Archive for the ‘Health’ Category

Friday, November 10th, 2017

Immune health probiotic

Boosting Immune Health with MELT Probiotic

Did you know 70% of your immune system lives in your gut? When you picture the human body as the big, hollow food tube that it is, it makes sense that the majority of our immune defenses would live where it is easiest for pathogens to hang out. Having a healthy gut gives your body a strong first line of defense against pathogens that enter the body through the mouth. If you want to be healthy, your gut has got to be healthy too.

That’s where probiotics come in. Probiotics are the key to a healthy gut.

The human gut contains good bacteria and bad bacteria. Probiotics help keep these in balance. There are many things that can tip the balance in favor of bad bacteria including diet and antibiotics.  According the Center for Disease Control 4 out of 5 Americans take antibiotics, and 30% of those prescribed are unnecessary. Adding probiotics to your daily diet can help restore the balance and help to get your immune system functioning properly.

MELT Probiotic is an easy and delicious way to help restore your gut biome to a healthy balance. With its creamy taste, MELT Probiotic enhances the flavor of the foods you love while delivering probiotics safely and deliciously. Just two servings, or two tablespoons, per day spread liberally on your morning toast, muffin, bagel or waffles deliver 1 billion CFU’s of probiotic to help support your digestive health. And even better, MELT Probiotic delivers active cultures 10x more effectively than yogurt!*

And it doesn’t stop at immune health. Here are some additional benefits of bacillus coagulans:



*In an independent lab study of a simulated gastric environment with a pH of 2.0 for two hours, GanedenBC30 cells were delivered 10x more effectively than common yogurt cultures.

Getting Your Fats Straight: Organic Virgin Coconut Oil is a Good Fat!

Tuesday, June 20th, 2017

Traditional and social media were awash with coconut oil news this week after the American Heart Association (AHA) issued its opinion on dietary fats. For more than a decade the AHA has ignored study after study extolling the benefits of organic virgin coconut oil only to pounce on a study that finally fit its industry-biased narrative of saturated fats being unhealthy. This is equivalent to firing an arrow into a wall and painting a bullseye around it. (Please note that when reading this blog, all emphasis is mine unless otherwise noted).

What we know from scores of studies is that all fats are not the same and all coconut oils are not the same.

Traditional coconut oil contains about 13 to 15% MCTs, but organic virgin coconut oil contains as much as 68% MCTs. The AHA study states that coconut oil is 82% saturated fat but fails to direct any focus on the fact that 83% of the saturated fat is in the form of medium chain fatty acids: 61% of which is Lauric Acid. Why is this important?

A 2015 study by Fabian Dayrit concluded “Coconut oil is rapidly metabolized because it is easily absorbed and lauric acid is easily transported. Detailed studies have shown that the majority of ingested lauric acid is transported directly to the liver where it is directly converted to energy and other metabolites rather than being stored as fat.”

The AHA points to an increase in LDL cholesterol in its justification for advising against consuming coconut oil. Many publications have seized this nugget to create clickbait headlines rife with hyperbole ranging from grossly misleading (Coconut Oil as Bad For Heart as Butter, Beef Fat) to patently false (So Coconut Oil Is Actually Really, Really Bad For You).

Here is the science that the AHA and the media are glossing over.

All cholesterol is not the same. The different types of fatty acids in organic virgin coconut oil contribute differently to blood cholesterol. The most important fact being ignored is according to the study the AHA is referencing, organic virgin coconut oil raises both low-density lipoprotein (LDL or bad cholesterol) and high-density lipoprotein (HDL or good cholesterol).

HDL is “good” cholesterol because it removes LDL cholesterol from the blood stream, hauling it off to the liver to be converted. When a doctor prescribes statins to a patient with high cholesterol it is because statins increase HDL thereby lowering LDL.

According to the AHA “A low HDL cholesterol level is associated with a high incidence of cardiovascular disease (CVD)… HDL can stimulate the removal of cholesterol from cells, including those involved in atherosclerosis, and can deliver the cholesterol to the liver where some of it may be secreted in bile and excreted, a process called reverse cholesterol transport.”

Another important finding in the study is that butter raised LDL more than coconut oil when compared to safflower oil, but butter has significantly lower levels of medium-chain fatty acids. According to the ACA study, “Both butter and coconut oil raised LDL cholesterol compared with safflower oil, butter more than coconut oil.” It is important to point out that the AHA advised against the use of coconut oil “because coconut oil increases LDL” but stopped short of advising against eating butter or beef fat when their “trials did not find a difference in raising LDL cholesterol between coconut oil and other oils high in saturated fat such as butter, beef fat, or palm oil.” Assumedly because the Beef and Dairy Councils are well funded and extremely powerful lobbies. Coconuts are not produced in the US therefore an equivalent council doesn’t exist.

FDA Set To Promote GMOs Using Your Tax Dollars

Monday, May 15th, 2017

Using the looming government shutdown as a smokescreen, our representatives in Washington snuck a deal into the most recent budget agreement that gives $3 million dollars of taxpayer money to the FDA to “promote understanding and acceptance of biotechnology.” This following on the heels of a letter submitted on April 18 to the FDA by 66 Bio-Ag and Food Industry groups supporting the outreach.

The FDA is currently mired in a hiring freeze and facing $40 million in proposed cuts under the “once-in-a-generation” budget proposal submitted by the current administration (which, at 62 pages it is inexplicably half the length of Monsanto’s Annual Report). I personally find it outrageous that tax dollars are being taken away from an agency put in place to protect consumers, while simultaneously slipping them taxpayer money to push propaganda benefiting a select few biotech companies like Bayer – Monsanto. A company with sales in one quarter that exceed the entire yearly budget of the FDA.

Bayer-Monsanto and the other bio-ag companies benefiting from this outreach have more than enough money to push their agenda on their own. What they don’t have is the credibility of the FDA, which ironically, isn’t saying much. But that goes to show how much credibility the bio-ag industry currently has with consumers.

Unfortunately, this budget deal has already passed and there is little or nothing that can be done to stop how the money is going to be allocated. However, the FDA has not announced what kind of educational programs they intend to implement. Which means there is still time to do something.

So what can you do?

Educate yourself. Learn both sides of the argument so that you can engage in educated discourse.

