Gehirnzellen ebenso von dieser alternativen Energiequelle wie auch jene Zellen, die durch oxidativen Stress oder Sauerstoffmangel in ihrer Funktion bereits beeinträchtigt sind.
Interessanterweise erzeugen die Ketone sogar bis zu einem Viertel mehr Energie als Glukose – und das bei einem geringeren Sauerstoffverbrauch während der Energieerzeugung. Darüber hinaus fallen bei der Keton-Verwertung im Vergleich zur GlukoseVerwertung auch noch weniger Abfallprodukte an.
Aus diesen Gründen stellt Kokosöl eine äusserst effiziente, alternative Energiequelle für das Gehirn dar.

Kokosöl und die Omega-3 Verfügbarkeit

Wie bei allen neurodegenerativen Erkrankungen spielen neben anderen Faktoren auch Omega-3-Fettsäuren bei Alzheimer eine wichtige Rolle. Aus diesem Grund haben sich Wissenschaftler mit der Frage beschäftigt, ob der Verzehr von MCTs Einfluss auf die im
Körper befindlichen Omega-3-Fettsäuren nimmt.
Sie kamen zu dem Ergebnis, dass der regelmässige Konsum von MCTs scheinbar die Verfügbarkeit von Omega-3-Fettsäuren im Gehirn erhöhen kann.
In den Untersuchungen wurde festgestellt, dass der tägliche Verzehr von MCTs bei Hunden mit einer „altersbedingten mentalen Degeneration“ in bestimmten Bereichen ihres Gehirns zu einer deutlichen Erhöhung der Omega-3-Fettsäuren (EPA und DHA) führte. [Quelle]
Omega-3-Fette kommen jedoch im Kokosöl nicht vor. Daher gehen die Forscher davon aus, dass die MCTs den Omega-3-Fetten ermöglichen, sich aus den Fettspeichern zu lösen und ins Gehirn zu gelangen – also genau dorthin, wo sie am dringendsten benötigt werden.

Kokosöl gegen Plaque?

Die Plaque-Theorie bei der Alzheimer-Erkrankung ist wissenschaftlich sehr umstritten. Lange Zeit wurde behauptet, dass Plaque-Ablagerungen im Gehirn für die Entstehung von Alzheimer verantwortlich sind. Später wurde diese Theorie jedoch widerlegt und stattdessen behauptet, dass die Plaques eine Art Schutzschild für die Nerven darstellen.
Dass die Plaque-Ablagerungen nicht die grundlegende Ursache für Alzheimer sind, ist eigentlich logisch, denn Studien belegten, dass auch bei „gesunden Menschen“ erhöhte Plaque-Mengen im Gehirn gefunden wurden. Mehr zu diesem Thema können Sie in folgendem Artikel nachlesen: Alzheimer: Plaque-Theorie ist falsch Sollte eine übermässige Plaque-Bildung im Gehirn dennoch in irgendeiner Art mit Alzheimer in Verbindung stehen, könnte Kokosöl auch in dieser Hinsicht interessant sein. Denn wissenschaftliche Studien an Hunden haben ergeben, dass der Verzehr von MCTs ein spezielles, Plaque abbauendes Protein aktivieren kann. [Quelle]
Vielleicht stellt sich Ihnen nun die Frage, ob dieser Abbau dem Körper nicht schadet, wenn Plaque den Nerven doch als Schutz dienen soll?
Diese Frage ist sicher berechtigt, doch der Körper fügt sich – zumindest in der Regel – nicht selbst einen Schaden zu. Daher wird er beim Verzehr natürlicher Lebensmittel diese immer zum Wohle seiner Gesundheit einsetzen, denn sein oberstes Ziel ist es, seine Gesundheit zurückzuerlangen.

Wie viel Kokosöl ist gut für mich?

Selbstverständlich können wir keine individuelle MengenEmpfehlung in Bezug auf die Einnahme von Kokosöl geben. Die Forschungsergebnisse sowie praktische Erfahrungswerte lassen jedoch den Schluss zu, dass folgende Empfehlungen Ihren Körper bei der Wiederherstellung seiner Gesundheit unterstützen können. Falls Sie bereits an einer neurodegenerativen Erkrankungen leiden, könnte die tägliche Einnahme von 6 bis 8 Esslöffeln Kokosöl sinnvoll sein. Zur Prävention reicht eine Menge von etwa 4 Esslöffeln täglich aus.
Da Kokosöl generell einen positiven Einfluss auf die Gehirntätigkeit zeigt und das Immunsystem in ebenso vielen Bereichen unterstützt wie das Verdauungssystem, sollte eigentlich jeder die vielfältigen gesundheitlichen Vorteile dieses wertvollen Öls nutzen.
Bislang wurde noch keine Obergrenze für die Verzehrmenge von Kokosöl gefunden, ab der der Konsum schädliche Auswirkungen für den Körper hätte. Daher können Sie problemlos mit der Einnahmemenge experimentieren.

Tipp

Es ist ratsam, während der erhöhten Kokosöl-Einnahme gleichzeitig auf den Verzehr konzentrierter Kohlenhydrate, wie z. B. Zucker, zuckerhaltige Nahrungsmittel und Getränke, Weissbrot, PommesFrites; Weizennudeln, weisser Reis etc., zu verzichten oder
zumindest auf ein Minimum zu reduzieren. Denn wenn ausreichend Glucose aus all diesen Nahrungsmitteln zur Verfügung steht, kommt der Körper nicht in Verlegenheit, Ketone zu nutzen.

Wichtiger Hinweis

Wenn Sie den Verzehr grösserer Fettmengen nicht gewohnt sind, sollten Sie zunächst mit 3 x täglich 1 Teelöffel beginnen und die Menge achtsam steigern. So geben Sie Ihrem Körper die Chance, sich langsam an die veränderte Fettzufuhr zu gewöhnen, so dass sie vollumfänglich von den wertvollen Inhaltsstoffen des Kokosöls profitieren können.
Sollte die Darmtätigkeit durch eine bestimmte Menge an Kokosöl zu stark angeregt werden, reduzieren Sie die Einnahme auf die zuvor gut vertragene Menge und versuchen Sie zu einem späteren Zeitpunkt noch einmal, die Verzehrmenge langsam zu erhöhen.
Das Kokosöl können Sie pur einnehmen, aufs Brot streichen, ins Müsli, Joghurt oder Quark mischen, in bereits fertiggestellte Suppen und Eintöpfe rühren oder als Topping über Gemüse und Kartoffeln geben.
Des Weiteren möchten wir Sie darauf hinweisen, dass Kokosöl trotz seiner zahlreichen gesundheitlichen Vorteile nicht als alleinige Fettquelle verwendet werden sollte. Da der Körper ebenso wie das Gehirn auch auf die Zufuhr mehrfach ungesättigter Fettsäuren
angewiesen ist, raten wir Ihnen ausserdem zur Verwendung einer hochwertigen Omega-3 Fettsäure-Quelle, wie beispielsweise dem Leinöl oder Hanföl.

 

Quellen

Whitmer RA. “Type 2 diabetes and risk of cognitive impairment and dementia.” Curr Neurol Neurosci Rep. 2007 Sep;7(5):373-80. (Typ-2-Diabetes und das Risikoder kognitiven Beeinträchtigungund Demenz.) 

Coker LH, Wagenknecht LE. “Advanced glycation end products, diabetes, and the brain.” Neurology. 2011 Sep 7 (Fortgeschrittene Glykations-Endprodukte, Diabetes und das Gehirn.) 

Taha AY, Henderson ST, Burnham WM “Dietary enrichment with medium chain triglycerides (AC-1203) elevates polyunsaturated fatty acids in the parietal cortex of aged dogs: implications for treating age-related cognitive decline.”
Neurochem Res. 2009 Sep;34(9):1619-25 (Anreicherung der Ernährung mitmittelkettigen Triglyceriden(AC-1203) hebt den Spiegel von mehrfach ungesättigtenFettsäurenim parietalen Kortexvonalten Hunden an: Implikationenfür die Behandlung vonaltersbedingtemkognitivem Verfall.) 

Christa M. Studzinski et al., “Induction of ketosis may improve mitochondrial function and decrease steady-state amyloid-β precursor protein (APP) levels in the aged dog” Brain Research Volume 1226, 21 August 2008, Pages 209-217 (Induktion der Ketosekanndie Funktion der Mitochondrienverbessernund den Steady-State-Amyloid-Precursor-Protein β(APP)-Spiegel bei alten Hunde verringern.)

