There is a lot of misinformation on the Internet regarding the differences between MCT oil and coconut oil. So let’s clearly define what each product is and how they differ. Once we have this proper understanding, the myths regarding MCT oil that are being propagated will become very obvious.
What are MCTs?
Before we can begin our comparison of MCT oil and coconut oil, the first thing we have to do is define “MCT.” MCTs stands for medium chain triglycerides. Another term for “triglycerides” is fatty acids. So another way of referring to MCTs is MCFA (medium chain fatty acids).
“Medium” references the chain length of the fatty acids. Oils can contain short chain, medium chain, or long chain fatty acids. Most oils are a combination of all three types.
Medium chain fatty acids contain between 6 and 12 carbon chains [1]. They are:
- C6 – Caproic Acid
- C8 – Caprylic Acid
- C10 – Capric Acid
- C12 – Lauric Acid
These medium chain fatty acids are known to have tremendous health benefits.
C6 through C10, although found in coconut oil, are more predominant in other places in nature, such as goat’s milk. This is reflected in their names, taken from “capra,” which means “goat.”
The most predominant MCT found in coconut oil, however, is lauric acid. Coconut oil is about 50% lauric acid, making it nature’s richest source of lauric acid.
While all the MCTs have known health benefits, lauric acid is the most well-known of the four. Lauric acid is prized around the world as a powerful antimicrobial agent, used in both food preservation as well as in drugs and nutraceuticals.
A recent search on the popular International Trading website Alibaba.com, for example, showed the following results when searching for each particular fatty acid:
- Lauric acid – 1,861 Products from 194 Suppliers
- Caprylic Acid – 451 Products from 66 Suppliers
- Caproic acid – 393 Products from 69 Suppliers
- Capric Acid – 206 Products from 56 Suppliers
Lauric acid products total more than the three capra MCT fatty acid products combined.
MCT Oil is Manufactured – Coconut Oil is Natural
Coconut oil in nature contains all four MCTs. In addition, it contains a small percentage of longer chain fatty acids.
MCT oil, on the other hand, is not an oil found in nature, but is manufactured by machine to separate out the medium chain fatty acids from the rest of the oil. The fatty acids are extracted through an industrial process of “fractionation”.
The logic is that since MCTs are healthy, the more the better. Therefore, it is a popular belief that MCT oil is healthier than coconut oil. But is this true?
What is MCT Oil?
Where the logic fails in comparing MCT oil to coconut oil, is in the assumption that all four MCTs are present in MCT oil, and only the longer chain fatty acids from coconut oil are removed. This assumption is false.
MCT oils generally contain only the capra fatty acids. Lauric acid is either missing, or present in minuscule amounts. Therefore, to assume that MCT oil is a fractionation of coconut oil, where the longer chain fatty acids have been removed, leaving all of the MCTs from coconut oil, is false. Lauric acid is the star component in coconut oil, but missing in MCT oil. If MCT oil was the fractionation of all of the MCTs in coconut oil, it would be about 80% lauric acid. But it is not. It is zero percent lauric acid.
This is not surprising if you think about it. Lauric acid is the most valuable component of coconut oil, and as we saw above, the most actively traded MCT fatty acid in the world market.
So what does one do with the remaining capra MCTs after removing the valuable lauric acid? Market it as MCT oil of course!
Is MCT Oil better than Coconut Oil?
No, of course not. How can a product that has the most famous and most dominant fatty acid removed from the original product be considered “better”?
Lauric acid is unique to coconut oil, comprising about 50% of its fatty acids. Coconut oil is nature’s richest source of lauric acid. The next highest source is human breast milk, at about 6 to 10%. So if you want lauric acid, coconut oil is the place to get it.
If, however, you want the capra medium chain fatty acids, you have many more alternatives, including goat’s milk and other animals’ milk.
The capra medium chain fatty acids have their own unique characteristics and benefits. But to refer to them as “better” than coconut oil is short-sighted. They are not better – just different.
Due to the recent rise in popularity of coconut oil, MCT oil has even been marketed as “liquid coconut oil” now. When lauric acid has been removed, the remaining MCTs stay liquid at much lower temperatures.
