FLAX UNLEASHED and FLAX UNBRIDLED – Scientific Research

Dr. Marion Smart DVM, PhD, Professor Emeritus and Veterinary Clinical Nutritionist who has had firsthand experience using Flax Unleashed, comments on this supplement:

“As a functional food, Flax Unleashed provides complex nutrients essential for life that must be found in the diet. Flax Unleashed captures the benefits of the whole flax seed, not just the oil which contains the valuable and essential omega-3 fatty acid. This oil is protected and preserved with naturally occurring components called Lignans, also found within the flax seed that add additional health giving qualities to this supplement placing it in a category of its own. This is not just another organic flax oil made by conventional means, but a nutritional powerhouse containing flax oil, vitamins, minerals, protein and one of natures' most potent natural anti-oxidants, Lignan. The plant based Omega 3 in flax is a precursor to EPA and DHA. Scientifically, this conversion is considered slow in our pets but metabolically the conversion is a natural, continuous step process in response to the inflammatory reaction created by the Omega 6 fatty acids that are very high in most North American pet food diets. Along with improving the Omega 6 : Omega 3 ratio in the diet, the Omega 3's are also critical for healthy and proper function of all cells in the body. We believe that the benefits of Flax Unleashed extend way beyond the Omega 3's and that through the gentle unrefined processing of the Canadian organic flax seed, a synergy (perhaps the greatest benefit of whole food products) is at least part of the reason that pet guardians consistently report improvement in their animal’s mobility, skin and hair coat, and overall vitality. This Certified Organic, functional whole food nutraceutical, contains one ingredient only – Canadian Organic, Non-GMO Flax seed and would be useful in the diet of every pet.”

Exerpts from Flax - A Health and Nutrition Primer

Chapter 2

Biologic Effects of Omega-3 Fatty Acids

The omega-3 fatty acids have biologic effects that make them useful in preventing and managing chronic conditions such as type 2 diabetes, kidney disease, rheumatoid arthritis, high blood pressure, coronary heart disease, stroke, Alzheimer disease, alcoholism and certain types of cancer (48). Key biologic effects of the three main omega-3 fatty acids – ALA, EPA and DHA – are described below. Alpha-linolenic acid (ALA) ALA has several biologic effects, which together contribute to its positive health effects:

1. Breast milk contains about 0.5-2.0% ALA and about 0.1-0.4% DHA (86) or roughly five times more ALA than DHA. ALA constitutes 75-80% of the total omega-3 fatty acids in breast milk (49,51-53), supporting a role for ALA in the growth and development of infants.

2. ALA is required for maintaining the nervous system. In humans, a deficiency of ALA results in poor growth and neurological problems such as numbness, weakness, pain in the legs, inability to walk and blurring of vision (87). These clinical deficiency symptoms can be alleviated by adding ALA to the diet (24,87-91).

3. ALA is the precursor of EPA, DPA and DHA. Thus, ALA-rich diets increase the ALA, EPA, DPA and total omega-3 fatty acid content of cell membrane phospholipids. In one study of 20 healthy men and women taking six flax oil capsules a day (providing 3.5 g of ALA/day) for 8 weeks, the ALA content of red blood cell membranes increased 100%, the EPA content increased 33%, and the DPA content increased 20%; the DHA content was unchanged (92). In other studies, diets containing more than 4.5 g of ALA/day (contained in about 1/2 tbsp of flax oil or 2 heaping tbsp of milled flax daily) increased the EPA content of plasma phospholipids between 33% and 370% and the DPA content between 5% and 50% (54). [The large ranges in the response of study volunteers to dietary ALA reflect differences in the amount of LA in their diets, among other factors (55).] Increasing the omega-3 fatty acid content of cell membrane phospholipids increases their flexibility and alters the way they behave in beneficial ways (93).

4. ALA dampens inflammatory reactions by blocking the formation of compounds that promote inflammation. Inflammation is a feature of many chronic diseases, such as heart disease, type 2 diabetes, metabolic syndrome, obesity, cancer and Alzheimer disease (94-96). ALA has several anti-inflammatory actions: • EICOSANOIDS. ALA affects eicosanoids in two ways. First, ALA is a precursor of EPA, which is itself a precursor of eicosanoids, as shown in Figure 3. Eicosanoids control inflammatory reactions. Their release is a normal response to injury, and their actions are required to help repair damaged tissue. However, not all eicosanoids are alike. The eicosanoids derived from EPA tend not to promote inflammation. This is one reason why nutrition experts advise consumers to eat more omega-3 fatty acids: A diet rich in omega-3 fatty acids produces more beneficial eicosanoids and less inflammation and decreases the risk of chronic diseases compared with diets rich in omega-6 fatty acids. Secondly, ALA interferes with the conversion of LA to AA and blocks the conversion of AA to its pro-inflammatory eicosanoids. For example, diets rich in ALA decreased significantly the concentration of AA in neutrophils (97) and in serum (98,99). The production of eicosanoids from AA in mononuclear cells decreased 30% in healthy men who consumed flax oil for four weeks (100). [Neutrophils and mononuclear cells are types of immune cells that help control infections and inflammation.]

• CYTOKINES. ALA blocks the formation of cytokines. Three cytokines that contribute to inflammation are tumor necrosis factor α, interleukin-1β and interleukin-6. A study of 20 men and women with high blood cholesterol found that the production of these cytokines by certain immune cells was decreased significantly when the volunteers ate a diet high in ALA compared with an average American diet. The high-ALA diet in this study provided about 19 g ALA/day obtained from walnuts, walnut oil and flax oil (99).

• PLATELET-ACTIVATING FACTOR. ALA may help block the formation of platelet-activating factor (PAF). In studies of mice used as a model of lupus nephritis (kidney inflammation), feeding flax in the diet for 14 weeks blocked PAF-caused platelet aggregation. According to the researchers, ALA may work synergistically with flax lignans to dampen the effects of PAF (101).

• C-REACTIVE PROTEIN. High blood levels of C-reactive protein (CRP) indicate the presence of systemic inflammation or infection (102). In a clinical trial, serum CRP levels decreased 75% when men and women ate a high-ALA diet containing walnuts, walnut oil and flax oil for 6 weeks (98).

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Eicosapentaenoic acid (EPA)EPA is the precursor of certain eicosanoids that tend not to promote inflammation because they are less biologically active than those derived from arachidonic acid (83). EPA affects inflammation in another way: It gives rise to potent compounds called resolvins, so named because they are found at sites recovering from inflammation (that is, when the inflammation is resolving) (103). The EPA-derived resolvins dampen inflammatory reactions (104).

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ocosahexaenoic acid (DHA)In the fetus and infant, DHA is required for the development and maturing of the eye, where it constitutes as much as 80% of total polyunsaturated fatty acids in the retina, and of the brain and nervous system, which contain high concentrations of DHA (105). The brain, retina and sperm have the highest concentrations of DHA of any tissue in the body (106). The demand for DHA is highest during the latter part of pregnancy and in the first few months of infancy. Like EPA, DHA also gives rise to resolvins. The DHA-derived resolvins are active in the brain, where they block the actions of pro-inflammatory cytokines (104).

Chapter 3

Food Sources of Omega-3 Fatty Acids

ALA is found in plants, animals, plankton and marine species (133). Up to 80% of the fatty acids in leafy green plants is in the form of ALA; but because their overall fat content is low, leafy plants do not contribute significant amounts of ALA to our diets (134). Flax is the richest source of ALA in the North American diet. ALA is also found in walnut oil, canola oil, olive oil, and soybean oil; in nuts such as butternuts and walnuts; in soybeans and pumpkin seeds; in omega-3-enriched eggs; and in purslane. Fish contain only trace amounts of ALA, although some species of fish, particularly fatty marine fish such as salmon, mackerel and herring, are rich in EPA and DHA (112, 122, 135). Table 11 shows the ALA content of some foods. EPA and DHA are found mainly in fatty fish such as mackerel, salmon, tuna, herring, lake trout and anchovy (135). Other sources include fish oil capsules; marine algae, which are rich in DHA but contain negligible amounts of the other omega-3 fatty acids (136); and omega-3-enriched eggs derived from laying hens fed a ration containing either microalgae, which increase the DHA content of the yolk (137), or flax, which increases the ALA, DPA and DHA content of the yolk (138).