Kathleen A. Page et al., “Medium Chain Fatty Acids Improve Cognitive Function in Intensively Treated Type 1 Diabetic Patients and Support in vitro Synaptic Transmission During Acute Hypoglycemia” Diabetes February 17, 2009 (Fettsäuren mittlerer Kettenlänge verbessern die kognitiveFunktionin intensivbehandeltenTyp 1 Diabetikernund unterstützen die synaptische Übertragunginvitrowährend einer akutenHypoglykämie) 

Marie-Pierre St-Onge et al., “The benefit of medium-chain triglyceride therapy on the cardiac function of SHRs is associated with a reversal of metabolic and signaling alterations” J Am. Coll. Nutr. October 2008 vol. 27 no. 5 547-552 (Der Vorteilmittelkettiger Triglyceride bei der Therapie auf dieHerzfunktion von SHRs wird mit derAuflösung vonmetabolischenÄnderungenund Signalisierungenassoziiert.)

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Die interessante Geschichte hinter dem Koksöl aus der Sicht der südlichen Länder

Mit den wissenschaftlichen Entdeckungen der gesundheitlichen Wirkungen von Kokosöl 

Coconut: In Support of Good Health in the 21st Century

Talk given 1999 at the Asian Pacific Coconut Community on the occasion of its 36th session celebrating
the 30th anniversary of APCC, by Mary G. Enig, Ph.D.

 

Abstract

Coconuts play a unique role in the diets of mankind because they are the source of important
physiologically functional components. These physiologically functional components are found in
the fat part of whole coconut, in the fat part of desiccated coconut, and in the extracted coconut oil.
Lauric acid, the major fatty acid from the fat of the coconut, has long been recognized for the unique
properties that it lends to nonfood uses in the soaps and cosmetics industry. More recently, lauric
acid has been recognized for its unique properties in food use, which are related to its antiviral,
antibacterial, and antiprotozoal functions. Now, capric acid, another of coconut’s fatty acids has been
added to the list of coconut’s antimicrobial components. These fatty acids are found in the largest
amounts only in traditional lauric fats, especially from coconut. Also, recently published research has
shown that natural coconut fat in the diet leads to a normalization of body lipids, protects against
alcohol damage to the liver, and improves the immune system’s anti-inflammatory response. Clearly,
there has been increasing recognition of health- supporting functions of the fatty acids found in
coconut. Recent reports from the U.S. Food and Drug Administration about required labeling of the
trans fatty acids will put coconut oil in a more competitive position and may help return to its use by
the baking and snack food industry where it has continued to be recognized for its functionality. Now
it can be recognized for another kind of functionality: the improvement of the health of mankind.

I. INTRODUCTION

Mr. Chairman and members of the Asian Pacific Coconut Community, I would like to thank you for
inviting me to once again speak to this gathering of delegates on the occasion of your 36th session as
you celebrate the 30th anniversary of APCC.
When I addressed the 32nd COCOTECH meeting in Cochin, India, I covered two areas of interest to
the coconut community. In the first part, I reviewed the major health challenge facing coconut oil at
that time, which was based on a supposed negative role played by saturated fat in heart disease. I
hope that my talk was able to dispel any acceptance of that notion. In the second part of my talk I
suggested that there were some new positive health benefits from coconut that should be recognized.
These benefits stemmed from coconut’s use as a food with major functional properties for
antimicrobial and anti-cancer effects.
In my presentation today, I will bring you up to date about the new recognition of functional foods as

important components in the diet. Additionally, I would like to briefly review the state of the anti-
saturated fat situation and bring you up to date on some of the research that compares the beneficial

effects of saturated fats with those of omega-6 polyunsaturates, as well as the beneficial effects of the
saturated fats relative to the detrimental effects of the partially hydrogenated fats and the trans fatty
acids. In particular I will review some of the surprising beneficial effects of the special saturates
found in coconut oil as they compare with those of the unsaturates found in some of the other food
oils. Components of coconut oil are increasingly being shown to be beneficial. Increasingly, lauric
acid, and even capric acid, have been the subject of favorable scientific reports on health parameters.

II. FUNCTIONAL PROPERTIES OF LAURIC FATS AS ANTIMICROBIALS

Earlier this year, at a special conference entitled, “Functional Foods For Health Promotion:
Physiologic Considerations”; EXPERIMENTAL BIOLOGY ’99, Renaissance Washington Hotel,
Washington, DC Saturday, April 17, 1999, which was sponsored by the International Life Sciences
Institute, ILSI NORTH AMERICA, Technical Committee on Food Components for Health
Promotion, the term “functional foods” was defined as “a functional food provides a health benefit
over and beyond the basic nutrients.”
This is exactly what coconut and its edible products such as desiccated coconut and coconut oil do.
As a functional food, coconut has fatty acids that provide both energy (nutrients) and raw material for
antimicrobial fatty acids and monoglycerides (functional components) when it is eaten. Desiccated
coconut is about 69% coconut fat, as is creamed coconut. Full coconut milk is approximately 24%
fat.
Approximately 50% of the fatty acids in coconut fat are lauric acid. Lauric acid is a medium chain
fatty acid, which has the additional beneficial function of being formed into monolaurin in the
human or animal body. Monolaurin is the antiviral, antibacterial, and antiprotozoal monoglyceride
used by the human or animal to destroy lipid-coated viruses such as HIV, herpes, cytomegalovirus,
influenza, various pathogenic bacteria, including listeria monocytogenes and helicobacter pylori, and
protozoa such as giardia lamblia. Some studies have also shown some antimicrobial effects of the
free lauric acid.
Also, approximately 6-7% of the fatty acids in coconut fat are capric acid. Capric acid is another
medium chain fatty acid, which has a similar beneficial function when it is formed into monocaprin
in the human or animal body. Monocaprin has also been shown to have antiviral effects against HIV
and is being tested for antiviral effects against herpes simplex and antibacterial effects against
chlamydia and other sexually transmitted bacteria. (Reuters, London June 29, 1999) See below for
details.
The food industry has, of course, long been aware that the functional properties of the lauric oils, and
especially coconut oil, are unsurpassed by other available commercial oils. Unfortunately, in the
U.S., both during the late 1930s and again during the 1980s and 1990s, the commercial interests of
the U.S. domestic fats and oils industry were successful in driving down usage of coconut oil. As a
result, in the U.S. and in other countries where the influence from the U.S. is strong, the manufacturer
has lost the benefit of the lauric oils in its food products. As we will see from the data I will present
in this talk, it is the consumer who has lost the many health benefits that can result from regular
consumption of coconut products.
The antiviral, antibacterial, and antiprotozoal properties of lauric acid and monolaurin have been
recognized by a small number of researchers for nearly four decades: this knowledge has resulted in
more than 20 research papers and several U.S. patents, and this past year it resulted in a
comprehensive book chapter, which reviewed the important aspects of lauric oils as antimicrobial
agents (Enig 1998). In the past, the larger group of clinicians and food and nutrition scientists has
been unaware of the potential benefits of consuming foods containing coconut and coconut oil, but
this is now starting to change.