Contact the FDA! Tell them what you think. Don’t forget, they work for you!

Contact your representatives! Tell them, this aggression will not stand. Here’s a handy-dandy list for contacting your reps – Don’t forget, they work for you!

And here is a list of your representatives that are taking money from the bio-ag industry and pushing their agenda –



The Scoop on Probiotics and Why We Love Probiotic MELT®!

Monday, March 28th, 2016

How do I choose a probiotic?

Not all probiotics strains are the same. Different strains offer different benefits and some probiotic strains survive manufacturing processes, shelf life and digestive transit better than others. When choosing a probiotic consider the following:

Is it safe and has the FDA reviewed the safety data?

Does it survive the extremes of manufacturing?

Does it survive the shelf life of the product?

Will it survive digestive transit?

Is there published research to support it?

Once you’ve gathered all of this information, then you’re ready to decide which probiotic is right for you.

What Are Probiotics?

Probiotics are live microorganisms that are intended to have health benefits. Although bacteria and other microorganisms are often thought of as harmful “germs,” many microorganisms are critical partners in helping our bodies function properly. For example, beneficial bacteria normally present in our intestines assist in digesting food, destroying disease-causing microorganisms, and producing vitamins. Large numbers of microorganisms live on and in our bodies. In fact, microorganisms in the human body outnumber human cells by 10 to 1. Many of the microorganisms in probiotic products are the same as or similar to microorganisms that naturally live in our bodies. Probiotics may include a variety of microorganisms with the most common including two broad groups of bacteria, known as Lactobacillus and Bifidobacterium. Other bacteria may also be used as probiotics such as Bacillus bacterial spores (e.g., Bacillus coagulans), and yeasts such as Saccharomyces boulardii.

Bacillus bacterial spores are of particular interest because they are uniquely designed to survive the harsh gastric environment and arrive at the intestinal system alive, ensuring full potency.

The Basics of Probiotic Survivability: If Its Not Live, Its Not a Probiotic

Probiotics are the fastest growing category in the supplement industry.  Recent research performed by the National Institute of Health has defined probiotics by three strict criteria:

  1. The organism must be a normally occurring organism in the digestive tract.
  2. In order to consistently trigger a healthy boost in immune function, the organism must be supplemented in concentrations higher than what normally occurs in the digestive tract.
  3. The organism must be able to survive in the digestive tract as well as in the environment.

Interestingly, there are almost no probiotic products in the marketplace that meet all three of these criteria, particularly the third criteria, which states the microorganism has to be live or it does not fit the definition of a probiotic. Studies by the Food Safety Authority of the United Kingdom and at least three different publications have confirmed that over 90% of strains used in probiotic products today do not survive the gastric system. Thus, they do not fit the profile of live microorganisms or meet the definition of a probiotic.

True probiotics must naturally survive the gastric barrier.

Physicians Exclusive commissioned Silliker Food Science Center, a leading food science laboratory, to test the survivability of probiotic strains of four products, including two probiotic dietary supplements and two yogurt products. The first probiotic supplement was a formulation composed of five Bacillus bacterial spores, including Bacillus coagulans. The second probiotic supplement formulation was composed of the most common Lactobacillus and Bifidobacterium species used in the probiotic market today. The third and fourth products in the study included a leading brand name yogurt and a leading brand name Greek Yogurt. The study looked at the survival of these probiotic sources in United States Pharmacopeia (USP) standard gastric solution, which is the most widely accepted simulated gastric model used in industry today.

The results of this study were consistent with the findings of several other publications on the survivability of common probiotic strains.  The blend of Bacillus bacterial spores was the only product to show 100% survival through the gastric barrier, while over 99.99% of the probiotic bacteria in all of the other tested products were killed by the stomach environment. If the probiotic contained in a food product or supplement does not survive and arrive at the site of colonization alive (i.e., your intestinal tract), it is not a probiotic.

What is GanedenBC30? Why is GanedenBC30 in Probiotic MELT®?

GanedenBC30 is a form of Bacillus coagulans, which is a spore-forming probiotic. Similar to a seed, GanedenBC30’s genetic material is protected by a hard shell. This spore safeguards the probiotic from the heat, cold and pressure of manufacturing processes, allows for stability during the product shelf life and protects the cells from the acid and bile they are exposed to during transit through the digestive system. Once it is safely inside the small intestine, the probiotic germinates and colonizes to provide benefits. GanedenBC30 survives conditions other probiotics cannot. Most probiotics are extremely fragile and thus few cells survive digestion to populate the intestines.  GanedenBC30 is different in that it was designed by nature to survive and thrive in conditions other probiotics cannot. While most probiotics are delivered in capsule or tablet form, or in cultured dairy products, like yogurt, GanedenBC30 can be consumed in a variety of foods and beverages like Probiotic MELT®.

GanedenBC30 is the only Bacillus that the FDA has reviewed for safety. Ganeden has conducted extensive safety studies on GanedenBC30, which have been published (Endres 2009, Endres2011) and culminated with Ganeden receiving FDA GRAS. These tests prove that even when GanedenBC30 is consumed at much higher levels than what is found in food and beverage products, that there are no safety concerns. FDA GRAS is strain specific, and GanedenBC30 is the only Bacillus that has been granted FDA GRAS status.

GanedenBC30 is the only Bacillus that has been the subject of over 20 studies published in peer reviewed journals. In multiple studies, GanedenBC30 supports digestive health when consumed daily. A large majority of the body’s immune system is located within the intestines. When GanedenBC30 is consumed daily, it creates a healthier intestinal environment, supporting immune function. GanedenBC30 is the only Bacillus that has been endorsed by Dr. Mehmet Oz, Dr. Michael Roizen, Dr. Andrew Weil.