 

Scientific Research - New Beginnings

‘The processes required for fermented foods were present on earth when man appeared on the scene… When we study these foods, we are in fact studying the most intimate relationships between man, microbe and foods.’ [1]

Prof. Keith H. Steinkraus, Cornell University, 1993

Functional microorganisms transform the chemical constituents of raw materials of plant/animal sources during food fermentation thereby enhancing the bio-availability of nutrients, enriching sensory quality of the food, imparting bio-preservative effects and improvement of food safety, degrading toxic components and anti-nutritive factors, producing antioxidant and antimicrobial compounds, stimulating the probiotic functions, and fortifying with some health-promoting bioactive compounds (Tamang et al., 2009, 2016; Farhad et al., 2010; Bourdichon et al., 2012; Thapa and Tamang, 2015).

Lactic acid bacteria present in fermented foods may decrease number of incidence, duration and severity of some gastrointestinal disorders (Verna and Lucak, 2010). Administration of some strains of Lactobacillus improves the inflammatory bowel disease, paucities and ulcerative colitis (Orel and Trop, 2014). L. rhamnosus GG is effective in the treatment of acute diarrhea (Szajewska et al., 2007) and administration of L. helveticus-fermented milk in healthy older adults produced improvements in cognition function (Chung et al., 2014). Consumption of fermented milk products containing live bacteria has immunomodulation capacity (Granier et al., 2013), and cures diarrhea (Balamurugan et al., 2014). Korean kimchi is suitable for control of inflammatory bowel diseases (Lim et al., 2011).

Citation: Tamang JP, Shin D-H, Jung S-J and Chae S-W (2016) Functional Properties of Microorganisms in Fermented Foods. Front. Microbiol. 7:578. doi: 10.3389/fmicb.2016.00578

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Modern advances in chemical preservation, refrigeration, and transportation efficiency have not resulted in the abandonment of fermented foods. At least in traditional dietary practices, fermented foods and beverages remain widespread, currently accounting for approximately one-third of the human diet globally [7]. Moreover, as scientists continue to uncover health-promoting properties of ancestral dietary patterns (for example, the Mediterranean diet, the traditional Japanese diet, and hunter-gatherer diets), by extension there is a renewed examination of the fermented foods that are so often a part of such ancient diets [8]. Emerging research, as reviewed here, indicates that fermentation may magnify the known benefits of a wide variety of foods and herbs, influencing the bioavailability and activity of the chemical constituents. In addition, as our knowledge of the human microbiome increases (the intestinal microbiota in particular), it is becoming increasingly clear that there are untold connections between the ways in which microbes act upon dietary items pre-consumption, and in turn, the ways in which these fermented dietary items influence our own microbiota.

Selhub EM, Logan AC, Bested AC. Fermented foods, microbiota, and mental health: ancient practice meets nutritional psychiatry. Journal of Physiological Anthropology. 2014;33(1):2. doi:10.1186/1880-6805-33-2.

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Modern lifestyles tend to impose stress on systems genetically adapted over millions of years. The consumption of food containing microorganisms has dramatically reduced, and as a consequence, the developing mucosal immune systems are faced with different microflora, particularly fewer pathogens than paleolithic man. Increases in observed incidence and severity of allergies and conditions such as IBD in the Western world have been linked with increases in standards of hygiene and sanitation, which have occurred concomitantly with decreases in the number and range of infectious challenges encountered by the growing and developing host. This lack of immune education impairs the development of the immune system and allows the host to over-react to non-pathogenic antigen-containing commensal flora, resulting in inflammatory damage, allergy and/or autoimmunity [51]. To combat these trends directly, the World Health Organisation currently advocates the implementation of alternative disease control strategies, such as exploiting the prophylactic and therapeutic potential of probiotic bacteria [52]. Most of these probiotic microorganisms, isolated from such sources as faeces of healthy individuals, are safe for human consumption and are available over the counter. Because of continued scepticism of such products, European Union funded research groups including medical, scientific and industrial interests, have agreed on criteria for selection and assessment of probiotics.

Co-evolution led to a symbiotic relationship between eukaryotes and prokaryotes with the development of sophisticated by-directional signaling systems of mucosal epithelia and lymphocytes in the intestinal tract [51]. It is estimated that over 400 species of bacteria, separated into two broad categories, namely beneficial (e.g., Bifidobacterium and Lactobacillus) and those considered detrimental (e.g., Enterobacteriaceae and Clostridium spp.) inhabit the human gastrointestinal tract. Bacterial end products of fermentation are essential mucosal nutrients including amino acids (arginine, cysteine and glutamine) and short chain fatty acids (SCFA: acetate, propionate and butyrate) [51]. These SCFAs serve as an energy source for the host, providing 10–30% of basal metabolic requirements including energy for liver cells, colonocytes and peripheral tissues with only about 5% excreted in the feces [51]. Besides fermentation, the metabolic products of the microflora includes vitamins K and B complex, secondary bile acid production, neutralization of dietary carcinogens such as nitrosamines, and conversion to active metabolites of some prodrugs. The indigenous intestinal (autochthonous) microbiota act as a further barrier against any transient (allochthonous) potential pathogens by competing for nutrients and mucosal adherence and by production of antigens (bacteriocins), which are active against pathogens. Furthermore, it has been clearly established that the gastrointestinal flora are essential for mucosal protection and immune education as it has been described as the most adaptable and renewable metabolic organ of the body. The composition and activities of gastrointestinal flora affect both intestinal and systemic physiology. The complex gastrointestinal microbial load is required for normal development and homeostasis of the humoral and cellular immune system. It is the interaction between the mucosal immune system and the enteric microflora which maintains the physiologically normal state or activation of immune organ, the latter resulting in secretion of antibodies against harmful antigens (pathogenic microorganisms) [51].

Cencic A, Chingwaru W. The Role of Functional Foods, Nutraceuticals, and Food Supplements in Intestinal Health. Nutrients. 2010;2(6):611-625. doi:10.3390/nu2060611.

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To understand how probiotics work, it is important to understand a little about the physiology, microbiology of GI tract and the digestive process. The digestive process begins as soon as food enters the mouth and to stomach, the microbes present in the GI tract have the potential to act in a favourable, a deleterious or a neutral manner. Microbes in small intestine and in the large intestine complete the digestion process.

Certain intestinal microbes are known to produce vitamins and they are nonpathogenic, their metabolism is non-putrefactive, and their presence is correlated with a healthy intestinal flora. The metabolic end products of their growth are organic acids (lactic and acetic acids) that tend to lower the pH of the intestinal contents, creating conditions less desirable for harmful bacteria. Probiotics may also influence other protective functions of the intestinal mucosa including synthesis and secretion of antibacterial peptides, mucins. The GI tract also serves as a large mucosal surface that bridges the gap between ‘inside the body’ and ‘outside the body’. Along this mucosal interface, microbes and foreign antigens colonizing or passing through the GI tract interact with important components of the immune system. This interaction serves to prime or stimulate the immune system for optimal functioning. Normal microbial inhabitants of the GI tract also reinforce the barrier function of the intestinal lining, decreasing ‘translocation’ or passage of bacteria or antigens from the intestine into the blood stream. This function has been suggested to decrease infections and possibly allergic reactions to food antigens.