MCT oil is not true coconut oil, however, since it contains little or no lauric acid. One should not expect the same benefits from cooking with MCT oil (which traditionally has been a supplement or skin care ingredient, and only recently has been marketed as a cooking oil), as with coconut oil.
So while we are not saying that MCT oil is “bad,” the hype saying it is “better” than coconut oil just does not reflect the facts. It suggests that people making such statements are falling for marketing claims, without really investigating the true nature of MCT oil.
References
1. Know Your Fats, by Mary Enig,
About the author: Unlike many people who write about coconut oil by simply reading about it, Brian Shilhavy actually lived in a coconut producing area of the Philippines for several years with his family. Marianita Jader Shilhavy grew up on a coconut plantation in the Philippines and in a culture that consumed significant amounts of coconut fat in their diet. She later went on to earn her degree in nutrition and worked as a nutritionist in the Philippines. Brian Shilhavy also lived in the Philippines for several years with Marianita and their 3 children observing firsthand the differences between the diet and health of the younger generation and those of Marianita’s parents’ generation still consuming a traditional diet. This led to years of studying Philippine nutrition and dietary patterns first hand while living in a rural farming community in the Philippines. Brian is the author of the best-selling book: Virgin Coconut Oil: How it has changed people’s lives and how it can change yours!
by Brian Shilhavy
Health Impact News
Candida albicans is the most common fungal microorganism in healthy individuals, as well as the most common fungal pathogen causing lethal infections (particularly in high-risk groups such as immunocompromised patients) (Cheng 2012; Douglas 2011). It can be found in up to 70% of healthy individuals at any given time (Cheng 2012; Hibino 2009; Schulze 2009).
Candida is considered an opportunistic pathogen because it can harmlessly colonize the human digestive tract, mouth, skin, and genitourinary tract (Kim 2011; Tampakakis 2009). However, when the balance of normal bacteria is upset (e.g., after antibiotic treatment) or the immune system of the host is weakened (e.g. treatment with systemic corticosteroids), candida can proliferate(Murzyn 2010).
Several areas of the body may be affected by fungal infection:
Urogenital tract - Although candida is often found in the lower female urogenital tract in asymptomatic women, proliferation and subsequent infestation of this fungal species accounts for approximately one-third of all infections in the vulva and/or vagina (i.e., vaginitis) (Sobel 2012). Also known as vulvovaginal candidiasis (VVC) or “yeast infection” (Powell 2010), this fungal infection represents the second most common cause of vaginitis in the U.S. (after bacterial vaginosis), and is diagnosed in up to 40% of women who present to their primary care provider with vaginal complaints (Ilkit 2011). Approximately 75% of women report having had at least one episode of VVC, and between 40%-45% will suffer from at least two or more episodes within their lifetime (Workowski 2010).
The most common symptoms of VVC include unrelenting itch, painful intercourse, malodorous vaginal discharge, and painful urination (Workowski 2010). Although the vast majority (up to 92%) of VVC cases are caused by Candida albicans, other candida species can also be responsible (e.g.,Candida glabrata and Candida parapsilosis). However, the various candida species tend to produce similar vulvovaginal symptoms. Recently, researchers have reported an increased frequency of VVC caused by non-albicans species (Sobel 2012). This trend may be attributed to selective pressure from the widespread use of over-the-counter and prescription antifungal drugs (Sobel 2012), especially since some non-albicans species are less susceptible to many of these medications (Iavazzo 2011).
Some evidence suggests that hormones influence the infectious process of VVC (Carrara 2010). This conclusion is supported by data indicating that a majority of VVC cases occur during the reproductive years. For example, 75% of women of childbearing age are affected by VVC (Sobel 2012; das Neves 2008; Špaček 2007), while only sporadic episodes of VVC are reported among premenstrual girls and postmenopausal women (Sobel 2012; Špaček 2007). Further research reveals that fluctuating hormone levels resulting from menstruation and pregnancy, as well as the use of oral contraceptives and hormone replacement (i.e., estrogen therapy), may predispose females to VVC (Yano 2011; Relloso 2012).