References for Ganeden BC30


Safety Assessment Of A Proprietary Preparation Of A Novel Probiotic, Bacillus Coagulans, As A Food Ingredient
Food and Chemical Toxicology, 2009; 47: 1231–1238
J.R. Endresa, A. Clewella, K.A. Jadea, T. Farberb, J. Hauswirthc A.G. Schaussa

One-Year Chronic Oral Toxicity With Combined Reproduction Toxicity Study Of A Novel Probiotic, Bacillus Coagulans, As A Food Ingredient
Food and Chemical Toxicology Article in Press
J.R. Endresa, I. Qureshia, T. Farberb, J. Hauswirthc, G. Hirkad, I. Pasicsd, A.G. Schaussa


A Prospective, Randomized, Double–blind, Placebo–controlled Parallel–group Dual Site Trial To Evaluate The Effects Of A Bacillus Coagulans–based Product On Functional Intestinal Gas Symptoms
BMC Gastroenterology, 2009, 9:85
Douglas S Kalman, Howard I Schwartz, Patricia Alvarez, Samantha Feldman, John C Pezzullo and Diane R Krieger

Survival And Metabolic Activity Of The GanedenBC30 Strain Of Bacillus Coagulans In A Dynamic In Vitro Model Of The Stomach And Small Intestine
Beneficial Microbes, 2010; 1(1): 31–36
A.J.H Maathuis, D. Keller, S. Farmer

Impact of GanedenBC30 (Bacillus coagulans GBI-30, 6086) on population dynamics of the human gut microbiota in a continuous culture fermentation system
International Journal of Probiotics and Prebiotics, 2011, 6 (1): 65-72
Harue Honda, Lesley Hoyles, Glenn R. Gibson, Sean Farmer, David Keller and Anne L. McCartney

Use Of A Continuous Culture Fermentation System To Investigate The Effect Of GanedenBC30 Bacillus Coagulans GBI-30, 6086) Supplementation On Pathogen Survival In The Human Gut Microbiota
Anarobe 2011, 17 (1): 36-42
H. Honda, G.R. Gibsona, S. Farmerb, D. Kellerb, A.L. McCartneya

Bacillus Coagulans GBI-30 (BC30) improves indices of Clostridium difficile-Induced colitis in mice
Gut Pathogens, 2011, 3:16
Leo R Fitzpatrick, Jeffrey S Small, Wallace H Greene, Kelly D Karpa and David Keller

Bacillus coagulans GBI-30, 6086 limits the recurrence of Clostridium difficile-Induced colitis following vancomycin withdrawal in mice
Gut Pathogens, 2012, 4:13
Leo R Fitzpatrick, Jeffrey S Small, Wallace H Greene, Kelly D Karpa, Sean Farmer and David Keller

Bacillus Coagulans Significantly Improved Abdominal Pain And Bloating In Patients With IBS
Postgraduate Medicine, 2009; 121(2): 119–124
Larysa Hun

Effects Of A Proprietary Bacillus Coagulans Preparation On Symptoms Of Diarrhea–Predominant Irritable Bowel Syndrome
Methods Find Exp Clin Pharmacol 2009; 31(10): 655–659
B.J. Dolin


Bacillus coagulans GBI-30, 6086 Modulates Faecalibacterium prausnitzii in Older Men and Women
The Journal of Nutrition May 2015
Edna P Nyangale, Sean Farmer, Howard A Cash, David Keller, David Chernoff, and Glenn R Gibson

Immunomodulation of Antiretroviral Drug-Suppressed Chronic HIV-1 Infection in an Oral Probiotic Double-Blind Placebo-Controlled Trial
AIDS Research and Human Retroviruses October 2014, 30(10): 988-995. doi:10.1089/aid.2014.0181.
Yang Otto O., Kelesidis Theodoros, Cordova Robert, and Khanlou Homayoon

GanedenBC30 Cell Wall And Metabolites: Anti–inflammatory And Immune Modulating Effects In vitro
BMC Immunology 2010, 11:15
Gitte S Jensen, Kathleen F Benson, Steve G Carter, John R Endres

Probiotic metabolites from Bacillus coagulans GanedenBC30 support maturation of antigen-presenting cells in vitro
World Journal of Gastroenterology, 2012, 18(16): 1875–1883
Kathleen F Benson, Kimberlee A Redman, Steve G Carter, David Keller, Sean Farmer, John R Endres and Gitte S Jensen

A review of probiotics studies in HIV research suggests improved immunological presentation and preservation of viral host restrictive factors of TH17 in HIV patients
Retrovirology, 2012, 9(Suppl 1):P22
M Selbovitz, Keller, Miller, Moore, Farmer and Bray

A Patented Strain Of Bacillus Coagulans Increased Immune Response To Viral Challenge
Postgraduate Medicine, 2009; 121(2): 114–118
Mira Baron

A Controlled Clinical Trial To Evaluate The Effect of GanedenBC30 On Immunological Markers
Methods and Findings in Experimental and Clinical Pharmacology 2010, 32(2): 129-132
M. Kimmel, D. Keller, S. Farmer, D.E. Warrino


Effect of prebiotics on the fecal microbiota of elderly volunteers after dietary supplementation of Bacillus coagulans GBI-30, 6086
Anaerobe Volume 30, December 2014, Pages 75–81
Edna P. Nyangale, Sean Farmer, David Keller, David Chernoff, Glenn R. Gibson

Bacillus coagulans : A Viable Adjunct Therapy For Relieving Symptoms Of Rheumatoid Arthritis According To A Randomized, Controlled Trial
BMC Complementary and Alternative Medicine 2010, 10:1
David R Mandel, Katy Eichas, Judith Holmes

Bacillus Coagulans As A Probiotic
Food Science & Technology Bulletin: Functional Foods 2010, 7 (7): 103-109
D. Keller, S. Farmer, A.L. McCartney, G. Gibson

Gluten-Free? Or Low-FODMAP diet?

Thursday, June 11th, 2015

Have you heard about the low-FODMAP diet, but have no idea what it is? This week’s blog attempts to shed some light on clarifying what FODMAPs are and why they are important for anyone with a history of digestive disorders (referred herein as IBS).

Reducing or eliminating food intolerances for managing IBS symptoms has been gaining momentum in health-conscious circles for decades. While dietary modifications are not a cure for IBS, they can improve symptoms and quality of life. In particular, the low-FODMAP diet has been shown to improve symptoms in at least 74% of patients with IBS. Non-celiac gluten intolerance has been reported (1), but further research is needed to identify the underlying mechanism. The relative ease of implementing the low-FODMAP diet combined with considerable evidence supporting its effectiveness suggests the low-FODMAP diet should be the first dietary approach in people diagnosed with IBS.

What are FODMAPs?