Lactic acid bacteria are known to release various enzymes and vitamins into the intestinal lumen. This exert synergistic effects on digestion, alleviating symptoms of intestinal malabsorption, and produced lactic acid, which lowers the pH of the intestinal content and helps to inhibit the development of invasive pathogens such as Salmonella spp. or strains of E. coli (Mallett et al. 1989; Mack et al. 1999). Bacterial enzymatic hydrolysis may enhance the bioavailability of protein and fat (Fernandes et al. 1987) and increase the production of free amino acids, short chain fatty acids (SCFA), lactic acid, propionic acid and butyric acid are also produced by lactic acid bacteria. When absorbed these SCFAs contribute to the available energy pool of the host (Rombeau et al. 1990; Rolfe 2000) and may protect against pathological changes in the colonic mucosa (Leavitt et al. 1978; Leopold and Eileler 2000). SCFA concentration helps to maintain an appropriate pH in the colonic lumen, which is critical in the expression of many bacterial enzymes and in foreign compound and carcinogen metabolism in the gut (Mallett et al. 1989).

In addition to nutrient synthesis, the action of micro-organisms either during the preparation of cultured foods or in the digestive tract can, to a limited extent, improve the digestibility of some dietary nutrients. Several lines of evidence show that the appropriate strain of lactic acid bacteria, in adequate amounts, can alleviate symptoms of lactose intolerance. Streptococcus thermophilus, Lactobacillus bulgaricus and other lactobacilli used in fermented milk products deliver enough bacterial lactase to the intestine and stomach where lactose is degraded to prevent symptoms in lactase nonpersistent individuals (Kilara and Shahani 1975; Martini et al. 1991).

Probiotic supplementation has both direct and indirect effects. Probiotics exhibit direct effects locally in the GI tract, including modulation of resident bacterial colonies and vitamin production. There are also indirect effects exerted at sites outside the GI tract, including the joints, lungs, and skin. Indirect effects most likely result from an impact on immunity, via changes in inflammatory mediators such as cytokines. Modulation of inflammatory responses may be related to regulating or modulating the immune system both locally in the GI tract.

It is speculated that inflammation associated with rheumatoid arthritis may be modulated by the use of probiotics (Marteau et al. 2001). Thirty patients with chronic juvenile arthritis were randomly allocated to receive Lactobacillus GG or bovine colostrum for a 2-week period (Malin et al. 1997). Immunological and nonimmunological gut defences were investigated in blood and faeces. It has been observed by different researchers that gut defence mechanisms are disturbed in chronic juvenile arthritis and suggested orally administered Lactobacillus GG has potential to reinforce mucosal barrier mechanisms in this disorder. When inflammed, the GI tract becomes permeable and serves as a link between inflammatory diseases of the GI tract and extra-inflammatory disorders such as arthritis. Modulation or downregulation of the immune system and subsequent reduction in GI permeability can result from consuming probiotics (Yukuchi et al. 1992; Vanderhoof 2000).

The potential of probiotics to control allergic inflammation at an early age was assessed in a randomized double-blind placebo-controlled study. The results provide the first clinical demonstration of specific probiotic strains modifying the changes related to allergic inflammation. The data further indicate that probiotics may counteract inflammatory responses beyond the intestinal milieu. The combined effects of these probiotic strains will guide infants through the weaning period, when sensitization to newly encountered antigens is initiated (Mack et al. 1999; Vanderhoof 2000).

In spite of inherent difficulties establishing good measures of probiotic efficacy (Rolfe 2000), studies on lactose intolerance, diarrhoea and colon cancer show that a daily dose of lactic acid bacteria is needed for any measurable effect (Rembacken et al. 1999).

Parvez, S., Malik, K.A., Ah Kang, S. and Kim, H.-Y. (2006), Probiotics and their fermented food products are beneficial for health. Journal of Applied Microbiology, 100: 1171–1185. doi:10.1111/j.1365-2672.2006.02963.x

Adams MR. 1999. Safety of industrial lactic acid bacteria. Journal of Biotechnology. 68: 171-178.  

Bourlioux P, Koletzko B, Guarner F og Braesco V. 2003. The Intelligent Intestine. Am J Clin Nutr. 78: 675-83.

Christensen HR, Kjar T, Brix S og Frokier H. 2004. Det vi spiser pavirker vores immunforsvar – men hvordan? Dansk Kemi. 84 (3): 26-27.

Corthesy B, Gaskins H Rex og Mercenier A. 2007. Cross-Talk between Probiotic Bacteria and the Host Immune System. J. Nutr. 137: 781S-790S.

Fink LN, Zeuthen LH og Frokiar H. 2007. Bakteriefloraen i tarmen afbalancerer immunsystemet. Dansk Kemi. 88 (3): 20-22.

Fooks LJ, Fuller R og Gibson GR. 1999. Prebiotics, probiotics and human gut microbiology. International Dairy Journal. 9: 53-61.

Fukuda S, Toh H, Hase K, Oshima K, Nakanishi Y, Yoshimura K, Tobe T,Clarke JM, Topping DL, Suzuki T, Taylor TD, Itoh K, Kikuchi J, Morita H,Hattori M og Ohno H. 2011. Bifidobacteria can protect from enteropathogenic infection through production of acetate. Nature 469: 543-547.

Fuller R. 1991. Probiotics in human medicine. Gut. 32: 439-442.Gilman J og Cashman KD. 2006. The Effect of Probiotic Bacteria on Transepithelial Calcium Transport and Calcium Uptake in Human Intestinal-like Caco-2 Cells. Curr. Issues Intestinal Microbiol. 7: 1-6.

Heyman M og Menard S. 2002. Review. Probiotic microorganisms: how they affect intestinal pathophysiology. Cellular and Molecular Life Science. 59: 1151-1165.

Heyman M. Effect of Lactic Acid Bacteria on Diarrheal Diseases. 2000. Journal of the American College of Nutrition. 19 (2): 137S-146S.

Nicoletti C, Regoli M, Bertelli E. 2009. Dendritic cells in the gut: to sample and to exclude? Nature 2 (5): 462.

Ohland CL og MacNaughton WK. 2010.Probiotic bacteria and intestinal epithelial barrier function. Am J Physiol Gastrointest Liver Physiol 298: G807–G819.

Pedersen SB og Frokiar H. 2006. Kan kosten pavirke vores risiko for at udvikle allergi? Miljo og sundhed. 31: 5-9.

Perdigon G, Fuller R og Raya R. Lactic Acid Bacteria and their Effect on the Immune System. 2001. Curr. Issues Intest. Microbiol. 2(1): 27-42.

Rescigno M, Urbano M, Valzasina B, Francolini M, Rotta G, Bonasio R, Granucci F, Kraehenbuhl JP, Ricciard-Castagnoli P. 2001. Dendritic cells express tight junction proteins and penetrate gut epithelial monolayers to sample bacteria. Nat. Immunol. 2 (4): 361-7.

Rupnik M, Wilcox MH og Gerding DN. Clostridium difficile infection: new developments in epidemiology and pathogenesis. 2009. Nature Reviews Microbiology 7: 526-536.

Taylor SL og Hefle SL. Food allergies and intolerances. 2006. Modern Nutrition in Health and Disease. Shils ME, Shike M, Ross, AC, Caballero B ogCousins RJ. 10: 1512-1530.

Wells J M, Rossi O, Meijerink M og Baarlen P van. 2010. Epithelial crosstalk at the microbiota-mucosal interface. PNAS Early Edition: 1-8.