Researchers have identified several factors that may increase susceptibility to fungal infections including (Sobel 2012):
- Diabetes (with poor glycemic control)
- Exposure to antibiotics (both during and after therapy)
- High levels of estrogen (e.g., oral contraceptives or estrogen therapy)
- Weakened immune system from drugs (e.g., corticosteroids) or disease (e.g., HIV/AIDS)
- Contraceptive device utilization (e.g., vaginal sponges, diaphragms, and intrauterine devices)
Although less common, men can get genital fungal infections as well (Aridogan 2011). Therefore, it is important that both members of a relationship receive treatment for fungal infections, even if symptoms are only evident in one person. If antifungal treatment is not initiated in both people in a relationship, the partners may continue to repeatedly infect one another (Brown Univ. 2012).
Skin – Fungal infections of the skin (i.e., cutaneous fungal infections) are a common phenomenon, affecting millions of people worldwide. While cutaneous fungal infection is not normally life threatening, it can be very uncomfortable and associated with a significant decrease in quality of life (Dai 2011; Jayatilake 2011). Candida is just one of a variety of microorganisms commonly found on human skin (NIH 2010). In healthy individuals, the overgrowth of candida is inhibited by resident skin microorganisms (normal bacterial skin flora). However, when there is an imbalance of this normal skin flora, candida can begin to reproduce in sufficient amounts to cause infection (i.e., candidiasis) (Evans 2003). Due to an increase in the number of immunocompromised individuals, the rate of candidiasis of the skin (i.e., cutaneous candidiasis) is currently on the rise (Scheinfeld 2011).
Candidiasis can be broadly classified into two forms based on the degree of fungal invasion: superficial/mucosal candidiasis and deep-seated/systemic candidiasis (Jayatilake 2011). However, superficial candidiasis of the skin and mucous membrane is much more common than deep-seated/systemic infection (Jayatilake 2011). Among the different species of candida that can be found on the skin, Candida albicans is by far the most common (Evans 2003). While cutaneous candidiasis can affect virtually any part of the human body (e.g., finger nails, external ear, in between fingers and toes), it most often occurs in warm, moist, creased areas such as the armpit or groin (NIH 2010; Jayatilake 2011; Kagami 2010; Cydulka 2009; Kauffman 2011). Major symptoms of cutaneous candidiasis include itch (unrelenting and often intense) and an enlarging skin rash. Occasionally, the rash will be surrounded by smaller rashes appearing along the outer edge of the main rash (NIH 2010). These types of fungal rashes may occur on skin that is exposed to feces (e.g., perineal skin), since this area is at a higher risk of becoming infected with candida fungus (Evans 2003).
Individuals whose hands and/or feet remain wet for prolonged periods of time may be prone to fungal infection around or under their finger and toe nails. In these cases, the nail area commonly becomes red and swollen. The nails themselves will become thick and brittle, ultimately becoming destroyed and detached (Cydulka 2009; Kauffman 2011; NIH 2012; NIH 2012). Although anyone’s nails can become infected by fungus, these types of infections are more common among adults older than 60, and among individuals with diabetes or poor circulation (AAFP 2008).
Mouth and throat – Candida infections of the mouth (i.e., oral candidiasis) are widespread among humans (Giannini 2011). In addition to the general factors that predispose an individual to candida infection (e.g., immunosuppressive drugs and antibiotics), oral candidiasis may also be caused by chronic dry mouth and oral prosthesis (dentures)(Junqueira 2012). Although oral infection can be caused by a variety of candida species, Candida albicans is the most common causative agent (Rautemaa 2011).
Oral candidiasis (thrush) is characterized by whitish, velvety sores or patches appearing on the mucous membranes lining the inside of the mouth (e.g., roof of the mouth and inside the lips and cheeks), as well as the throat and tongue (Abe 2004; NIH 2011). These whitish sores may slowly increase in size, quantity, and may bleed easily (NIH 2011). Occasionally, oral candida infections can manifest as subjective feelings of pain or taste abnormalities (Yamamoto 2010).