Kabara (1978) and others have reported that certain fatty acids (FAs) (e.g., medium-chain saturates)
and their derivatives (e.g., monoglycerides (MGs)) can have adverse effects on various
microorganisms: those microorganisms that are inactivated include bacteria, yeast, fungi, and
enveloped viruses. Additionally, it is reported that the antimicrobial effects of the FAs and MGs are
additive, and total concentration is critical for inactivating viruses (Isaacs and Thormar 1990).
The properties that determine the anti-infective action of lipids are related to their structure: e.g.,
monoglycerides, free fatty acids. The monoglycerides are active; diglycerides and triglycerides are
inactive. Of the saturated fatty acids, lauric acid has greater antiviral activity than either caprylic acid
(C-8), capric acid (C-10), or myristic acid (C-14). In general, it is reported that the fatty acids and
monoglycerides produce their killing/inactivating effect by lysing the plasma membrane lipid bilayer.
The antiviral action attributed to monolaurin is that of solubilizing the lipids and phospholipids in the
envelope of the virus, causing the disintegration of the virus envelope. However, there is evidence
from recent studies that one antimicrobial effect in bacteria is related to monolaurin’s interference
with signal transduction (Projan et al 1994), and another antimicrobial effect in viruses is due to
lauric acid’s interference with virus assembly and viral maturation (Hornung et al 1994).
Recognition of the antiviral aspects of the antimicrobial activity of the monoglyceride of lauric acid
(monolaurin) has been reported since 1966. Some of the early work by Hierholzer and Kabara (1982)
that showed virucidal effects of monolaurin on enveloped RNA and DNA viruses was done in
conjunction with the Center for Disease Control of the U.S. Public Health Service. These studies
were done with selected virus prototypes or recognized representative strains of enveloped human
viruses. The envelope of these viruses is a lipid membrane, and the presence of a lipid membrane on
viruses makes them especially vulnerable to lauric acid and its derivative monolaurin.
The medium-chain saturated fatty acids and their derivatives act by disrupting the lipid membranes of
the viruses (Isaacs and Thormar 1991; Isaacs et al 1992). Research has shown that enveloped viruses
are inactivated in both human and bovine milk by added fatty acids and monoglycerides (Isaacs et al
1991), and also by endogenous fatty acids and monoglycerides of the appropriate length (Isaacs et al
1986, 1990, 1991, 1992; Thormar et al 1987).
Some of the viruses inactivated by these lipids, in addition to HIV, are the measles virus, herpes
simplex virus-1 (HSV-1), vesicular stomatitis virus (VSV), visna virus, and cytomegalovirus (CMV).
Many of the pathogenic organisms reported to be inactivated by these antimicrobial lipids are those
known to be responsible for opportunistic infections in HIV-positive individuals. For example,
concurrent infection with cytomegalovirus is recognized as a serious complication for HIV+
individuals (Macallan et al 1993). Thus, it would appear to be important to investigate the practical
aspects and the potential benefit of an adjunct nutritional support regimen for HIV-infected
individuals, which will utilize those dietary fats that are sources of known antiviral, antimicrobial,
and antiprotozoal monoglycerides and fatty acids such as monolaurin and its precursor lauric acid.
Until now, no one in the mainstream nutrition community seems to have recognized the added
potential of antimicrobial lipids in the treatment of HIV-infected or AIDS patients. These
antimicrobial fatty acids and their derivatives are essentially nontoxic to man; they are produced in
vivo by humans when they ingest those commonly available foods that contain adequate levels of
medium-chain fatty acids such as lauric acid. According to the published research, lauric acid is one
of the best “inactivating” fatty acids, and its monoglyceride is even more effective than the fatty acid
alone (Kabara 1978, Sands et al 1978, Fletcher et al 1985, Kabara 1985).

The lipid-coated (envelope) viruses are dependent on host lipids for their lipid constituents. The
variability of fatty acids in the foods of individuals as well as the variability from de novo synthesis
accounts for the variability of fatty acids in the virus envelope and also explains the variability of
glycoprotein expression, a variability that makes vaccine development more difficult.
Monolaurin does not appear to have an adverse effect on desirable gut bacteria, but rather on only
potentially pathogenic microorganisms. For example, Isaacs et al (1991) reported no inactivation of
the common Escherichia coli or Salmonella enteritidis by monolaurin, but major inactivation of
Hemophilus influenzae, Staphylococcus epidermidis and Group B gram positive streptococcus.
The potentially pathogenic bacteria inactivated by monolaurin include Listeria monocytogenes,
Staphylococcus aureus, Streptococcus agalactiae, Groups A,F & G streptococci, gram-positive
organisms, and some gram-negative organisms if pretreated with a chelator (Boddie & Nickerson
1992, Kabara 1978, Kabara 1984, Isaacs et al 1990, Isaacs et al 1992, Isaacs et al 1994, Isaacs &
Schneidman 1991, Isaacs & Thormar 1986, Isaacs & Thormar 1990, Isaacs & Thormar 1991,
Thormar et al 1987, Wang & Johnson 1992).
Decreased growth of Staphylococcus aureus and decreased production of toxic shock syndrome
toxin-1 was shown with 150 mg monolaurin per liter (Holland et al 1994). Monolaurin was 5000
times more inhibitory against Listeria monocytogenes than ethanol (Oh & Marshall 1993).
Helicobacter pylori is rapidly inactivated by medium-chain monoglycerides and lauric acid, and there
appears to be very little development of resistance of the organism to the bactericidal effects
(Petschow et al 1996) of these natural antimicrobials.
A number of fungi, yeast, and protozoa are inactivated or killed by lauric acid or monolaurin. The
fungi include several species of ringworm (Isaacs et al 1991). The yeast reported is Candida albicans
(Isaacs et al 1991). The protozoan parasite Giardia lamblia is killed by free fatty acids and
monoglycerides from hydrolyzed human milk (Hernell et al 1986, Reiner et al 1986, Crouch et al
1991, Isaacs et al 1991). Numerous other protozoa were studied with similar findings; these findings
have not yet been published (Jon J. Kabara, private communication, 1997).
Research continues in measuring the effect of the monoglyceride derivative of capric acid
monocaprin as well as the effects of lauric acid. Chlamydia trachomatis is inactivated by lauric acid,
capric acid, and monocaprin (Bergsson et al 1998), and hydrogels containing monocaprin are potent
in vitro inactivators of sexually transmitted viruses such as HSV-2 and HIV-1 and bacteria such as
Neisseria gonorrhoeae (Thormar 1999).

III. ORIGINS OF THE ANTI-SATURATED FAT AGENDA

The coconut industry has suffered more than three decades of abusive rhetoric from the consumer
activist group Center for Science in the Public Interest (CSPI), from the American Soybean
Association (ASA) and other members of the edible oil industry, and from those in the medical and
scientific community who learned their misinformation from groups like CSPI and ASA. I would
like to review briefly the origins of the anti-saturated fat, anti-tropical oil campaigns and hopefully
give you some useful insight into the issues.
When and how did the anti-saturated fat story begin? It really began in part in the late 1950s, when a
researcher in Minnesota announced that the heart disease epidemic was being caused by hydrogenated vegetable fats. The edible oil industry’s response at that time was to claim it was only
the saturated fat in the hydrogenated oils that was causing the problem. The industry then announced
that it would be changing to partially hydrogenated fats and that this would solve the problem.
In actual fact, there was no change because the oils were already being partially hydrogenated, and
the levels of saturated fatty acids remained similar, as did the levels of the trans fatty acids. The only
thing that really changed was the term for hydrogenation or hardening listed on the food label.
During this same period, a researcher in Philadelphia reported that consuming polyunsaturated fatty
acids lowered serum cholesterol. This researcher, however, neglected to include the information that
the lowering was due to the cholesterol going into the tissues, such as the liver and the arteries. As a
result of this research report and the acceptance of this new agenda by the domestic edible oils
industries, there was a gradual increase in the emphasis on replacing “saturated fats” in the diet and
on the consuming of larger amounts of the “polyunsaturated fats.” As many of you probably know,
this strong emphasis on consuming polyunsaturates has backfired in many ways: the current
adjustments being recommended in the U.S. by groups such as the National Academy of Sciences
replace the saturates with monounsaturates instead of with polyunsaturates and replace
polyunsaturates with monounsaturates.
Early promoters of the anti-saturated fat ideas included companies such as Corn Products Company
(CPC International) through a book written by Jeremiah Stamler in 1963, with the professional
edition published in 1966 by CPC. This book took some of the earliest pejorative stabs at the
tropical oils. In 1963, the only tropical fat or oil singled out as high in saturated fats was coconut oil.
Palm oil had not entered the U.S. food supply to any extent, had not become a commercial threat to
the domestic oils, and was not recognized in any of the early texts. An observation by the editorial
staff of Consumer Reports noted that
“…in 1962…one writer observed, the average American now fears fat (saturated fat, that is) ‘as he
once feared witches.'”
In 1965, a representative of Procter and Gamble told the American Heart Association to change its
Diet/Heart statement, removing any reference to the trans fatty acids. This altered official document
encouraged the consumption of partially hydrogenated fats. In the 1970s, this same Procter and
Gamble employee served as nutrition chairman in two controlling positions for the National Heart
Lung and Blood Institute’s Lipid Research Clinic (LRC) trials and as director of one of the LRC
centers. These LRC trials were the basis for the 1984 NIH Cholesterol Consensus Conference, which
in turn spawned the National Cholesterol Education Program (NCEP). This program encourages
consumption of margarine and partially hydrogenated fats, while admitting that trans should not be
consumed in excess. The official NCEP document states that “…coconut oil, palm oil, and palm
kernel oil…should be avoided…”
In 1966, the U.S. Department of Agriculture documents on fats and oils talked about how unstable
the unsaturated fats and oils were. There was no criticism of the saturated fats. That criticism of
saturated fat was to come later to this agency when it came under the influence of the domestic edible
fats and oils industry, and when it developed the U.S. Dietary Guidelines. These Dietary Guidelines
became very anti-saturated fat and remain so to this day. Nevertheless, as we will learn later in my
talk, there has started some reversal of the anti-saturated fat stance in the works in this agency in
1998.