FODMAPs are short-chain carbohydrates and related alcohols that are poorly absorbed in the small intestine. The term FODMAP is an acronym, derived from “Fermentable Oligo-, Di-, Mono-saccharides And Polyols” (2). The low FODMAP diet was developed at Monash University in Melbourne by Peter Gibson and Susan Shepherd (3,4).

How was the low-FODMAP diet discovered?

Throughout the 1980s and 1990s, evidence was building for the role of poorly absorbed, short-chain carbohydrates (lactose and fructose) in inducing IBS symptoms, with dietary restriction providing symptomatic relief (5-8). It was clear, however, that these sugars were not the only culprits. Other short-chain carbohydrates were identified as poorly absorbed in the human GI tract, such as fructo-oligosaccharides (fructans), galacto-oligosaccharides (GOS), and sugar polyols, sorbitol and mannitol (artificial sweeteners also found naturally in some foods).

Gibson and Shepherd were the first to publish a description of FODMAPs in 2005 (9) with the first published research trial in 2006 (10). A total of 74% of patients reported symptomatic improvement on the low-FODMAP dietary regimen. The efficacy of the low-FODMAP diet was confirmed and reconfirmed in subsequent trials and studies (11, 12).

Two additional trials (13, 14) identified the mechanisms that explained the gastrointestinal (GI) effects of FODMAPs: poor absorption in the small intestine, increased water content of the output (explaining why some experience diarrhea), and fermentation of the short-chain carbohydrates, which induced bloating, distension, abdominal pain and excessive flatulence. The low-FODMAP diet reduces fermentation and associated gas production, which is likely to reduce symptom severity of IBS patients.

Other potential factors include alterations in the gut microbiota number, composition, function and location. Some patients with IBS have small intestine bacterial overgrowth (SIBO) with fermentation of malabsorbed carbohydrates occurring in the narrow lumen of the small intestine, the location of which may be associated with abdominal pain and discomfort. With more predominant methane-producing bacteria, fermenting malabsorbed carbohydrates would produce methane gas, which is linked to delayed transit and constipation (15-17).

Since these initial studies, the FODMAP approach has been fine-tuned to include GOS, sorbitol and mannitol, in addition to fructose, lactose and fructans. These six carbohydrates make up the low-FODMAP diet as it is today, with published tables of food composition available on fruits and vegetables and breads and cereals (18-20). The table below summarizes the richest FODMAP food sources.

FODMAP foods table60

What does this mean for you?

Not all FODMAPs will trigger symptoms and will depend on whether they are malabsorbed by the individual. Importantly, fructans and GOS are always malabsorbed and fermented by intestinal microflora (21-23) as are the sugar polyols, sorbitol and mannitol (24-27). Other FODMAP carbohydrates will only induce symptoms in the proportion of patients with IBS that malabsorb them.

Breath testing is useful for clarifying which FODMAP foods to avoid on an individual basis by providing a reliable measure of test sugar absorption via measurement of breath hydrogen lev­els (28). A significant rise in breath hydrogen following ingestion of the test sugar (e.g. fructose) demon­strates poor absorption with fermen­tation by intestinal microflora. Negative breath tests demonstrate complete absorption of the sugar and suggest that the patient can consume this sugar without a negative impact on their symptoms.

Commonly offered breath tests for detecting FODMAP intolerances are typically for fructose, lactose and sorbitol (28). Regardless of breath test results, there are three other FODMAP carbohydrates that need to be considered as potential triggers. Fructans and GOS are not breath tested as they are always mal­absorbed. They are always fermented and should be considered as triggers in all IBS patients. Mannitol is rarely offered as a breath test because it is not found widely in the diet and can be inves­tigated as a trigger through simple dietary elimi­nation and rechallenge (28).

The results from breath tests can be used to implement a low-FOD­MAP diet without restricting sugars shown to be well absorbed. This individu­alizes the diet and avoids unnecessary restrictions as well as assisting with the long-term nutritional composition of the diet (28). In addition, FODMAPs have prebiotic effects due to the production of short-chain fatty acids after fermentation. Therefore, everyone is encouraged to try and reintroduce FODMAPs to a level that they can comfortably tolerate (28).