 

Solid Ground - Scientific Research

Flax Lignan:

Flaxseed is one of the richest sources of lignans and is increasingly used in food products or as a supplement. Plant lignans can be converted by intestinal bacteria into the so-called enterolignans, enterodiol and enterolactone. For a proper evaluation of potential health effects of enterolignans, information on their bioavailability is essential. The aim of this study was to investigate whether crushing and milling of flaxseed enhances the bioavailability of enterolignans in plasma. In a randomized, crossover study, 12 healthy subjects supplemented their diet with 0.3 g whole, crushed, or ground flaxseed/(kg body weight · d). Each subject consumed flaxseed for 10 successive days separated by 11-d run-in/wash-out periods, in which the subjects consumed a diet poor in lignans. Blood samples were collected at the end of each run-in/wash-out period, and at the end of each supplement period. Plasma enterodiol and enterolactone were measured using LC-MS-MS. The mean relative bioavailability of enterolignans from whole compared with ground flaxseed was 28% (P ≤ 0.01), whereas that of crushed compared with ground flaxseed was 43% (P ≤ 0.01). Crushing and milling of flaxseed substantially improve the bioavailability of the enterolignans.

Among foods consumed by humans, flaxseed contains the highest concentration of enterolignan precursors, mainly secoisolariciresinol diglucoside. Other seeds, nuts, whole grains, fruits and vegetables, and beverages such as coffee and tea contain smaller amounts (24). The most important sources of lignan precursors in Western diets are beverages such as tea and coffee, seeds, cereals, berries, fruits and vegetables (25,26). Flaxseed is a relatively minor dietary component in most countries, but because of its potential health benefits [flaxseed also contains a high quantity of (n-3) fatty acids as well as dietary fiber], it is increasingly being incorporated into a variety of food products, such as bread, muesli bars, and breakfast cereals, or used as a supplement. For example, in the Netherlands, whole flaxseed is used in commercial breads (up to 3.5 g flaxseed/100 g bread); therefore is an important potential source of dietary lignans. In a case-control study carried out in Texas, Strom et al. (27) found that flaxseed bread was one of the main food sources of lignans.

The Relative Bioavailability of Enterolignans in Humans Is Enhanced by Milling and Crushing of Flaxseed1

J. Nutr. December 1, 2005  vol. 135 no. 12 2812-2816

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Milk Thistle:

Silymarin (SM) is a C25 containing flavonoid mixture, extracted from the Silybum marianum (milk thistle) plant. Today’s standardized (according to its silibinin, often called silybin, content) SM extract contains approximately 65% to 80% flavonolignans (silybin A and silybin B, isosilybin A, isosilybin B, silychristin and silydianin), with small amounts of flavonoids, and approximately 20% to 35% of fatty acids and polyphenolic compounds possessing a range of metabolic regulatory effects [1]. Silybin was discovered as the first member of a new family of natural compounds called flavonolignans in 1959 [2] and it is known as the predominant and primary active ingredient in SM [3,4]. That is why compounds containing milk thistle ingredients showing silybin content and silybin antioxidant, as well as other activities in various model systems, are used to explain the biological activity of SM. In particular, SM has been the gold standard drug to treat liver disorders of different etiologies and milk thistle extracts have been used as traditional herbal remedies (“liver tonics”) for almost 2000 years. Therefore, SM is most well known for its antioxidant and chemoprotective effects on the liver [5,6,7,8,9,10,11] and it is often prescribed and self-prescribed as a complementary and alternative hepatoprotective medicine [12]. SM is being studied as a hepato-, neuro-, nephro- and cardio-protective ingredient due to its strong antioxidant and tissue regenerative properties [12,13,14,15,16,17]. There is a range of recent comprehensive reviews covering various routes and mechanisms of action of SM in animal models and human trials [13,14,15,16,17] very often referring to its antioxidant properties. However, it seems likely that direct antioxidant (AO) activity of polyphenols does not contribute directly to the antioxidant defence of the body [18,19] and only limited work has been carried out to explore SM/silybin impact on the induction of cellular antioxidant defence via the modulation of various transcription factors, including Nrf2 and NF-κB and respective gene and protein expressions. Potential molecular proliferative signaling targets for anti-cancer activity of silibinin include the receptor tyrosine kinase, STAT, androgen receptor and NF-κB pathways [20], however, anti-cancer activity of SM is beyond the scope of the present review. Therefore, this review focuses on evaluating recent studies on SM (silibinin) antioxidant effects in various in vitro and in vivo model systems in the context of its contribution to the antioxidant systems regulation and participation in cell signaling.

Surai PF. Silymarin as a Natural Antioxidant: An Overview of the Current Evidence and Perspectives. Abourashed E, ed. Antioxidants. 2015;4(1):204-247. doi:10.3390/antiox4010204.

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Spirulina:

Spirulina (Arthrospira platensis), is a free-floating filamentous cyanobacterium that has a long history of recorded use. There is evidence that the Mayan and Aztec civilizations widely consumed dried Spirulina cakes in pre-Columbian times, and for centuries, communities in Central Africa have harvested Spirulina from the waters of Lake Chad for use as food9,10. Spirulina has received considerable attention for its 60–70% protein content and high concentrations of phenolic acids, tocopherols, essential fatty acids, and B vitamins10,11. Extracts of Spirulina have been reported to have multiple therapeutic effects, including cholesterol reduction, immunomodulation, antioxidant, anti-cancer, and anti-viral effects11.

Chen Y-H, Chang G-K, Kuo S-M, et al. Well-tolerated Spirulina extract inhibits influenza virus replication and reduces virus-induced mortality. Scientific Reports. 2016;6:24253. doi:10.1038/srep24253.

 

 

 

Lignan Works - Scientific Research

The flaxseed (Linum usitatissimum L.) is the seed from the flax plant, an annual herb which belongs to Linaceae family with more than 200 species. The Latin name of flaxseed means “very useful”, and it has brown and golden varieties. The shape of flaxseed is flat or oval up to 4–6 mm size with a pointed tip. Flaxseed has been a part of human diet for thousands of years in Asia, Europe, Africa, North America and more recently in Australia. The world flaxseed production remained static about 2.6 million tonnes as compared with other oilseed crops and represents 1 % of total world oilseeds supply. Currently, flaxseed has been the focus of increased interest in the field of diet and disease research due to the potential health benefits associated with some of its biologically active components such as dietary fiber (25–28 %) and α-linolenic acid (50–55 % of total fatty acids composition) [1].

Among the compounds that present biological activity, phenolic compounds are of special interest. Lignans, very complex classes of bioactive polyphenolic phytochemicals, formed by the coupling of two coniferyl alcohol residues are widely distributed in the plant kingdom [2]. There are two general types of lignans: i) those found in plant seeds like secoisolariciresinol diglucoside (SDG), isolariciresinol, matairesinol, lariciresinol and ii) those found in animals and humans known as mammalian lignans [3]. Phenolic lignans are found in most fiber-rich plants, including pumpkin seed, sesame seed, grains such as wheat, barley, rye and oats; legumes such as beans, lentils, and soybeans; and vegetables such as garlic, asparagus, broccoli, and carrots. Flaxseed is particularly the richest known source of lignans (9–30 mg per g), with lignan production at 75–800 times that of other oil seeds, cereals, legumes, and fruit and vegetables [4]. The principal dietary lignan present in flaxseed is SDG which occurs as a component of a linear ester-linked complex. Chemically, the C6-OH of the glucose of SDG is esterified to the carboxylic acid of hydroxymethylglutaric acid. Accumulation of SDG is coherent with LuPLR gene expression and synthesis of PLR enzyme during mature seed development [5]. The understanding of the action mechanism of these SDG compounds is crucial for their possible exploitation as neutraceutical supplement in biological system.