In the early 1970s, although a number of researchers were voicing concerns about the trans fats, the edible oil industry and the U.S. Food and Drug Administration (FDA) were engaging in a revolving-
door exchange that would (i) promote the increasing consumption of partially hydrogenated vegetable oils, (ii) would condemn the saturated fats, and (iii) hide the trans issue. As an example of this “oily”
exchange, in 1971 the FDA’s general counsel became president of the edible oil trade association, and
he in turn was replaced at the FDA by a food lawyer who had represented the edible oil industry.
From that point on, the truth about any real effects of the dietary fats had to play catch-up. The
American edible oil industry sponsored “information” to educate the public, and the natural dairy and
animal fats industries were inept at countering any of that misinformation. Not being domestically
grown in the U.S., coconut oil, palm oil, and palm kernel oil were not around to defend themselves at
that time. The government agencies responsible for disseminating information ignored those
protesting “lone voices,” and by the mid-1980s, American food manufacturers and consumers had
made major changes in their fats and oils usage — away from the safe saturated fats and headlong into
the problematic trans fats.
Enig and Fallon (1998/1999) have reviewed the above history in “The Oiling of America” published
in the Australian magazine Nexus. The magazine has placed this review on the internet and it can be
viewed or downloaded from the Nexus website. The internet addresses for the websites are
https://www.peg.apc.org/~nexus/OilingAmerica.1.html and
https://www.peg.apc.org/~nexus/OilingAmerica.2.html.

IV. THE DAMAGING ROLE OF THE U.S. CONSUMER ACTIVIST GROUP CSPI

Some of the food oil industry (especially those connected with the American Soybean Association
(ASA)) and some of the consumer activists (especially the Center for Science in the Public Interest
(CSPI) and also the American Heart Savers Association) further eroded the status of natural fats
when they sponsored the major anti-saturated fat, anti-tropical oils campaign in the late 1980s.
Actually, an active anti-saturated fat bias started as far back as 1972 in CSPI. But beginning in 1984,
this very vocal consumer activist group started its anti-saturated fat campaign in earnest. In
particular, at this time, the campaign was against the “saturated” frying fats, especially those being
used by fast-food restaurants. Most of these so-called saturated frying fats were tallow based, but
also included was palm oil in at least one of the hotel/restaurant chains.
Then in a “News Release” in August 1986, CSPI criticized what it called “Deceptive Vegetable Oil
Labeling: Saturated Fat Without The Facts,” referring to “palm, coconut, and palm kernel oil” as “rich
in artery-clogging saturated fat.” CSPI further announced that it had petitioned the Food and Drug
Administration to stop allowing labeling of foods as having “100% vegetable shortening”if they
contained any of the “tropical oils.” CSPI also asked for mandatory addition of the qualifier “a
saturated fat” when coconut, palm or palm kernel oils were named on the food label.
In 1988, CSPI published a booklet called “Saturated Fat Attack.” This booklet contained lists of
processed foods “surveyed” in Washington, DC supermarkets. The lists were used for developing
information about the saturated fat in the products. Section III is entitled “Those Troublesome
Tropical Oils,” and it contains statements encouraging pejorative labeling. There were lots of
substantive mistakes in the booklet, including errors in the description of the biochemistry of fats and
oils and completely erroneous statements about the fat and oil composition of many of the products.

At the same time CSPI was conducting its campaign in 1986, the American Soybean Association
began its anti-tropical oil campaign by sending inflammatory letters, etc., to soybean farmers. The
ASA took out advertisements to promote a “[tropical] Fat Fighter Kit.” The ASA hired a Washington
DC “nutritionist” to survey supermarkets to detect the presence of tropical oils in foods.

Then early in 1987, the ASA petitioned the FDA to require labeling of “Tropical Fats,” and by mid-
1987, the Soybean Digest continued an active and increasing anti-tropical oils campaign. At about

the same time (June 3, 1987), the New York Times published an editorial, “The Truth About
Vegetable Oil,” in which it called palm, palm kernel, and coconut oils “the cheaper, artery-clogging
oils from Malaysia and Indonesia” and claimed that U.S. federal dietary guidelines opposed tropical
oils, although it is not clear that this was so. The “artery-clogging” terminology was right out of
CSPI.
Two years later in 1989, the ASA held a press conference with the help of the CSPI in Washington
DC in an attempt to counter the palm oil group’s press conference of 6 March. The ASA “Media
Alert” stated that the National Heart Lung and Blood Institute and National Research Council
“recommend consumers avoid palm, palm kernel and coconut oils.” Only months before these press
conferences, millionaire Phil Sokolof, the head of the National Heart Savers Association (NHSA),
purchased the first of a series of anti-saturated fats and anti-tropical fats advertisements in major
newspapers. No one has found an overt connection between Sokolof (and his NHSA) and the ASA,
but the CSPI bragged about being his advisor.

V. WHAT ABOUT HEART DISEASE AND COCONUT OIL?

The research over four decades concerning coconut oil in the diet and heart disease is quite clear:
coconut oil has been shown to be beneficial. This research leads us to ask the question, “should
coconut oil be used to both prevent and treat coronary heart disease?”
This statement is based on several reviews of the scientific literature concerning the feeding of
coconut oil to humans. Blackburn et al (1988) have reviewed the published literature of “coconut
oil’s effect on serum cholesterol and atherogenesis” and have concluded that when “…[coconut oil is]
fed physiologically with other fats or adequately supplemented with linoleic acid, coconut oil is a
neutral fat in terms of atherogenicity.”
After reviewing this same literature, Kurup and Rajmohan (1995) conducted a study on 64 volunteers
and found “…no statistically significant alteration in the serum total cholesterol, HDL cholesterol,
LDL cholesterol, HDL cholesterol/total cholesterol ratio and LDL cholesterol/HDL cholesterol ratio
of triglycerides from the baseline values…” A beneficial effect of adding the coconut kernel to the
diet was noted by these researchers.
Kaunitz and Dayrit (1992) have reviewed some of the epidemiological and experimental data
regarding coconut-eating groups and noted that the “available population studies show that dietary
coconut oil does not lead to high serum cholesterol nor to high coronary heart disease mortality or
morbidity.” They noted that in 1989 Mendis et al reported undesirable lipid changes when young
adult Sri Lankan males were changed from their normal diets by the substitution of corn oil for their
customary coconut oil. Although the total serum cholesterol decreased 18.7% from 179.6 to 146.0
mg/dl and the LDL cholesterol decreased 23.8% from 131.6 to 100.3 mg/dl, the HDL cholesterol
decreased 41.4% from 43.4 to 25.4 mg/dl (putting the HDL values very much below the acceptable lower limit of 35 mg/dl) and the LDL/HDL ratio increased 30% from 3.0 to 3.9. These latter two
changes are considered quite undesirable. Mendis and Kumarasunderam (1990) also compared the
effect of coconut oil and soy oil in normolipidemic young males, and again the coconut oil resulted in
an increase in the HDL cholesterol, whereas the soy oil reduced this desirable lipoprotein. As noted
above, Kurup and Rajmohan (1995), who studied the addition of coconut oil alone to previously
mixed fat diets, had reported no significant difference from baseline.
Previously, Prior et al (1981) had shown that islanders with high intakes of coconut oil showed “no
evidence of the high saturated fat intake having a harmful effect in these populations.” When these
groups migrated to New Zealand, however, and lowered their intake of coconut oil, their total
cholesterol and LDL cholesterol increased, and their HDL cholesterol decreased. Statements that any
saturated fat is a dietary problem is not supported by evidence (Enig 1993).
Studies that allegedly showed a “hypercholesterolemic” effect of coconut oil feeding, usually only
showed that coconut oil was not as effective at lowering the serum cholesterol as was the more
unsaturated fat to which coconut oil was being compared. This appears to be in part because coconut
oil does not “drive” cholesterol into the tissues as does the more polyunsaturated fats. The chemical
analysis of the atheroma shows that the fatty acids from the cholesterol esters are 74% unsaturated
(41% of the total fatty acids is polyunsaturated) and only 24% are saturated. None of the saturated
fatty acids were reported to be lauric acid or myristic acid (Felton et al 1994).
There is another aspect to the coronary heart disease picture. This is related to the initiation of the
atheromas that are reported to be blocking arteries. Recent research shows that there is a causative
role for the herpes virus and cytomegalovirus in the initial formation of atherosclerotic plaques and
the reclogging of arteries after angioplasty. (New York Times 1991) What is so interesting is that
the herpes virus and cytomegalovirus are both inhibited by the antimicrobial lipid monolaurin, but
monolaurin is not formed in the body unless there is a source of lauric acid in the diet. Thus,
ironically enough, one could consider the recommendations to avoid coconut and other lauric oils as
contributing to the increased incidence of coronary heart disease.
Chlamydia pneumoniae, a gram-negative bacteria, is another of the microorganisms suspected of
playing a role in atherosclerosis by provoking an inflammatory process that would result in the
oxidation of lipoproteins with induction of cytokines and production of proteolystic enzymes, a
typical phenomena in atherosclerosis (Saikku 1997). Some of the pathogenic gram-negative bacteria
with an appropriate chelator have been reported to be inactivated or killed by lauric acid and
monolaurin as well as capric acid and monocaprin (See above, Bergsson et al 1997 and Thormar et al
1999).
However, the microorganisms most frequently identified as probable causative infecting agents are in
the herpes virus family and include cytomegalovirus, type 2 herpes simplex (HSV-2), and Coxsackie
B4 virus. The evidence for a causative role for cytomegalovirus is the strongest (Ellis 1997, Visseren
et al 1997, Zhou et al 1996, Melnick et al 1996, Epstein et al 1996, Chen & Yang 1995), but a role for
HSV-2 is also shown (Raza-Ahmad et al 1995). All members of the herpes virus family are reported

to be killed by the fatty acids and monoglycerides from saturated fatty acids ranging from C-6 to C-
14 (Isaacs et al 1991), which include approximately 80% of the fatty acids in coconut oil.