  1. Biesiekierski, J.R., Newnham, E.D., Irving, P.M., Barrett, J.S., Haines, M., Doecke, J.D. et al. (2010) Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. AmJ Gastroenterol 106: 508–514; quiz 515.
  2. Shepherd, S. (2013) Low FODMAP Recipes. Melbourne, Australia: Penguin. ISBN 9780143567561.
  3. FODMAPS. King’s College, London. Diabetes & Nutritional Sciences.
  4. Gibson, P.R., Gibson, P.R., Shepherd, S.J. (2010). Evidence-based dietary management of functional gastrointestinal symptoms: The FODMAP approach. Journal of Gastroenterology and Hepatology 25 (2): 252–258. doi:10.1111/j.1440-1746.2009.06149.x. PMID 20136989.
  5. Goldstein, R., Braverman, D. and Stankiewicz, H. (2000) Carbohydrate malabsorption and the effect of dietary restriction on symptoms of irritable bowel syndrome and functional bowel complaints. Isr Med Assoc J 2: 583–587.
  6. Nelis, G.F., Vermeeren, M.A. and Jansen, W. (1990) Role of fructose-sorbitol malabsorption in the irritable bowel syndrome. Gastroenterology 99: 1016–1020.
  7. Rumessen, J.J. and Gudmand-Hoyer, E. (1988) Functional bowel disease: malabsorption and abdominal distress after ingestion of fructose, sorbitol, and fructose-sorbitol mixtures. Gastroenterology 95: 694–700.
  8. Symons, P., Jones, M.P. and Kellow, J.E. (1992) Symptom provocation in irritable bowel syndrome. Effects of differing doses of fructose-sorbitol. Scand J Gastroenterol 27: 940–944.
  9. Gibson, P.R. and Shepherd, S.J. (2005) Personal view: food for thought – western lifestyle and susceptibility to Crohn’s disease. The FODMAP hypothesis. Aliment Pharmacol Ther 21: 1399–1409.
  10. Shepherd, S.J. and Gibson, P.R. (2006) Fructose malabsorption and symptoms of irritable bowel syndrome: guidelines for effective dietary management. J Am Diet Assoc 106: 1631–1639.
  11. Shepherd, S.J., Parker, S.C., Muir, J.G. and Gibson, P.R. (2008) Randomised, placebo-controlled evidence of dietary triggers for abdominal symptoms in patients with irritable bowel syndrome. Clin Gastroenterol Hepatol 6: 765–771.
  12. Staudacher, H.M., Whelan, K., Irving, P.M. and Lomer, M.C.E. (2011) Comparison of symptom response following advice for a diet low in fermentable carbohydrates (FODMAPs) versus standard dietary advice in patients with irritable bowel syndrome. J Hum Nutr Diet 24: 487–495.
  13. Barrett, J.S., Gearry, R.B., Muir, J.G., Irving, P.M., Rose, R., Rosella, O. et al. (2010) Dietary poorly absorbed, short-chain carbohydrates increase delivery of water and fermentable substrates to the proximal colon. Aliment Pharmacol Ther 31: 874–882.
  14. Ong, D.K., Mitchell, S.B., Barrett, J.S., Shepherd, S.J., Irving, P.M., Biesiekierski, J.R. et al. (2010) Manipulation of dietary short chain carbohydrates alters the pattern of gas production and genesis of symptoms in irritable bowel syndrome. J Gastroenterol Hepatol 25: 1366–1373.
  15. Chatterjee, S., Park, S., Low, K., Kong, Y. and Pimentel, M. (2007) The degree of breath methane production in IBS correlates with the severity of constipation. Am J Gastroenterol 102: 837–841.
  16. Fiedorek, S.C., Pumphrey, C.L. and Casteel, H.B. (1990) Breath methane production in children with constipation and encopresis. J Pediatr Gastroenterol Nutr 10: 473–477.
  17. Pimentel, M., Lin, H.C., Enayati, P., van den Burg, B., Lee, H.R., Chen, J.H. et al. (2006) Methane, a gas produced by enteric bacteria, slows intestinal transit and augments small intestinal contractile activity. Am J Physiol Gastrointest Liver Physiol 290: G1089–G1095.
  18. Pimentel, M., Mayer, A.G., Park, S., Chow, E.J., Hasan, A. and Kong, Y. (2003) Methane production during lactulose breath test is associated with gastrointestinal disease presentation. Dig Dis Sci 48: 86–92.
  19. Biesiekierski, J.R., Rosella, O., Rose, R., Liels, K., Barrett, J.S., Shepherd, S.J. et al. (2011) Quantification of fructans, galacto-oligosacharides and other short-chain carbohydrates in processed grains and cereals. J Hum Nutr Diet 24: 154–176.
  20. Muir, J., Rose, R., Rosella, O., Liels, K., Barrett, J., Shepherd, S. et al. (2009) Measurement of short chain carbohydrates (FODMAPs) in common Australian vegetables and fruit by high performance liquid chromatography. J Agric Food Chem 57: 554–565.
  21. Muir, J.G., Shepherd, S.J., Rosella, O., Rose, R., Barrett, J.S. and Gibson, P.R. (2007) Fructan and free fructose content of common Australian vegetables and fruit. J Agric Food Chem 55: 6619–6627.
  22. Macfarlane, G., Steed, H. and Macfarlane, S. (2008) Bacterial metabolism and health-related effects of galacto-oligosaccharides and other prebiotics. J Appl Microbiol 104: 305–344.
  23. Rumessen, J.J. and Gudmand-Hoyer, E. (1998) Fructans of chicory: intestinal transport and fermentation of different chain lengths and relation to fructose and sorbitol malabsorption. Am J Clin Nutr 68: 357–364.
  24. Saunders, D.R. and Wiggins, H.S. (1981) Conservation of mannitol, lactulose, and raffinose by the human colon. Am J Physiol 241: G397–G402.
  25. Ong, D.K., Mitchell, S.B., Barrett, J.S., Shepherd, S.J., Irving, P.M., Biesiekierski, J.R. et al. (2010) Manipulation of dietary short chain carbohydrates alters the pattern of gas production and genesis of symptoms in irritable bowel syndrome. J Gastroenterol Hepatol 25: 1366–1373.
  26. Evans, P.R., Piesse, C., Bak, Y.T. and Kellow, J.E. (1998) Fructose-sorbitol malabsorption and symptom provocation in irritable bowel syndrome: relationship to enteric hypersensitivity and dysmotility. Scand J Gastroenterol 33: 1158–1163.
  27. Fernandez-Banares, F., Esteve-Pardo, M., Humbert, P., de Leon, R., Llovet, J.M. and Gassull, M.A. (1991) Role of fructose-sorbitol malabsorption in the irritable bowel syndrome. Gastroenterology 101: 1453–1454.
  28. Barrett, J.S. and Gibson, P.R. (2012) Fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) and nonallergic food intolerance: FODMAPs or food chemicals? Ther Adv Gastroenterol 5(4) 261–268. DOI: 10.1177/ 1756283X11436241

New Study Shows Probiotic Supplementation May Prevent Symptoms of Child Autism

Thursday, April 30th, 2015

Autism spectrum disorder (ASD) is a complex developmental disability that impairs social interaction and communication. A child with autism has difficulty interacting with others, shows little interest in others, and lacks social awareness. Autism is more prevalent among boys than girls, with the ratio estimated at 4:1. Autism is a multifactorial disorder; several factors must be considered when determining the case. These factors include complex genetic interactions, nutritional deficiencies or overloads, pre- and postnatal exposure to chemicals or viruses, errors during the embryonic neural tube closure process, dysfunctional immune systems, and allergies. Recent studies have correlated gut dysfunction with ASD and suggest a possible role of the gastrointestinal (GI) microflora in symptomatology and or severity of symptoms in autistic children. Many autistic children experience severe dietary or GI problems including abdominal pain, constipation, diarrhea, and bloating. These symptoms may be due to the disruption of the indigenous gut flora promoting the overgrowth of potentially pathogenic microorganisms.

A growing body of medical research indicates that alterations in the type of bacteria that live in the GI tract can influence brain function, mood and overall mental health. Recently, Hsaio and colleagues (2013) linked gut microbes to ASD in a mouse model. They showed that ASD symptoms are triggered by compositional and structural shifts of microbes and associated metabolites. More importantly, they provided some of the first conclusive evidence of reversing symptoms of ASD via administration of Bacteroides fragilis probiotic. The broader potential of this research is identifying an analogous probiotic that can treat subsets of individuals with ASD; probiotics may provide therapeutic strategies for neurodevelopmental disorders. Therapies that target the gut microbiome may hold the key for making progress against a wide range of notoriously difficult psychiatric illnesses.