Diabetes is a metabolic syndrome and is characterized by increases in central adiposity, serum triglycerides, serum glucose, blood pressure, inflammation and decreases in HDL-cholesterol that elevates risk of insulin resistance [44]. The animal and human studies revealed that high fat diet containing 0 · 5 to 1 · 0 % SDG reduces liver triglycerides content, serum triglycerides, total cholesterol, and insulin and leptin concentrations that resulted in significantly reduced visceral fat gain as compared to group of mice receiving high fat diet without SDG [45]. Another study have shown that female rats receiving glucosuria induced diet with SDG have 80 % less chances of glucosuria as compared to rats have 100 % chances of glucosuria receiving diet without SDG [46]. SDG reduces C-reactive protein concentrations which are associated with insulin resistance and diabetes mellitus in type 2 diabetics [47]. Daily consumption of low-fat muffin enriched with SDG (500 mg/day) for 6 week can reduce CRP concentrations [48]. The earlier studies indicate that flaxseed lignan supplements have beneficial associations with C-reactive protein and also suggest that lignans have possible lipid- and blood pressure-lowering associations [49].

The occurrence of menopause is associated with an increased risk of cardiovascular events and this has partially been attributed to the decline in circulating levels of estrogen. SDG supplementation produces a dose-related cessation or lengthening (by 18–39 %) of estrous cycles, reduces immature ovarian relative weight and delays puberty in experimental animals [61, 62]. The daily consumption of a low-fat muffin enriched with SDG (500 mg/day) for 6 week had no effect on endothelial functioning in healthy postmenopausal women [63]. Dietary flaxseed SDG (600 mg/day) can appreciably improve lower urinary tract symptoms in benign prostatic hyperplasia subjects [64]. Urinary composition or blood levels of radioactive lignans were not affected by the duration of SDG exposure while chronic SDG exposure alters lignan disposition in rats, however; it does not change the metabolite profile [65]. There were no significant effects of exposing male or female offspring to SDG during suckling on any measured reproductive indices [66]. SDG affects the reproductive development of offspring with caution when consuming flaxseed during pregnancy and lactation [67].

Imran M, Ahmad N, Anjum FM, et al. Potential protective properties of flax lignan secoisolariciresinol diglucoside. Nutrition Journal. 2015;14:71. doi:10.1186/s12937-015-0059-3.

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Flaxseed is the richest plant source of the ω-3 fatty acid i.e. α-linolenic acid (ALA) (Gebauer et al. 2006). Flaxseed oil is low in saturated fatty acids (9 %), moderate in monosaturated fatty acids (18 %), and rich in polyunsaturated fatty acid (73 %) (Cunnane et al. 1993). Of all lipids in flaxseed oil, α- linolenic acid is the major fatty acid ranging from 39.00 to 60.42 % followed by oleic, linoleic, palmitic and stearic acids (Table 2), which provides an excellent ω-6:ω-3 fatty acid ratio of approximately 0.3:1 (Pellizzon et al. 2007). Although flaxseed oil is naturally high in anti-oxidant like tocopherols and beta-carotene, traditional flaxseed oil gets easily oxidized after being extracted and purified (Holstun and Zetocha 1994). The bioavailability of ALA is dependent on the type of flax ingested (ALA has greater bioavailability in oil than in milled seed, and has greater bioavailability in oil and milled seed than in whole seed) (Austria et al. 2008).

Plant lignans are phenolic compounds formed by the union of two cinnamic acid residues. Lignans are ubiquitous within the plant kingdom and are present in almost all plants (Tarpila et al. 2005). Lignans act as both antioxidants and phytoestrogens. Phytoestrogens can have weak estrogen activity in animals and humans. Flax contains up to 800 times more lignans than other plant foods (Mazur et al. 1996; Westcott and Muir 1996). Lignan content in flaxseed is principally composed of secoisolariciresinol diglucoside (SDG) (294–700 mg/100 g), matairesinol (0.55 mg/100 g), lariciresinol (3.04 mg/100 g) and pinoresinol (3.32 mg/100 g) (Tourre and Xueming 2010; Milder et al. 2005). Johnsson et al. (2000) reported SDG content in the range of 11.7 to 24.1 mg/g and 6.1 to 13.3 mg/g in defatted flaxseed flour and whole flaxseed, respectively. Besides lignans, other phenolic compounds found in flaxseed are p-coumaric acid and ferulic acid (Strandas et al. 2008). The SDG found in flax and other foods is converted by bacteria in the gut to the lignans- enterodiol and enterolactone which can provide health benefits due to their weak estrogenic or anti-estrogenic, as well as antioxidant effects (Adlercreutz 2007). Flax lignans have shown promising effects in reducing growth of cancerous tumors, especially hormone-sensitive ones such as those of the breast, endometrium and prostate (Tham et al. 1998).

Dietary fibers, lignans, and ω-3 fatty acids, present in flaxseed have a protective effect against diabetes risk (Prasad et al. 2000; Prasad 2001; Adlercreutz 2007). Flaxseed lignan SDG has been shown to inhibit expression of the phosphoenolpyruvate carboxykinase gene, which codes for a key enzyme responsible for glucose synthesis in the liver (Prasad 2002). Supplementation of diet of type 2 diabetics with 10 g of flaxseed powder for a period of 1 month reduced fasting blood glucose by 19.7 % and glycated hemoglobin by 15.6 % (Mani et al. 2011). It could be due to lower content of glycemic carbohydrates and higher content of dietary fibers of flaxseed. Several small studies using a fasting glucose tolerance approach have found a reduction in postprandial blood glucose levels of women consuming flaxseed (Cunnane et al. 1993, 1995). Kelley et al. (2009) studied that when conjugated linoleic acid (0.5 %) and flax oil (0.5 %) was supplemented in diet of rats susceptible to obesity and diabetic tumors, a 20 % reduction in glycemia was observed. Kapoor et al. (2011) studied the effect of supplementation of flaxseed powder on diabetic human females. Patients were provided 15 and 20 g/day of flaxseed powder for a period of 2 months. Post-prandial blood glucose levels were found to be decreased by 7.9 and 19.1 %, respectively. Similar results has also been reported by Nazni et al. (2006) who conducted a study on 25 diabetic subjects and supplemented flaxseed powder in bread form for 90 days and reported a significant reduction in blood glucose levels after supplementation. However, Dodin et al. (2008) measured fasting serum glucose and insulin levels and reported no change after flaxseed supplementation. Similarly, ingestion of 10 g/day of flaxseed oil had no effect on fasting blood serum glucose and insulin levels (Barre et al. 2008). Utilization of flaxseed for glycemic control may also be associated to the decrease in risk of obesity and dyslipidemia, since these are risk factors for the development of diabetes and resistance to insulin (Wu et al. 2010; Morisset et al. 2009).

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Tumor and Cancer reducing effects