In spite of what has been said over the past four or more decades about the culpability of the saturated
fatty acids in heart disease, they are ultimately going to be held blameless. More and more research is showing the problem to be related to oxidized products. One protection man has against oxidized
products is the naturally saturated fats such as coconut oil.

VI. THE LATEST ON THE TRANS FATTY ACIDS

Both the United States and Canada will soon require labeling of the trans fatty acids, which will put
coconut oil in a more competitive position than it has been in the past decade. A fear of the vegetable
oil manufacturers has always been that they would have to label trans fatty acids. The producers of
trans fatty acids have relied on the anti-saturated fat crusade to protect their markets. However, the
latest research on saturated fatty acids and trans fatty acids shows the saturated fatty acids coming out
ahead in the health race.
It has taken this last decade, from 1988 to 1998, to see changes in perception. During this period, the
trans fatty acids have taken a deserved drubbing. Research reports from Europe have been emerging
since the seminal report by Mensink and Katan in 1990 that the trans fatty acids raised the low
density lipoprotein (LDL) cholesterol and lowered the high density lipoprotein (HDL) cholesterol in
serum. This has been confirmed by studies in the U.S. (Judd et al 1994, Khosla and Hayes 1996,
Clevidence 1997).
In 1990, the lipids research group at the University of Maryland published a paper (Enig et al 1990)
correcting some of the erroneous data sponsored by the food industry in the 1985 review by the Life

Sciences Research Office of Federation of American Societies for Experimental Biology (LSRO-
FASEB) (Senti 1985) of the trans fatty acids.

Also, in 1993, a group of researchers at Harvard University, led by Professor Walter Willett, reported
a positive relationship between the dietary intake of the trans fatty acids and coronary heart disease in
a greater than 80,000 cohort of nurses who had been followed by the School of Public Health at
Harvard University for more than a decade.
Pietinen and colleagues (1997) evaluated the findings from the large cohort of Finnish men who were
being studied for a cancer prevention study. After controlling for the appropriate variables including
several coronary risk factors, the authors observed a significant positive association between the
intake of trans fatty acids and the risk of death from coronary disease. There was no association
between intakes of saturated fatty acids, or dietary cholesterol and the risk of coronary deaths. This is
another example of the differences between the effects of the trans fatty acids and the saturated fatty
acids and further challenge to the dietary cholesterol hypothesis.
The issue of the trans fatty acids as a causative factor in remains underexplored, but recent reports
have found a connection. Bakker and colleagues (1997) studied the data for the association between
breast-cancer incidence and linoleic acid status across European countries since animal and
ecological studies had suggest a relationship. They found that the mean fatty acid composition of
adipose did not show an association with omega-6 linoleic acid and breast, colon or prostate cancer.
However, cancers of the breast and colon were positively associated with the trans fatty acids.
Kohlmeier and colleagues (1997) also reported that data from the EURAMIC study showed adipose
tissue concentration of trans fatty acids having a positive association with postmenopausal breast
cancer in European women.
In 1995 a British documentary on the trans fatty acids aired on a major television station in the U.K.
This documentary included an expose of the battle between the edible oil industry and some of the major researchers of the trans fatty acids. Just this year, this same documentary has been aired on
television in France where it was requested by a major television station.
Several of the early researchers into the trans problems, Professor Fred Kummerow and Dr. George
Mann, have continued their research and/or writing (Mann 1994). The popular media has continued
to press the issue of the amounts of trans in the foods, for which there are still no comprehensive
government data bases, and a recent published paper from a U.S. Department of Agriculture
researcher states:
“Because trans fatty acids have no known health benefits and strong presumptive evidence suggests
that they contribute markedly to the risk of developing CHD, the results published to date suggest
that it would be prudent to lower the intake of trans fatty acids in the U.S. diet.”(Nelson 1998).
Professor Meir Stampfer from Harvard University refers to trans fats as “one of the major nutritional
issues of the nation,” contending that “they have a large impact” and “…we should completely
eliminate hydrogenated fats from the diet” (Gottesman 1998).
Lowering the trans fatty acids in the foods in the U.S. can only be done by returning to the use of the
natural unhydrogenated and more saturated fats and oils.
Predictions can be made regarding the future of the trans fatty acids. Our ability to predict has been
pretty good; for example when Enig Associates started producing the marketing newsletter Market
Insights written by Eric Enig, we predicted that trans fatty acids would eventually be swept out of the
market. It appears that this prediction may be close to coming true.
Also in the early 1990s, Market Insights predicted that CSPI would change its mind about the trans
fatty acids, which it had spent years defending. CSPI did change its mind, and in fact went on the
attack regarding the trans, but CSPI never admitted that it had originally been promoting the trans or
that the high levels of trans found in the fried foods in the fast food and other restaurants and in many
other foods are directly due to CSPI lobbying. While its change was welcome, CSPI’s revisionist
version of its own history of support of partially hydrogenated oils and trans fatty acids would have
fit perfectly into George Orwell’s “1984”

VII. COMPARISON OF SATURATED FATS WITH THE TRANS FATS

The statement that trans fatty acids are like saturated fatty acids is not correct for biological systems.
A listing of the biological effects of saturated fatty acids in the diet versus the biological effects of
trans fatty acids in the diet is in actuality a listing of the good (saturated) versus the bad (trans).
When one compares the saturated fatty acids and the trans fatty acids, we see that
(1) saturated fatty acids raise HDL cholesterol, the so-called good cholesterol, whereas the trans fatty
acids lower HDL cholesterol (Mensink and Katan 1990, Judd et al 1994);
(2) saturated fatty acids lower the blood levels of the atherogenic lipoprotein [a], whereas trans fatty
acids raise the blood levels of lipoprotein [a] (Khosla and Hayes 1996, Hornstra et al 1991,
Clevidence et al 1997);
(3) saturated fatty acids conserve the elongated omega-3 fatty acids (Gerster 1998), whereas trans
fatty acids cause the tissues to lose these omega-3 fatty acids (Sugano and Ikeda 1996);
(4) saturated fatty acids do not inhibit insulin binding, whereas trans fatty acids do inhibit insulin
binding;
(5) saturated fatty acids are the normal fatty acids made by the body, and they do not interfere with
enzyme functions such as the delta-6-desaturase, whereas trans fatty acids are not made by the body,
and they interfere with many enzyme functions such as delta-6-desaturase;
and
(6) some saturated fatty acids are used by the body to fight viruses, bacteria, and protozoa, and they
support the immune system, whereas trans fatty acids interfere with the function of the immune
system.

VIII. WHAT ABOUT THE UNSATURATED FATS?

The arteries of the heart are also compromised by the unsaturated fatty acids. When the fatty acid
composition of the plaques (atheromas) in the arteries has been analyzed, the level of saturated fatty
acids in the cholesterol esters is only 26 percent compared to that in the unsaturated fatty acids, which
is 74 percent. When the unsaturated fatty acids in the cholesterol esters in these plaques are analyzed,
it is shown that 38 percent are polyunsaturated and 36 percent are monounsaturated. Clearly the
problem in not with the saturated fatty acids.
As an aside, you need to understand that the major role of cholesterol in heart disease and in cancer is
as the body’s repair substance, and that cholesterol is a major support molecule for the immune
system, an important antioxidant, and a necessary component of neurotransmitter receptors. Our
brains do not work very well without adequate cholesterol. It should be apparent to scientists that the
current approach to cholesterol has been wrong.
The pathway to cholesterol synthesis starts with a molecule of acetyl CoA that comes from the
metabolism of excess protein forming ketogenic amino acids and from the metabolism of excess
carbohydrate, as well as from the oxidation of excess fatty acids. Grundy in 1978 reported that the
degree of saturation of the fat in the diet did not affect the rate of synthesis of cholesterol. Research
reported in 1997 (Jones 1997), however, showed that the polyunsaturated fatty acids in the diet
increase the rate of cholesterol synthesis relative to other fatty acids. Furthermore, research reported
in 1993 (Hodgsons et al 1993) had shown that dietary intake of the omega-6 polyunsaturated fatty
acid linoleic acid was positively related to coronary artery disease.
Thus, those statements made by the consumer activists in the United States to the effect that the
saturated fatty acids increase cholesterol synthesis is without any foundation. What happens when
there is an increase or a decrease of cholesterol in the serum is more like a shift from one
compartment to another as the body tries to rectify the potential damage from the excess
polyunsaturated fatty acids. Research by Dr. Hans Kaunitz reported in 1978 clearly showed the
potential problems with excess polyunsaturated fatty acids.