In a new study from Finland, Pärtty and colleagues (2015) are the first to show that probiotic supplementation early in life may be effective for reducing attention deficit hyperactivity disorder (ADHD) and ASD in children.

Researchers in Finland tested the hypothesis that probiotic supplementation may protect against the development of ADHD and AS by reviewing data from a study that was originally designed to test the effect of early supplementation with a probiotic in infancy on the later development of eczema. The mothers of 159 children were recruited in a randomized, double-blind, placebo-controlled study and received 10 billion colony-forming units of Lactobacillus rhamnosus or placebo daily for 4 weeks before expected delivery. After delivery, the capsule contents were given either to the children or continuously to the mothers (if breast-feeding) for 6 months.

To evaluate the possible link between probiotic supplementation and ADHD or AS, 75 of these children were evaluated by an experienced third party child psychiatrist or neurologist and the children were randomized and blinded so as not to produce any study bias. Results showed that ADHD or AS was diagnosed in 6/35 (17.1%) children in the placebo and none in the probiotic group (0/40). The probability value of this occurring was 0.008, indicating that it was not due to chance, but rather to a clear effect.

Previously stored fecal samples allowed the researchers to analyze the children for gut bacteria during their first six months of life. The researchers found that the numbers of Bifidobacterium species bacteria in feces during the first 6 months of life was lower in children with ADHD and AS compared to the healthy children.

The researchers concluded “Probiotic supplementation early in life may reduce the risk of neuropsychiatric disorder development later in childhood possible by mechanisms not limited to gut microbiota composition.”


Gilbert JA, Krajmalnik-Brown R, Porazinska DL, Weiss SJ, Knight R. 2013. Toward Effective Probiotics for Autism and Other Neurodevelopmental Disorders. Cell 155(7):1446-1448.

Hsaio EY, McBride SW, Hsien S, Sharon G, Hyde ER, McCue T, Codelli JA, Chow J, Reisman SE, Petrosino JF, et al. 2013. Cell 155(7):1451–1463.

Kaluzna-Czaplinska J, Blaszczyk S. 2012. The level of arabinitol in autistic children after probiotic therapy. Nutrition 28:124-126.

Pärtty A, Kalliomäki M, Wacklin P, Salminen S, Isolauri E. 2015. A possible link between early probiotic intervention and the risk of neuropsychiatric disorders later in childhood: a randomized trial. Pediatr Res. doi: 10.1038/pr.2015.51.

What is the difference between Palm Fruit and Palm Kernel Oils?

Thursday, January 1st, 2015

frogWhile palm fruit and palm kernel oils have noteworthy differences, the most important question is how and where these oils are sourced.  The organic, non-GMO certified palm fruit oil we use in all MELT products is sourced from Columbia (South America) and certified Fair Trade/ Ecosocial by the RSPO and Rainforest Alliance ( palm fruit oil we source is not linked to the destruction of old growth rain forests, the release of greenhouse gases, the displacement of native people, or the extinction of orangutans or Sumatran tigers (which only live in Borneo and Sumatra in Indonesia). Our certifications verify the palm plantations we source from are not developed by removing rain forests, but by converting pre-existing agricultural land to palm oil production. Because our supplier has several Fair Trade programs above and beyond the standards set forth by the RSPO, they are currently in the process of achieving Fair Trade certification by the end of 2015.

We often receive inquiries asking the difference between palm fruit and palm kernel oils, which we are happy to address. First, it is important to note that both palm fruit and palm kernel oils are better to consume than oxidized oils, hydrogenated or partially hydrogenated oils, and other “bad” fats. We only use palm fruit oil in our products, not because palm kernel oil is “bad”, but because palm fruit oil contributes a better overall balance of fatty acids in MELT®’s Perfect Blend. The concept behind the Perfect Blend is balancing a variety of fatty acids in the diet for wellness.

Both palm fruit oil and palm kernel oil come from palm trees, but there the similarity ends.

Palm fruit oil comes from the palm fruit, the orange flesh that surrounds the palm seed. About 37 percent of palm fruit oil is monounsaturated fat, 50 percent is saturated fat, and 9 percent is polyunsaturated fat (see below). Unrefined, palm fruit oil’s reddish or golden color indicates the presence of carotenoids, which the body converts into vitamin A. Most importantly, palm fruit oil is high in tocotreinols, a form of vitamin E. We use palm fruit oil over palm kernel oil because of its monounsaturated fat content and high levels of Vitamin E.

Palm kernel oil is extracted from the palm seed and has a fatty acid composition that is almost identical to coconut oil (see below), high in medium-chain fatty acids (i.e., caprylic, capric, and lauric acids) and with a total saturated fat content of over 80 percent. For MELT Organic spreads, we use palm fruit oil over palm kernel oil for its monounsaturated fat content, which provides a better overall balance to the fatty acid composition of MELT Organic spreads.




New Study Shows Sustained Improvement in Child Behavior with Omega-3 Supplementation

Friday, October 17th, 2014

A new study conducted by researchers from the University of Pennsylvania reported that daily supplementation of an omega-3 blend improved antisocial and aggressive behavior in children between the ages of eight and sixteen. Furthermore, daily supplementation of an omega-3 blend over a six month period reduced behavioral problems in children both at the end of treatment and for six months thereafter.

It is worth noting this study used a blend of omega-3 for supplementation and not just fish oils, which are high in EPA and DHA. Currently, some individuals (e.g., Dr. Mercola, Dr. Murray) are virtually dogmatic about fish oils as the ONLY legitimate source of omega-3, as if the alpha-linolenic acid (ALA) found in flax and chia seed serves no nutritional benefit. This generalization has led some in the blogosphere to circulate the idea that flax oil is “bad” because of its ALA content, which is categorically incorrect unless it’s rancid.

426 highHistorically, flax oil was promoted over fish oils in part because of very low quality, rancid fish oils in capsules that did more harm than good. Now high quality liquid sources are available (e.g., Carlson’s, Nordic Naturals) so more emphasis is being placed on consuming cod liver oil, and for good reason since not everyone converts ALA to EPA and DHA. However, there are also several studies that show ALA consumption is critical for optimal absorption of specifically DHA.