Interest in research on the association between flaxseed ingestion and risk of cancer emerged when epidemiologic evidences suggested a beneficial relationship. Research in laboratories has shown that flaxseed inhibits the formation of colon, breast, skin, and lung tumors and also reduces blood vessel cell formation in female rats, all suggesting a protective effect against breast, colon and ovarian cancer (Truan et al. 2012). Higher levels of insulin and insulin-like growth factor 1 (IGF-1) increase cancer risk by stimulating cell proliferation and increasing survival of DNA-damaged cells through antiapoptotic mechanisms (Sturgeon et al. 2011). Blood insulin has also been associated with increased risk of pancreatic and colorectal cancers (Pisani 2008). Various studies suggest that flaxseed added to the diet may lower circulating levels of insulin and IGF-1 (Woodside et al. 2006; Chen et al. 2011a). However, Sturgeon et al. (2011) reported that incorporation of 7.5 g of flaxseed daily for 6 weeks and 15 g of flaxseed for an additional 6 weeks into the diet of healthy postmenopausal women had little short-term effect on blood levels of IGF-1. Flaxseed has a breast tumor-reducing effect, possibly because of its high content of SDG lignan (Truan et al. 2012; Chen et al. 2011a; Chen et al. 2009; Saggar et al. 2010a, b; Wang et al. 2005). Enterodiol (ED) and enterolactone (EL) are produced from flax lignans in animal body. Because they are structurally similar to human estrogen-17β-estradiol (E2), they have binding affinity to estrogen receptors (ER) (Penttinen et al. 2007). Flaxseed and its SDG component have been shown to attenuate tumorigenesis through a reduction in cell proliferation and angiogenesis, as well as an increase in apoptosis via modulation of the estrogen receptor (ER)- and growth factor- signaling pathways (Saggar et al. 2010a; Chen et al. 2009). The potential breast cancer protective effect of flax lignans could be due to their weak estrogenic activity and antioxidant properties. Flaxseed oil with its exceptionally high ALA content was also shown to reduce human estrogen receptor-positive breast tumors (MCF-7) growth by 33 % compared to control (Truan et al. 2010). Chen et al. (2007) studied that the groups of mice that received 5 % and 10 % flaxseed in the diet for 8 weeks inhibited tumor growth by 26 % and 38 %, respectively. The researchers suggested the ability of flaxseed to help maintain more early stages of cancer is due to the fact that flaxseed contains the highest level of plant lignans, which have antioxidant activities (Hall et al. 2006) and have also been shown to alter estrogen metabolism, which may decrease ovarian cancer risk and improve health (McCann et al. 2007).

Based on the information, it is evident that flaxseeds are the richest source of α-linolenic acid and lignans. It is also a considerable potential source of soluble fiber, antioxidants and high quality protein. Its long journey from being a medicine in ancient times to the health food source in 21st century has opened the doors for a large population. The role of flaxseed lignans and ω-3 fatty acid in reducing the risks associated with cardiac and coronary disease, cancer (breast, colon, ovary and prostate) and other human health risk factors has been well known. When healthy heart is one of the most desired and highly demanded health benefits from functional foods; and where food industry’s goal is to develop innovative solutions to address nutritional challenges, flaxseed is going to play a vital role for the same. Flaxseed can contribute in improving the availability of healthy food choices, specifically by improving the nutrient profile of foods through reductions in the salt, sugar and saturated fat content; and by increasing the content of ω-3 fatty acids and other bioactive compounds. With contribution from such factors, worldwide market for healthy heart foods is estimated to grow rapidly in the coming years. As a result, flax and flaxseed oil may be preferred ingredients of functional foods and nutraceuticals in future. There is no doubt that a change to an omega-3 rich and high fiber diet would be beneficial. Therefore the use of flaxseed in whole seed or ground form can be recommended as a dietary supplement. Modern techniques like high power ultrasound, micro-fluidization, spray granulation and nanoencapsulation will pave way for new approaches to the processing, stabilization and utilization of flaxseed oil. Further, enrichment of diets of the animals with flax/flaxseed oil for production of ω-3 enriched eggs, milk, meat and other animal origin products could be another approach in utilizing flaxseeds.

Goyal A, Sharma V, Upadhyay N, Gill S, Sihag M. Flax and flaxseed oil: an ancient medicine & modern functional food. Journal of Food Science and Technology. 2014;51(9):1633-1653. doi:10.1007/s13197-013-1247-9.

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Our results suggest that flaxseed and its lignans have potent antiestrogenic effects on estrogen receptor–positive breast cancer and may prove to be beneficial in breast cancer prevention strategies in the future.

Flaxseed and Its Lignans Inhibit Estradiol-Induced Growth, Angiogenesis, and Secretion of Vascular Endothelial Growth Factor in Human Breast Cancer Xenografts In vivo

Malin Bergman Jungeström, Lilian U. Thompson, Charlotta Dabrosin

Clin Cancer Res Feb 2007 (13) (3) 1061-1067; DOI: 10.1158/1078-0432.CCR-06-1651

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Flaxseed is one of the richest sources of lignans and is increasingly used in food products or as a supplement. Plant lignans can be converted by intestinal bacteria into the so-called enterolignans, enterodiol and enterolactone. For a proper evaluation of potential health effects of enterolignans, information on their bioavailability is essential. The aim of this study was to investigate whether crushing and milling of flaxseed enhances the bioavailability of enterolignans in plasma. In a randomized, crossover study, 12 healthy subjects supplemented their diet with 0.3 g whole, crushed, or ground flaxseed/(kg body weight · d). Each subject consumed flaxseed for 10 successive days separated by 11-d run-in/wash-out periods, in which the subjects consumed a diet poor in lignans. Blood samples were collected at the end of each run-in/wash-out period, and at the end of each supplement period. Plasma enterodiol and enterolactone were measured using LC-MS-MS. The mean relative bioavailability of enterolignans from whole compared with ground flaxseed was 28% (P ≤ 0.01), whereas that of crushed compared with ground flaxseed was 43% (P ≤ 0.01). Crushing and milling of flaxseed substantially improve the bioavailability of the enterolignans.

Among foods consumed by humans, flaxseed contains the highest concentration of enterolignan precursors, mainly secoisolariciresinol diglucoside. Other seeds, nuts, whole grains, fruits and vegetables, and beverages such as coffee and tea contain smaller amounts (24). The most important sources of lignan precursors in Western diets are beverages such as tea and coffee, seeds, cereals, berries, fruits and vegetables (25,26). Flaxseed is a relatively minor dietary component in most countries, but because of its potential health benefits [flaxseed also contains a high quantity of (n-3) fatty acids as well as dietary fiber], it is increasingly being incorporated into a variety of food products, such as bread, muesli bars, and breakfast cereals, or used as a supplement. For example, in the Netherlands, whole flaxseed is used in commercial breads (up to 3.5 g flaxseed/100 g bread); therefore is an important potential source of dietary lignans. In a case-control study carried out in Texas, Strom et al. (27) found that flaxseed bread was one of the main food sources of lignans.

The Relative Bioavailability of Enterolignans in Humans Is Enhanced by Milling and Crushing of Flaxseed1J. Nutr. December 1, 2005, vol. 135 no. 12 2812-2816

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Flax Lignans

Flax is one of the richest sources of plant lignans, being very rich in the lignan secoisolariciresinol diglucoside (SDG). Flax contains other lignans as well – namely, matairesinol, pinoresinol, lariciresinol, isolariciresinol and secoisolariciresinol (often abbreviated Seco or SECO) (143,144).

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Metabolism of Lignans

The lignans SDG, SECO, pinoresinol, lariciresinol and matairesinol in flax are converted by bacteria in the colon to the mammalian lignans, enterodiol and enterolactone. [The flax lignan isolariciresinol is not converted to mammalian lignans (145).] Enterodiol and enterolactone are called mammalian lignans or enterolignans because they are produced in the gut of humans and other mammals; they are not found in plants. A simplified diagram showing the conversion of flax lignans to mammalian lignans is given in Figure 4. Enterodiol can be converted to enterolactone (146). The biologic activity of flax and other plant lignans depends on the presence of certain bacteria in the gut (146). Some humans appear to lack either the right type or a sufficient number of gut bacteria to convert SDG and other lignans to mammalian lignans (147), and taking antibiotics virtually stops the production of enterodiol and enterolactone in the gut for several weeks (140). Enterodiol and enterolactone have three metabolic fates: 1) They can be excreted directly in the feces; 2) They can be taken up by epithelial cells lining the human colon, conjugated with glucuronic acid or sulfate and excreted in the feces or enter the circulation (148); or 3) They can be absorbed from the gut and transported to the liver, where free forms are conjugated before being released into the bloodstream (140). Eventually, they undergo enterohepatic circulation – that is, they are secreted into bile and reabsorbed from the intestine – and are excreted in the urine in conjugated form (149). Based on a kinetic study involving 12 healthy adults, the mammalian lignans appear to be absorbed from the colon about 8-10 hours after the plant lignans are eaten and reach a maximum concentration in the bloodstream about 7-10 hours later (150). The concentration of enterodiol and enterolactone in the feces, blood and urine is related to the concentration of plants lignans in the diet – large intakes of plant lignans result in large amounts of these mammalian lignans in biological fluids. Eating flax or flax-containing food products increases the blood levels of mammalian lignans (151-154) and the excretion of mammalian lignans and/or total lignans in feces (155) and urine (151,152,154,156-159). Consuming a diet supplemented with a lignan/SDG complex derived from flax also increases mammalian lignan excretion in urine (160). The bioavailability of the mammalian lignans can be enhanced by crushing and milling flax (161).