IX. RESEARCH SHOWING BENEFICIAL EFFECTS OF EATING THE MORE SATURATED FATS

One major concern expressed by the nutrition community is related to whether or not people are
getting enough elongated omega-3 fatty acids in their diets. The elongated omega-3 fatty acids of
concern are eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Some research has shown that (the basic omega-3 fatty acid) -linolenic acid is not readily converted to the elongated
forms in humans or animals, especially when there is ingestion of the trans fatty acids and the
consequent inhibition of the delta-6-desaturase enzyme. One recent study (Gerster 1998), which used
radioisotope-labeled -linolenic acid to measure this conversion in adult humans, showed that if the
background fat in the diet was high in saturated fat, the conversion was approximately 6% for EPA
and 3.8% for DHA, whereas if the background fat in the diet was high in omega-6 polyunsaturated
fatty acids (PUFA), the conversion was reduced 40-50%.
Nanji and colleagues (1995) report that a diet enriched in saturated but not unsaturated fatty acids
reversed alcoholic liver injury in their animals, which was caused by dietary linoleic acid. These
researchers conclude that this effect may be explained by the down-regulation of lipid peroxidation.
This is another example of the need for adequate saturated fat in the diet. Cha and Sachan (1994)
studied the effects of saturated fatty acid and unsaturated fatty acid diets on ethanol
pharmacokinetics. The hepatic enzyme alcohol dehydrogenase and plasma carnitines were also
evaluated. The researchers concluded that dietary saturated fatty acids protect the liver from alcohol
injury by retarding ethanol metabolism, and that carnitine may be involved.
Hargrove and colleagues (1999) noted the work of Nanji et al and postulated that they would find that
diets rich in linoleic acid would also cause acute liver injury after acetaminophen injection. In the
first experiment, two levels of fat (15 g/100 g protein and 20 g/100 g protein) were fed using corn oil
or beef tallow. Liver enzymes indicating damage were significantly elevated in all the animals except
for those animals fed the higher level of beef tallow. These researchers concluded that “diets with
high [linoleic acid] may promote acetaminophen-induced liver injury compared to diets with more
saturated and monounsaturated fatty acids.”

X. RESEARCH SHOWING GENERAL BENEFICIAL EFFECTS FROM FEEDING COCONUT OIL

Research that compares coconut oil feeding with other oils to answer a variety of biological questions
is increasingly finding beneficial results from the coconut oil.
Obesity is a major health problem in the United States and the subject of much research. Several
lines of research dealing with metabolic effects of high fat diets have been followed. One study used
coconut oil to enrich a high fat diet and the results reported were that the “coconut-oil enriched diet is
effective in…[producing]…a decrease in white fat stores.” (Portillo et al 1998)
Cleary et al (1999) fed genetically obese animals high fat diets of either safflower oil or coconut oil.
Safflower oil-fed animals had higher hepatic lipogenic enzyme activities than did coconut oil fed
animals. When the number of fat cells were measured, the safflower oil-fed also had more fat cells
than the coconut oil-fed.
Many of the feeding studies produce results at variance with the popular conception. High fat diets
have been used to study the effects of different types of fatty acids on membrane phospholipid fatty
acid profiles. When such a study was performed on mice, the phospholipid profiles were similar for
diets high in linoleic acid from high-linoleate sunflower oil relative to diets high in saturated fatty
acids from coconut oil. However, those animals fed the diets high in oleic acid (from the high-oleate
sunflower oil) or high in elongated omega-3 fatty acids (from menhaden oil) were not only different from the other two diets, but they also resulted in enlarged spleens in the animals. (Huang and Frische
1992)
Oliart-Ros and colleagues (1998), Instituto Technologico de Veracruz, Mexico, reported on effects of
different dietary fats on sucrose-induced cardiovascular syndrome in rats. The most significant
reduction in parameters of the syndrome was obtained by the n-3 PUFA-rich diet. These researchers
reported that the diet thought to be PUFA-deficient presented a tissue lipid pattern similar to the n-3
PUFA-rich diet (fish oil), which surprised and puzzeled them. When questioned, it turned out that
the diet was not really PUFA-deficient, but rather just a normal coconut oil (nonhydrogenated), which
conserved the elongated omega-3 and normalized the omega-6-to-omega-3 balance.
A recent study measured the effect of high-fat diets, fed for more than three months to the neonatal
pig, on the HMG-CoA reductase enzyme’s function and gave some surprises. There were two
feeding protocols: one with the added cholesterol and one without added cholesterol, but both with
coconut oil. The hepatic reductase activity, which was the same in all groups at the beginning of the
feeding on the third day and similar on the 42nd day, was increased with and without added
cholesterol on the 13th day and then decreased on the 25th day. The data was said to suggest that
dietary cholesterol suppressed hepatic reductase activity in the young pigs regardless of their genetic
background, that the stage of development was a dominant factor in its regulation, and that both
dietary and endogenously synthesized cholesterol was used primarily for tissue building in very
young pigs. (McWhinney et al 1996) The feeding of coconut oil did not in any way compromise the
normal development of these animals.
When compared with feeding coconut oil, feeding two different soybean oils to young females
caused a significant decrease in HDL cholesterol. Both soybean oils, one of which was extracted
from a new mutant soybean thought to be more oxidatively stable, were not protective of the HDL
levels (Lu Z et al 1997).
Trautwein et al (1997) studied cholesterol-fed hamsters on different oil supplements for plasma,
hepatic, and biliary lipids. The dietary oils included butter, palm stearin, coconut oil, rapeseed oil,
olive oil, and sunflowerseed oil. Plasma cholesterol concentrations were higher (9.2 mmol/l) for
olive oil than for coconut oil (8.5 mmol/l), hepatic cholesterol was highest in the olive oil group, and
none of the diet groups differed for biliary lipids. Even in this cholesterol-sensitive animal model,
coconut oil performed better than olive oil.
Smit and colleagues (1994) had also studied the effect of feeding coconut oil compared with feeding
corn oil and olive oil in rats and measured the effect on biliary cholesterol. Bile flow was not
different between the three diets, but the hepatic plasma membranes showed more cholesterol and
less phospholipid from corn and olive oil feeding relative to coconut oil feeding.
Several studies (Kramer et al 1998) have pointed out problems with canola oil feeding in newborn
piglets, which result in the reduction in number of platelets and the alteration in their size. There is
concern for similar effects in human infants. These undesirable effects can be reversed when coconut
oil or other saturated fat is added to the feeding regimen (Kramer et al 1998).
Research has shown that coconut oil is needed for good absorption of fat and calcium from infant
formulas. The soy oil (47%) and palm olein (53%) formula gave 90.6% absorption of fat and 39%
absorption of calcium, whereas the soy oil (60%) and coconut oil (40%) gave 95.2% absorption of fat
and 48.4% absorption of calcium (Nelson et al 1996). Both fat and calcium are needed by the infant for proper growth. These results clearly show the folly of removing or lowering the coconut oil in
infant formulas.