As one might expect, omega-3 supplementation is not about taking one type of omega-3 over another. Omega-3 supplementation is about combining omega-3 into one’s diet, such as eating one tsp of Carlson’s lemon-flavored cod liver with your morning toast with MELT® Organic (which contains 425 mg ALA per serving). Or, grinding one to two tbsp of flax or chia seed and adding it to your favorite yogurt in addition to one tsp of cod liver oil.

Methods and Results

A community sample of 8 to 16 year old children were randomized into a treatment group (100 subjects total) and a placebo-control group (100 subjects total) in a randomized, double-blind, placebo-controlled, stratified, parallel-group trial. Supplementation consisted of a fruit drink containing 1000 mg/day of an omega-3 blend or a placebo consisting of the same fruit drink without omega-3. The omega-3 blend included 300 mg DHA, 200 mg EPA, 400 mg ALA, and 100 mg of docosapentaenoic acid [DPA]. Treatment lasted for 6 months, and all participants were followed for another 6 months after discontinuation of treatment. Changes in behavior problems were reported by both the child subjects and their caregivers.

Primary outcome measures were externalizing behavior problems that included acting out, being aggressive, and reactive. Secondary outcome measures looked at the impact on internalizing behavior (social withdrawal, feelings of loneliness or guilt, fearfulness, etc.). The children were assessed by the parents and researchers, as well as through a self-assessment questionnaire. The parents also completed a self-assessment questionnaire.

While the children themselves did not report improvement, the parents reported a significant improvement in children’s behavior in the treatment group for all behavioral issues. Specifically, omega-3 supplementation for 6 months resulted in a 41.6% reduction in parent-rated child externalizing behavior compared to the placebo group. This effect persisted 6 months after the treatment period had ended. An even larger reduction of 68.4% was seen for internalizing behavior.

Findings provide evidence that omega-3 supplementation can produce sustained reductions in externalizing and internalizing behavior problems in children between eight and sixteen years old.


Raine A, Portnoy J, Liu J, Mahoomed T, Hibbeln J. 2014. Reduction in behavior problems with omega-3 supplementation in children aged 8-16 years: a randomized, double-blind, placebo-controlled, stratified, parallel-group trial. J Child Psychol Psychiatry. doi: 10.1111/jcpp.12314. [Epub ahead of print]

Barceló-Coblijn G, Murphy EJ. 2009. Review: Alpha-linolenic acid and its conversion to longer chain n-3 fatty acids: Benefits for human health and a role in maintaining tissue n-3 fatty acid levels. Progress in Lipid Research 48:355–374.




Gourmet Spicy Kraut

Wednesday, August 13th, 2014

Canning, pickling, and freezing are all worthy methods for preserving your garden’s bounty, but fermenting your gorgeous surplus of vegetables is even better. When performed correctly, raw fermentation is a miracle of nature with infinite possibilities for nutritional therapy – all in a delicious, tangy side dish perfectly paired with your favorite meats or eaten alone. Like kefir and other fermented foods, fermented vegetables provide highly concentrated sources of probiotics with a wide range of benefits from naturally lifting one’s mood to strengthening the immune system and boosting gut health. Done correctly, fermented vegetables can be stored up to 8 months. Since probiotic strains vary with the vegetable, this recipe is especially healthful (and addictive) because of the array of vegetables included.

This week’s fermentation is a gourmet spicy kraut reminiscent of kimchi but easier to make and fun to improvise with new variations. It is DELICIOUS! Other fermentation recipes call for using whey, but I believe it’s unnecessary and worth avoiding. Enjoy our other fermented food recipes, including German Sauerkraut, Organic Ginger Beet Kvass, Lacto-Fermented Garlic, and Traditional Korean Kimchi.

spicy kraut


1 small green cabbage, outer leaves removed, 1” wide slices, coarsely chopped

6 bok choy, coarsely chopped

3 carrots, sliced into thin rounds

3” diakon radish, sliced into thin rounds, then in half (half rounds)

4 big garlic cloves, chopped

1½” length of ginger, peeled and grated

1 bunch scallions, chopped

1/8 to 1/4 cup Korean chili powder (gochugaru) to taste

2 to 3 tablespoons sea salt to taste


Gallon fermentation jar with airlock system

Weights for keeping spicy kraut immersed in its own brine

Mason quart jars for storage

Please note fermentation jars with airlocks and glass weights can be purchased online from Cultures For Health or The Probiotic Jar.


  • Clean and sanitize kitchen surfaces; the cleaner your environment the better.
  • Clean and sanitize the equipment (fermentation jar, weights) to ensure the absence of pathogenic bacteria. Be sure to rinse off the equipment after sanitizing it so doesn’t kill off the beneficial bacteria needed for fermentation.
  • After washing and prepping the produce, add it all to a large mixing bowl.
  • With latex gloves on, hand-mix together the kraut with the Korean chili powder and salt until thoroughly mixed together. The salt will draw moisture from the produce, which is essential for developing the brine.
  • Pack the kraut salad tightly into your fermentation jar. Add any leftover juices to the fermentation jar.
  • Add weight on top of the packed kraut to ensure the produce is well submerged in liquid –the anaerobic environment is critical for proper fermentation and preventing contamination. Spicy kraut wants to be suffocated!
  • If the kraut is light on liquid, then add salted water as needed. (Over the next 24 hours, the kraut will produce more liquid as the salt pulls moisture out of the vegetables.)
  • Tighten the airlock lid and fill the airlock with water to the fill line. Make sure the lid is on tight and the airlock is screwed in securely – we only want gases leaving the container. When properly sealed, the airlock lid makes contamination or spoilage practically impossible.
  • Ideal fermentation temperature is around 68-72 degrees and ok up to 75 degrees. Technically, the kraut is ready in 2 weeks, but is at its best in terms of flavor and probiotic content when it ferments for 3.5 to 4 weeks. More than 4 weeks, the kraut can turn mushy.
  • A little bit of white froth or a white film may form on the liquid surface; this is harmless and will resolve itself. If black mold develops on the surface, then don’t eat it. For information on common mistakes and troubleshooting, read Food Renegades blog on the matter.
  • After 3.5 to 4 weeks of fermentation, move the spicy kraut into quart mason jars, pack it down, top off with brine, and store in the refrigerator. It’s good for up to 8 months.