In addition to infections inside the mouth, candida can also take the form of perlèche (angular cheilitis) (Gonsalves 2007; Sharon 2010), which is commonly identified by reddish lesions and crusting at the corners of the mouth (Park 2011). Perlèche can be associated with long-term use of ill-fitting dentures and incorrect use of dental floss (resulting in cuts at the corners of the mouth) (Sharon 2010).
Systemic infection – Although candida species are normal residents of the gastrointestinal and genitourinary tracts of humans, they occasionally cause a deep-seated or systemic (disseminated) infection (Kauffman 2012b). These serious fungal infections usually indicate the host has a weakened immune system, and can occur as a result of a superficial skin infection that invades deeper tissues, eventually reaching the blood stream (i.e., candidemia). Once the fungus is circulating throughout the body, it has the capacity to reach vital organs such as the brain, heart, and kidneys. While this form of candidiasis is rare, it is the most severe (Jayatilake 2011). These types of fungal infections can be fatal and require prompt diagnosis and aggressive treatment in order to achieve a favorable outcome (Emiroglu 2011).
Since the clinical symptoms of a systemic candida infection can vary, and are often very similar to that of a bacterial infection, the gold standard for its proper diagnosis is a positive blood culture (Kauffman 2012a). Advancements in blood culturing technology now allow for the rapid identification of a variety of candida species in as little as 90 minutes. This reduction in laboratory turnaround time enables clinicians to optimize antifungal drug selection much faster, and ultimately improve care (Advandx 2010; Hall 2012).
Intestinal Candidiasis – Candida organisms are a common part of the normal gastrointestinal flora (Kumamoto 2011), and are present in the gut of approximately 70% of healthy adults (Schulze 2009). However, high levels of candida colonization in the GI tract may be an urgent problem (Zlatkina 2005), especially since it is associated with several gastrointestinal diseases (e.g., irritable bowel syndrome) and certain allergic reactions. (Kumamoto 2011; Schulze 2009). Furthermore, candida colonization in the gut can also promote inflammation, which in turn promotes further fungal colonization in a vicious cycle (Kumamoto 2011).
Intestinal candida colonization can also lead to superficial and systemic candidiasis if the innate host barriers (i.e., mucosa, immune system, intestinal microflora) are not stable (Schulze 2009). Benign strains of intestinal candida can also become more virulent when their gene expression is altered in such a way that they are able to form biofilms, destroy tissues, and escape host immune system defenses (Kumamoto 2011; Schulze 2009). While antimycotics (e.g., nystatin) are available for the treatment of intestinal candida overgrowth, probiotics (having demonstrated positive results in controlled clinical trials) may also be beneficial. Probiotics may exert this affect by rebalancing the normal flora of the gut, thereby suppressing local candida colonization.
Some research questions the clinical significance of yeast infestation of the intestinal mucosa, and suggests that clinical action may not always be necessary (Schulze 2009).
Fungal Sinusitis – Overgrowth of fungus in the nasal cavity (i.e., fungal sinusitis or fungal rhinosinusitis) and the subsequent human immune response (e.g., allergic fungal sinusitis) is currently believed to be responsible for some cases of chronic sinusitis (Ivker 2012). This condition can be classified as either invasive or non-invasive, depending on the extent of fungal infection. Invasive forms of fungal sinusitis are largely limited to immunocompromised populations (Riechelmann 2011), and are characterized by infection of the submucosal tissue, which often causes tissue necrosis and destruction (Montone 2012).
Although optimal treatment options for fungal sinusitis are still debated, (Dabrowska 2011), they typically include systemic antifungal therapy as well as surgical debridement & evacuation of infected tissue (Riechelmann 2011). In addition to these conventional treatment options, some experts believe fungal sinusitis may also respond to probiotics as well as an anti-fungal diet. An anti-fungal diet calls for avoidance of sugar and concentrated sweets, and consists primarily of protein and fresh vegetables, along with a small amount of fruit, complex carbohydrates, and fat-containing foods (Ivker 2012).