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Biological Effects of Lignans

Flax lignans and the mammalian lignans (enterodiol and enterolactone) are biologically active. Lignans have anticancer and antiviral effects, influence gene expression (activation) and may protect against estrogen-related diseases such as osteoporosis (139-141). Diets high in lignans may help maintain good cognitive function in postmenopausal women (164); reduce the risk of uterine fibroids in middle-aged women (165); reduce breast cancer risk in women (166); and reduce the risk of acute fatal coronary events (167) and prostate cancer (168) in men. Specific actions of lignans include the following:

• The main flax lignan SDG is an antioxidant. It scavenges for certain free radicals like the hydroxyl ion (•OH) (169). Our bodies produce free radicals continually as we use (oxidize) fats, proteins, alcohol and some carbohydrates for energy. Free radicals can damage tissues and have been implicated in the pathology of many diseases like atherosclerosis, cancer and Alzheimer disease (170). In a rat study, feeding flax at levels of 5% and 10% in the diet prior to administering a liver toxin protected against oxidative stress in liver tissue compared with a normal diet not containing flax (171). The mammalian lignans, enterodiol and enterolactone, also act as antioxidants (172). Indeed, the antioxidant action of SECO and enterodiol is greater than that of vitamin E (173).

• The mammalian lignans affect receptors found on the surface of cell membranes. For instance, they activate the pregnane X receptor, which is involved in the metabolism of bile acids, steroid hormones and many drugs. Enterolactone is a moderate activator of the receptor, suggesting it has the ability to affect the metabolism of some drugs (174). A study conducted in France suggested that some plant lignans, along with enterodiol and enterolactone, affect hormone receptors in breast tissue. Among 58,049 French women who did not eat soy regularly, a high dietary intake of lignans (>1395 μg/day) was associated with a reduced risk of breast cancer. The benefit was limited to women with estrogen receptor positive (ER+) and progesterone receptor positive (PR+) tumours, suggesting that the biologic effects of lignans derive in part from their effects on cell hormone receptors (166).

• The mammalian lignans stimulate the synthesis of sex hormonebinding globulin (SHBG) (175), which binds sex hormones and reduces their circulation in the bloodstream, thus decreasing their biologic activity. In a meta-analysis, higher blood levels of SHBG were associated with an 80% lower risk of type 2 diabetes in women and a 52% lower risk in men (176). Low blood levels of SHBG have been found in postmenopausal women with breast cancer (177).

• The mammalian lignans inhibit the activity of aromatase, an enzyme involved in the production of estrogens (178). Decreased aromatase activity may be one way in which lignans protect against breast cancer (179).

Coconut Oil - Scientific Research

Excerpts from The Coconut Oil Miracle by Bruce Fife

Page 68 - One of the most amazing aspects about coconut oil is its ability to fight infections.  When coconut oil is eaten, the body transforms its unique fatty acids into powerful antimicrobial defense forces capable of defeating some of the most notorious disease-causing microorganisms.  Even super-germs are vulnerable to these lifesaving coconut derivatives.  The unique properties of coconut oil make it, in essence, a natural antibacterial, antiviral, anti-fungal, and antiprotozoal food.

Coconut oil's antimicrobial effects come from its unique composition of MCFAs.  All of these fatty acids (when converted into free fatty acids or monoglycerides) exhibit antimicrobial properties, some to a greater extent than others.  This is an exciting area of research because it involves a readily available food source that can be used to both treat and prevent infection illness.

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Page 69 - The marvellous thing about using coconut oil to treat or prevent these conditions is that while coconut oil is deadly to disease-causing microorganisms, it is harmless to humans.  The fatty acids that make coconut oil so effective against germs are the same ones nature has put into mother's milk to protect children. Human breast milk and the milk of other mammals all contain small amounts of MCFAs.  This is why butter, which is concentrated milk fat, also contains MCFA.  Breast milk, with its medium-chain fatty acids, protects the newborn baby from harmful germs while its immune system is still developing, its most vulnerable time of life.  This is one of the reasons why coconut oil or MCFAs are added to infant formula.  A mother who consumes coconut oil will have more MCFAs in her milk to help protect and nourish her baby.  If it's safe enough for a newborn baby, it is safe enough for us.  Nature made MCFAs to nourish and protect us against infection illnesses.

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Page 73 - Coconut oil is comprised of about 48 percent lauric acid, 18 percent myristic acid, 7 percent capric acid, 8 percent caprylic acid and 0.5 percent caproic acid.  These fatty acids give coconut oil its amazing antimicrobial properties and are generally absent from all other vegetable and animal oils, with the exception of palm kernel oil.  Most of the remaining fatty acids in coconut oil have little, if any, antimicrobial effect.

Coconut Crumble - Scientific Research

Excerpt from http://coconutresearchcenter.org/hwnl_2-4.htm

Coconut Dietary Fiber

Nutritionists recommend that we get 20-35 grams of dietary fiber a day. Most Americans only get about 15 grams. Good sources of dietary fiber are whole grains, legumes, and nuts.  Coconut is an ideal source of dietary fiber. Coconut has one of the highest percentages of fiber among all plant foods. Seventy-five percent of the total carbohydrate content is fiber. In comparison, the carbohydrate in green beans is only 30 percent fiber, in okra it is only 25 percent, and—corn it is 18 percent.

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Intestinal Health

Although we do not get nourishment from fiber, it feeds friendly bacteria in our gut that are essential for good health. These bacteria produce vitamins and other substances that are beneficial in promoting health and wellness. When we eat adequate amounts of fiber, intestinal bacteria flourish. Harmful bacteria and yeast such as candida, which compete for space in the intestinal tract, are kept under control.

One of the most important reasons why friendly bacteria are important to our health is that they produce short-chain fatty acids (SCFAs). Short-chain fatty acids are fats that are synthesized from dietary fiber by intestinal bacteria and are vital to our health and the health of the colon.

While these SCFAs are harmless to our tissues and friendly bacteria, they are deadly to many forms of disease-causing bacteria and yeasts that can infect the intestinal tract. SCFAs can kill these troublesome organisms. The benefits which intestinal bacteria provide us are dependent on the amount of fiber we feed them. The more fiber we eat, the more friendly bacteria will thrive and produce SCFAs, thus keeping our colon healthy and nasty microorganisms in check.

Another benefit is SCFAs ability to pass through cell membranes and into the mitochondria without the aid of special hormones (insulin) or enzymes (carnitine). Therefore, they can easily enter the cells in the colon where they are utilized as fuel to power metabolism. SCFAs are an important source of nutrition for the cells in the colon. In fact, SCFAs are the preferred food of colonic cells and are necessary for a healthy intestinal environment.

Researchers have discovered that an abnormally low level of SCFAs in the colon can lead to nutritional deficiencies, which can cause inflammation and bleeding. Researchers found that SCFAs administered rectally into the colon relieve these conditions.

The fiber in coconut acts as food for gut bacteria. Consequently, coconut helps increase SCFAs in the gut and helps prevent and relieve symptoms associated with Crohn's disease, irritable bowel syndrome, colitis, and other digestive disorders. Many people have reported that even eating as little as two coconut macaroon cookies a day relieves their symptoms.