XI. RESEARCH SHOWING A ROLE FOR COCONUT IN ENHANCING IMMUNITY AND MODULATING METABOLIC FUNCTIONS

Coconut oil appears to help the immune system response in a beneficial manner. Feeding coconut oil
in the diet completely abolished the expected immune factor responses to endotoxin that were seen
with corn oil feeding. This inhibitory effect on interleukin-1 production was interpreted by the
authors of the study as being largely due to a reduced prostaglandin and leukotriene production (Wan
and Grimble 1987). However, the damping may be due to the fact that effects from high omega-6
oils tend to be normalized by coconut oil feeding. Another report from this group (Bibby and
Grimble 1990) compared the effects of corn oil and coconut oil diets on tumor necrosis factor-alpha
and endotoxin induction of the inflammatory prostaglandin E2 (PGE2) production. The animals fed
coconut oil did not produce an increase in PGE2, and the researchers again interpreted this as a
modulatory effect that brought about a reduction of phospholipd arachidonic acid content. A study
from the same research group (Tappia and Grimble 1994) showed that omega-6 oil enhanced
inflammatory stimuli, but that coconut oil, along with fish oil and olive oil, suppressed the production
of interleukin-1.
Several recent studies are showing additional helpful effects of consuming coconut oil on a regular
basis, thus supplying the body with the lauric acid derivative monolaurin. Monolaurin and the ether
analogue of monolaurin have been shown to have the potential for damping adverse reactions to toxic
forms of glutamic acid (Dave et al 1997). Lauric acid and capric acid have been reported to have
very potent effects on insulin secretion (Garfinkel et al 1992). Using a model system of murine
splenocytes, Witcher et al 1996 showed that monolaurin induced proliferation of T cells and inhibited
the toxic shock syndrome toxin-1 mitogenic effects on T cells.
Monserrat and colleagues (1995) showed that a diet rich in coconut oil could protect animals against
the renal necrosis and renal failure produced by a diet deficient in choline (a methyl donor group).
The animals had less or no mortality and increased survival time as well as decreased incidence or
severity of the renal lesions when 20% coconut oil was added to the deficient diet. A mixture of
hydrogenated vegetable oil and corn oil did not show the same benefits.
The immune system is complex and has many feedback mechanism to protect it, but the wrong fat
and oils can compromise these important mechanisms. The data from the several studies show the
helpful effects of coconut fat. Additionally, there are anecdotal reports that consumption of coconut
is beneficial for individuals with the chronic fatigue and immune dysfunction syndrome known as
CFIDS.

XII. U.S. PATENTS FOR MEDICAL USES OF LAURIC OILS, MEDIUM-CHAIN FATTY ACIDS, AND THEIR DERIVATIVES SUCH AS MONOLAURIN

A number of patents have been granted in the United States for medical uses of lauric oils, lauric
acid, and monolaurin. Although one earlier patent was granted to Professor Kabara more than three
decades ago, the rest of these patents have been granted within the past decade.

In 1989 a patent was issued to the New England Deaconess Hospital (Bistrian et al 1989) for the
invention titled “Kernel Oils and Disease Treatment.” This treatment required lauric acid as the
primary fatty acid source with lauric oils constituting up to 80% of the diet “using naturally occurring
kernel oils.”
In 1991 and 1995, two patents were issued to the group of researchers whose work has been reviewed
above. The first invention (Isaacs et al 1991) was directed to antiviral and antibacterial activity of
both fatty acids and monoglycerides, primarily against enveloped viruses. The claims were for “a
method of killing enveloped viruses in a host human…wherein the enveloped viruses are AIDS
viruses…[or]…herpes viruses…[and the]…compounds selected from the group consisting of fatty acids
having from 6 to 14 carbon atoms and monoglycerides of said fatty acids…[and]…wherein the fatty
acids are saturated fatty acids.”
The second patent (Isaacs et al 1995) was a further extension of the earlier one. This patent also
included discussion of the inactivation of envelop viruses and specifically cited monoglycerides of
caproic, caprylic, capric, lauric, and myristic acid. These fatty acids make up more than 80% of
coconut oil. Also included in this patent was a listing of susceptible viruses and some bacteria and
protozoa.
Although these latter patents may provide the owners of the patents with the ability to extract
royalties from commercial manufacturers of monoglycerides and fatty acids, they cannot require
royalties from the human gastrointestinal tract when it is the “factory” that is doing the manufacturing
of the monoglycerides and fatty acids. Clearly though, these patents serve to illustrate to us that the
health-giving properties of monolaurin and lauric acid are well-recognized by some individuals in the
research arena, and they lend credence to our appropriate choice of lauric oils for promoting health
and as adjunct treatment of viral diseases.

XIII. HOW CAN WE GET SUFFICIENT COCONUT FAT INTO THE FOOD SUPPLY IN THE U.S. AND OTHER COUNTRIES THAT NEED ITS BENEFITS?

I would like to review for you my perception of the status regarding the coconut and coconut
products market in the North American countries such as the United States and Canada at the end of
the 20th century and the beginning of the 21st century.
Coconut products are trying to regain their former place in several small markets. The extraction of
oil from fresh coconut has been reported in the past decade and my impression is that this is being
considered as a desirable source of minimally processed oil, which produces an oil with desirable
characteristics for the natural foods market.
There have been some niche markets for coconut products developing during the past half-decade.
These are represented primarily by the natural foods and health foods producers. Some examples are
the new coconut butters produced in the U.S. and Canada by Omega Nutrition and Carotec, Inc. And,
this is no longer as small a market as it has been in past years. Desiccated coconut products, coconut
milk, and even coconut oil are appearing on the shelves of many of these markets. After years of
packaging coconut oil for skin use only, one of the large suppliers of oils to the natural foods and
health foods stores has introduced coconut oil for food use, and it has appeared within the last few
months on shelves in the Washington, DC metropolitan area along with other oils. I believe I
indirectly had something to do with this turn of events.

XIV. CONCLUSIONS AND RECOMMENDATIONS

As we come close to the end of the year 1999 and set our sights on what could happen in the year
2000 and beyond, there is much to be gained from pursuing the functional properties of coconut for
improving the health of humanity.
On the occasion of the 30th anniversary of the Asian Pacific Coconut Community, at this 36th
meeting of APCC, I wanted to bring you a message that I hope will encourage you to continue your
endeavors on behalf of all parts of the coconut industry. Coconut products for inedible and especially
edible uses are of the greatest importance for the health of the entire world.
Some of what I have been telling you, most of you already know. But in saying these things for the
record, it is my intention to tell those who did not know all the details until they heard or read this
paper about the positive properties of coconut.
Coconut oil is a most important oil because it is a lauric oil. The lauric fats possess unique
characteristics for both food industry uses and also for the uses of the soaps and cosmetic industries.
Because of the unique properties of coconut oil, the fats and oils industry has spent untold millions to
formulate replacements from those seed oils so widely grown in the world outside the tropics. While
it has been impossible to truly duplicate coconut oil for some of its applications, many food
manufacturers have been willing to settle for lesser quality in their products. Consumers have also
been willing to settle for a lesser quality, in part because they have been fed so much misinformation
about fats and oils.
Desiccated coconut, on the other hand, has been impossible to duplicate, and the markets for
desiccated coconut have continued. The powdered form of desiccated coconut now being sold
in Europe and Asia has yet to find a market in the U.S., but I predict that it will become an
indispensable product in the natural foods industry. Creamed coconut, which is desiccated
coconut very finely ground, could be used as a nut butter.
APCC needs to promote the edible uses of coconut, and it needs to promote the reeducation of the
consumer, the clinician, and the scientist. The researcher H. Thormar (Thormar et al 1999)
concluded his abstract with the statement that monocaprin “…is a natural compound found in certain
foodstuffs such as milk and is therefore unlikely to cause harmful side effects in the concentrations
used.” It is not monocaprin that is found in milk, but capric acid. It is likely safe at most any level
found in food. However, the levels in milk fat are at most 2 percent whereas the levels in coconut fat
are 7 percent.
One last reference for the record. Sircar and Kansra (1998) have reviewed the increasing trend of
atherosclerotic disease and type-2 diabetes mellitus in the Indians from both the subcontinent of India
and abroad. They note that over the time when there has been an alarming increase in the prevalence
of these diseases, there has been a replacement of traditional cooking fats with refined vegetable oils
that are promoted as heart-friendly, but which are being found to be detrimental to health. These
astute researchers suggest that it is time to return to the traditional cooking fats like ghee, coconut oil,
and mustard oil.
There are a number of areas of encouragement. The nutrition community in the United States is
slowly starting to recognize the difference between medium chain saturated fatty acids and other saturated fatty acids. We predict now that the qualities of coconut, both for health and food function,
will ultimately win out.

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1) Studie zu mittelkettigen gesättigten Fettsäuren: A Geliebter, N Torbay, EF Bracco, SA Hashim and TB Van Itallie, Overfeeding with medium-chain triglycerides diet results in diminished deposition of fat. American Journal of Clinical Nutrition, Vol 37, 1-4, Copyright © 1983 by The American Society for Clinical Nutrition, Inc Abstract: The study was designed to determine whether overfeeding rats with a diet containing medium-chain triglyceride (MCT) as the major fat source (45% of calories) would impede the expected gain in weight and body fat as compared to rats overfed with isocaloric amounts of diet containing long-chain triglyceride (LCT). For 6 wk rats were fed either MCT diet or LCT diet twice daily via a gastrostomy tube. MCT-fed rats gained 20% less weight (P less than 0.001) and possessed fat depots weighing 23% less (p less than 0.001) than LCT-fed rats. Mean adipocyte size was smaller (p less than 0.005) in MCT- than in LCT-fed rats. Weights of carcass protein and water were similar for both groups as were concentrations of serum insulin and levels of physical activity. The decreased deposition of fat in the MCT-fed rats may have resulted from obligatory oxidation of MCT-derived fatty acids in the liver after being transported there via the portal vein, leaving almost no MCT derivatives for incorporation into body fat. MCT may have potential for dietary prevention of human obesity.