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Vermifuge

An interesting benefit of coconut fiber, not found in other fibers, as far as I'm aware, is that it acts as a vermifuge (i.e., expels parasitic worms). Eating coconut to get rid of parasites is a traditional practice in India that was even recognized among the early medical profession. It was included in a handbook of tropical medicine published in India in 1936 and in an Indian Materia Medica with Ayurvedic medicine published in 1976.

In 1984 researchers in India published a study on the effectiveness of this traditional remedy. Fifty individuals infected with tapeworm participated in the study. Various coconut preparations followed by Epsom salt were administered to the volunteers. The researchers found that within 12 hours after eating dried coconut, 90 percent of the tapeworms were expelled. Some of those tapeworms were over six feet long. Continued use resulted in 100% expulsion.

At the time of the study, the researchers reported that except for Niclosomide, no drug was as effective in the treatment of tapeworm infestation as was coconut. Niclosomide, however, causes tapeworms to waste away or separate, releasing toxins that can cause undesirable side effects. The researchers concluded that since coconut is nontoxic, palatable, easily available, and fairly cheap, and because it is highly effective in expelling tapeworms without causing side effects, it is a safe and effective treatment for tapeworm infestation. They recommended the use of coconut dietary fiber as a good source of fiber to use for the purpose of removing intestinal parasites.

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Mineral Absorption

Many researchers believe that the fiber in our foods can influence mineral absorption. The foods with the highest fiber content are legumes and grains like soy, wheat, and oats. One drawback that has been reported by researchers with the bran or fiber from these sources is that they contain phytic acid, which binds with minerals in the digestive tract and pulls them out of the body. Consequently, mineral absorption is decreased. Some of the minerals that are bound to phytic acid include zinc, iron, and calcium. It has been suggested that eating too much phytic acid can lead to mineral deficiencies. Even dietary fiber levels of 10 to 20 percent are believed to interfere with absorption of minerals in the digestive tract. Yet, we are counseled to get between 20 and 35 percent dietary fiber in our diets. What are we to do? We need fiber for good digestive health, but too much may cause nutritional problems. The perfect solution to this problem is not to reduce fiber consumption, but to replace some of the fiber we get from grains and legumes with fiber that does not pull minerals out of the body. Coconut flour fits that description. Coconut does not contain phytic acid and does not remove minerals from the body. You can eat all the coconut you want without worrying about it negatively affecting your mineral status.

If anything, coconut fiber improves mineral status. Fiber slows down the emptying of the stomach, allowing foods to be bathed in gastric juices for a longer amount of time. This allows more minerals to be released from the food we eat; so more are available for absorption.

Excerpt from http://coconutresearchcenter.org/hwnl_2-1.htm

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Blood Sugar and Diabetes

Blood sugar is an important issue for anyone who is concerned about heart disease, overweight, hypoglycemia, and especially diabetes because it affects all of these conditions.

Carbohydrates in our foods are broken down in the digestive tract and converted into glucose (blood sugar). Meals that contain a high concentration of carbohydrates, particularly simple carbohydrates such as sugar and refined flours, cause a rapid rise in blood sugar. Since elevated blood sugar can lead to a coma and death, insulin is frantically pumped into the blood stream to avoid this. If insulin is produced in adequate amounts, blood sugar is soon brought back down to normal. This is what happens in most individuals. However, if insulin is not produced quickly enough or if the cells become desensitized to the action of insulin, blood glucose can remain elevated for extended periods of time. This is what happens in diabetes.

Dietary fiber helps moderate swings in blood sugar by slowing down the absorption of sugar into the bloodstream. This helps keep blood sugar and insulin levels under control. Coconut fiber has been shown to be very effective in moderating blood sugar and insulin levels. For this reason, coconut is good for diabetics.

Diabetics are encouraged to eat foods that have a relatively low glycemic index. The glycemic index is a measure of how foods affect blood sugar levels. The higher the glycemic index, the greater an effect a particular food has on raising blood sugar. So diabetics need to eat foods with a low glycemic index. When coconut is added to foods, including those high in starch and sugar, it lowers the glycemic index of these foods. This was clearly demonstrated by T. P. Trinidad and colleagues in a study published in the British Journal of Nutrition in 2003. In their study, both normal and diabetic subjects were given a variety of foods to eat. Some of the types of food included cinnamon bread, granola bars, carrot cake, and brownies—all foods that a diabetic must ordinarily limit because of their high sugar and starch content. It was found that as the coconut content of the foods increased, the blood sugar response between the diabetic and non-diabetic subjects became nearly identical. In other words, coconut moderated the release of sugar into the bloodstream so that there was no spike in blood glucose levels. As the coconut content in the foods decreased, the diabetic subjects’ blood sugar levels became elevated, as would normally be expected from eating foods high in sugar and white flour. This study showed that adding coconut to foods lowers the glycemic index of the foods and keeps blood sugar levels under control. Sweet foods such as cookies and cakes made using coconut flour do not affect blood sugar levels like those made with wheat flour. This is good news for diabetics who want a treat now and then without adversely affecting their blood sugar.

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Cancer

Fiber acts like a broom, sweeping the intestinal contents through the digestive tract. Parasites, toxins, and carcinogens are swept along with the fiber, leading to their timely expulsion from the body. This cleansing action helps prevent toxins that irritate intestinal tissues and cause cancer from getting lodged in the intestinal tract. Colon cancer is second only to lung cancer as the world’s most deadly form of cancer. Many studies have shown a correlation between high-fiber diets and a low incidence of colon cancer. For example, in one of the most extensive studies to date, involving over 400,000 people from nine European countries, it was found that those who had the highest fiber intake were 40 percent less likely to develop colon cancer.

Fiber readily absorbs fluids. It also appears to absorb harmful carcinogens and other toxic substances. Researchers at the University of Lund, Sweden, found that fiber in the diet can absorb toxins that promote cancer. Various types of fiber were examined for their absorption capacity and found to absorb 20 to 50 percent of these carcinogenic compounds.

Dr. B. H. Ershoff of Loma Linda University summarized studies reported by the Committee on Nutrition in Medical Education. The studies compared groups of rats and mice, some given high-fiber diets and others given low-fiber diets. The animals were fed various drugs, chemicals, and food additives. These substances proved to be poisonous to the animals on the low-fiber diets, yet those given high-fiber diets showed no deleterious effects.

Logically you can see the relationship between dietary fiber and its protective effect in the colon, but studies also show it protects against breast, prostate, and ovarian cancers as well. One explanation for this is that toxins lingering in the colon are absorbed into the bloodstream, and the blood then carries these toxins to other parts of the body where they can cause cancer.

Another explanation involves estrogen. Estrogen is required for the early growth and development of breast and ovarian cancer. The liver collects estrogen and sends it into the intestines where it is reabsorbed into the bloodstream. A high-fiber diet interrupts this process. Less estrogen is allowed back into the bloodstream because the activities of bacterial enzymes in the intestine are reduced. Studies show that serum estrogen can be significantly reduced by a high-fiber diet. Progesterone, which is an antagonist to estrogen and helps protect against cancer, is not affected or reduced by fiber.

One of the primary reasons given to explain why dietary fiber protects against colon and other cancers is that it decreases intestinal transit time. If carcinogenic substances, hormones, and toxins are quickly moved through the digestive tract and out of the body, they don’t get a chance to irritate tissues and instigate cancer. Coconut fiber not only absorbs and sweeps carcinogenic toxins out of the intestinal tract, it also helps prevent the conditions that promote cancer. Evidence suggests that coconut fiber may also prevent the formation of tumors in the colon by moderating the harmful effects of tumor-promoting enzymes.

Additional Information: Canadian Flax Council