2) Die „Verbrennung“ ist bei mittelkettigen gesättigten Fettsäuren um 12% gesteigert, gegenüber 4% bei langkettigen gesättigten Fettsäuren.

3) Studie zu thermischen Wirkungen von mittel- und langkettigen gesättigten Fettsäuren auf den Menschen: Seaton T., Welles S.,Warenko W.,Thermic effects of MCT and LCT in man, American Journal of Clinical Nutrition 1986; 44, 630-634

4) verschiedene Kapitel zu gesättigten Fettsäuren im Buch ?Fat That Heals, Fat That Kills?, Udo Erasmus, Alive Books, Revised, updated & expanded 1993, ISBN-10: 0920470386

5) Fat metabolism, article discussing the specifications of MCT oil, why we use it and how it works, by Arthur E. Roberson, Ph.D

I. Introduction
Nomenclature of Fats

Fats, or lipids, are found in all cells and perform a variety of functions essential for life. These include their roles in energy storage, membrane structure, and incorporation in vitamins, hormones, and prostaglandins (Zubay, 1983). Fats are used to cushion and insulate the body and function as electrical insulation in the nervous system. Triglycerides are the most common form of fat found in foods and stored in body fat depots. Most naturally occuring triglycerides contain fatty acids 16-20 carbon atoms in length. Such fatty acids are called ?long chain fatty acids? (LCFAs), and their corresponding triglycerides are called ?long chain triglycerides? (LCTs). Medium chain triglycerides (MCTs) are comprised of medium chain fatty acids (MCFAs), which are 6-12 carbons in length. Although the carboxylic acid part of fatty acids is soluble in water, the hydrocarbon chain is not. Thus, LCFAs are not water soluble. Since the hydrocarbon chains of MCFAs are shorter, MCFAs are more water soluble than LCFAs. Likewise, MCTs are also relatively soluble in water, due to ionization of the carboxylic acid groups and the small size of the hydrocarbon chains. Their small molecular size and greater water solubility cause MCTs to undergo a different metabolic path than that experienced by LCTs (Bach and Babayan, 1982).

Occurrence and Purification of MCTs
Medium chain triglycerides occur naturally in small quantities in a variety of foods, and are present naturally in the blood of the human fetus and in human milk (Bach and Babayan, 1982; Souci, Fachmann, Kraut, 1989/90)? MCT oil has a caloric density of 8.3 calories per gram; one tablespoon equals 14 grams and contains 115 calories. MCTs are not drugs and have no pharmacological effects (Bach and Babayan, 1982).

Historical Uses of MCTs

Since their introduction in 1950 for the treatment of fat malabsorption problems, medium chain triglycerides have enjoyed wide application in enteral and parenteral nutrition regimens (Bach and Babayan, 1982). Fat emulsions can be used to provide up to 60% of nonprotein calories. Before the availability of lipid emulsions suitable for intravenous use, glucose was used as the only nonprotein source of calories (Mascioli et al, 1987). Not only did this result in essential fatty acid deficiencies, but it was also undesirable because it increased hepatic lipogenesis and respiratory work. Although inclusion of LCTs in intravenous feedings represented an improvement, problems remained with slow clearance of LCTs from the bloodstream and interference with the RES component of the immune system. When medium chain triglycerides or structured lipids (triglycerides containing both MCFAs and LCFAs) are added to the regimen, calories are provided in a more readily oxidizable form (Schmidl, Massaro, and Labuza; 1988), and less interference with the RES is observed (Mascioli et al, 1987). In one case, MCT was fed as the exclusive source of fat (along with a small amount of LCT to provide essential fatty acids) to a patient with chyluria (a fat malabsorption disease) for over 15 years without producing side effects (Geliebter et al, 1983).

Sports Nutrition
Although MCTs have been used in hospital environments for years, their use by healthy individuals is relatively new. Recently, athletes have begun to use MCTs to increase caloric consumption, thereby providing energy and facilitating weight gain. Their low food efficiency, due to the thermogenic effect, means that MCTs have very little tendency to be converted to body fat. The calories from MCTs represent an additional energy source which (in contrast to conventional fats) can be used concurrently with glucose.

II. Metabolism
Digestion and Absorption of Fats

Since LCTs are not very soluble in water, the body has to go through an elaborate digestive process in order to absorb these nutrients. Bile salts are secreted by the gall bladder to help dissolve the LCTs. Upon ingestion, LCTs interact with bile in the duodenum (upper small intestine) and are incorporated into mixed micelles (Record et al, 1986). Enzymes called lipases (pancreatic lipase and phospholipase A2) remove the fatty acid molecule from the glycerol backbone. The mixed micelles are passively absorbed into the intestinal mucosa where the free fatty acids are re-esterified with glycerol. The intestinal mucosa synthesizes a lipoprotein carrier called a chylomicron to transport the reformed triglyceride. Chylomicrons are secreted into the lymph and are released into the venous circulation via the thoracic duct. In the bloodstream, lipoprotein lipase again breaks down the triglycerides into two free fatty acids and a monoglyceride. The monoglycerides go to the liver to be further degraded, while many of the circulating free fatty acids are taken up and stored by adipocytes (fat cells). When carbohydrates are consumed insulin is released, and insulin stimulates adipocytes to re-esterify the fatty acids into triglycerides and store them as body fat. In general, body fat stores are not mobilized and used for energy to any significant extent in the presence of insulin.

In contrast, since MCFAs are more water soluble they are more easily absorbed and do not require this complicated digestive process. MCTs can be absorbed intact and do not require the action of pancreatic lipase or incorporation into chylomicrons. Instead, a lipase within the intestinal cell degrades the MCT into free MCFAs and glycerol. The MCFAs are bound to albumin, released into the bloodstream, and transported directly to the liver by the portal vein. The vast majority of MCFAs are retained by the liver where they are rapidly and extensively oxidized. Whereas conventional fats are largely deposited in fat cells, MCTs are transported directly to the liver and used for energy. Very little of the MCFAs ever escape the liver to reach the general circulation (Bach and Babayan, 1982). Only 1-2% of MCTs are incorporated into depot fat (Geliebter et al, 1983; Baba, Bracco, and Hashim, 1982). Medium chain triglycerides are digested and absorbed much faster than conventional fats (in fact, as rapidly as glucose) and are immediately available for energy.

References
1. Baba, Bracco, and Hashim, Enhanced thermogenesis and diminished deposition of fat in response to overfeeding with diet containing medium chain triglyceride. Am. J. Clin. Nutr. 35: 678-682 (1982).
2. Bach and Babayan, Medium chain triglycerides: an update. Am. J. Clin. Nutr. 36:950-962 (1982).
3. Christensen, Hagve, Gronn, and Christophersen, Beta-oxidation of medium chain (C8-C14) fatty acids studied in isolated liver cells. Biochem. et Biophys. Acta 1004: 187-195 (1989).
4. Geliebter, Torbay, Bracco, Hashim, and Van Itallie, Overfeeding with medium chain triglyceride diet results in diminished deposition of fat. Am. J. Clin. Nutr. 37: 1-4 (1983).
5. Mascioli, Bistrian, Babayan, and Blackburn, Medium chain triglycerides and structured lipids as unique nonglucose energy sources in hyperalimentation. Lipids 22: 421-423 (1987).
6. Record, Kolpek, and Rapp, Long chain versus medium chain length triglycerides – a review of metabolism and clinical use. Nutr. Clin. Prac. 1:129-135 (1986).
7. Schmidl, Massaro, and Labuza, Parenteral and enteral food systems. Food Tech. 77-87 (July, 1988).
8. Souci, Fachmann, and Kraut, Food Composition and Nutrition Tables 1989/90. Published by Wissenschaftliche Verlagsgesellschaft (1989).
9. Sucher, Medium chain triglycerides: a review of their enteral use in clinical nutrition. Nutr. Clin. Prac. 44: 146-150 (1986).
10. Zubay, Biochemistry, chapter 13: ?Metabolism of Fatty Acids and Triacylglycerols,? by Denis E. Vance. Published by Addison-Wesley Publishing Company (1983).