MELT® Organic Love

Monday, July 28th, 2014

Cygnia had the pleasure of connecting with Mariya of Tahoe about why she loves MELT and how its been an essential part of her lactose- and gluten-free diet.

What health issues necessitated your search for healthier foods?

“I had painful stomach issues throughout college that I left undiagnosed because I was afraid of anything getting in the way of keeping up with classes, socializing, working, and eating at the cafeteria. I didn’t want to make my time in college any harder than it needed to be. As a result, I didn’t feel well during all four years in college and I didn’t take care of myself.

A couple of years after I graduated, I decided to get to the bottom of my declining health. By then, my symptoms extended well beyond the gastrointestinal stuff to other issues like anxiety, skin rashes, and a fear of food – every time I ate, I felt like I was going to make myself sick. I started seeing specialists and doctors and with the help of a Naturopathic Doctor I finally got to the bottom of it three years ago.

My Naturopath ran an allergy panel and found I am severely allergic to wheat, gluten, and yeast. I immediately stopped eating wheat, gluten, and yeast; my symptoms subsided for the most part, but I noticed I was still feeling sick when I ate dairy. Even though my allergy panel didn’t show a dairy allergy, I still noticed it was making me sick. My Naturopath confirmed many people suffering from prolonged, unaddressed wheat, gluten, and yeast allergies can develop a secondary allergy to lactose.

I have felt 1000 times better ever since I removed lactose from my diet.”

How do you like eating MELT?

“I am a meat, potatoes, and butter kind of girl – it’s the diet I was raised on, so my transition to a gluten- and lactose-free diet was hard. Three years later, it is much easier but I never found a butter substitute that tastes as good or is as versatile as MELT. MELT feels luxurious to eat and I LOVE it with my food where I haven’t LOVED other butter substitutes. I use on everything and it is awesome.

I use MELT wherever I use butter: gluten-free oats, baked acorn squash, corn on the cob, broccoli, all of my vegetables, gluten-free bread, quinoa… I use it on anything and everything I normally put butter on.”

Parting thoughts?

“I LOVE butter, but it just doesn’t work for me anymore. I have tried tons of other butter substitutes, but yours – bar none – takes the cake. It is amazingly delicious. I find myself craving it during the middle of the day. Thank you for creating such a good product!!! I am telling my family and friends.

I hope I see you guys in every grocery store I go into. I am a diehard fan – I have NEVER written a brand or a product rave. I was sitting at the table eating MELT by the spoonful when my boyfriend said, “You are addicted to that stuff.”  “I know I should just write them a letter and tell them.”  All I keep thinking is the grocery store better have MELT the next time I am there.

I want to help young people make healthier food choices for themselves so they don’t have to suffer for years and years. I want to help get the message out on products like MELT. You can eat healthier without sacrificing anything. It’s all there – the taste, the texture – so why not make a healthier choice for yourself?  I want to thank you and I am super stoked on MELT.”

UC Santa Barbara Scientists Discover Potential of Cinnamon to Prevent Alzheimer’s Disease

Friday, June 6th, 2014

According to a new study in the Journal of Alzheimer’s Disease – “Interaction of Cinnamaldehyde and Epicatechin with Tau: Implications of Beneficial Effects in Modulating Alzheimer’s Disease Pathogenesis” – the compound responsible for giving cinnamon its sweet, bright smell could potentially play a role in delaying the onset of or warding off Alzheimer’s disease.

Alzheimer’s disease is the most common form of dementia, a neurodegenerative disease that progressively worsens over time as it kills brain cells. No cure has yet been found, nor has the major cause of Alzheimer’s been identified.

However, two compounds found in cinnamon –– cinnamaldehyde and epicatechin –– are showing some promise in the effort to fight the disease. According to Roshni George and Donald Graves, scientists at UC Santa Barbara, these compounds have been shown to prevent the development of the filamentous “tangles” found in the brain cells that characterize Alzheimer’s.

Responsible for the assembly of microtubules in a cell, a protein called tau plays a large role in the structure of the neurons, as well as their function.

“The problem with tau in Alzheimer’s is that it starts aggregating,” said George, a graduate student researcher. When for the protein does not bind properly to the microtubules that form the cell’s structure, it has a tendency to clump together, she explained, forming insoluble fibers in the neuron. The older we get the more susceptible we are to these twists and tangles, Alzheimer’s patients develop them more often and in larger amounts.

The use of cinnamaldehyde, the compound responsible for the bright, sweet smell of cinnamon, has proven effective in preventing the tau knots. By protecting tau from oxidative stress, the compound, an oil, could inhibit the protein’s aggregation. To do this, cinnamaldehyde binds to two residues of an amino acid called cysteine on the tau protein. The cysteine residues are vulnerable to modifications, a factor that contributes to the development of Alzheimer’s.

“Take, for example, sunburn, a form of oxidative damage,” said Graves, adjunct professor in UCSB’s Department of Molecular, Cellular, and Developmental Biology. “If you wore a hat, you could protect your face and head from the oxidation. In a sense this cinnamaldehyde is like a cap.” While it can protect the tau protein by binding to its vulnerable cysteine residues, it can also come off, Graves added, which can ensure the proper functioning of the protein.

Oxidative stress is a major factor to consider in the health of cells in general. Through normal cellular processes, free radical-generating substances like peroxides are formed, but antioxidants in the cell work to neutralize them and prevent oxidation. Under some conditions however, the scales are tipped, with increased production of peroxides and free radicals, and decreased amounts of antioxidants, leading to oxidative stress.

Epicatechin, which is also present in other foods, such as blueberries, chocolate, and red wine, has proven to be a powerful antioxidant. Not only does it quench the burn of oxidation, it is actually activated by oxidation so the compound can interact with the cysteines on the tau protein in a way similar to the protective action of cinnamaldehyde.

“Cell membranes that are oxidized also produce reactive derivatives, such as Acrolein, that can damage the cysteines,” said George. “Epicatechin also sequesters those byproducts.”

Studies indicate that there is a high correlation between Type 2 diabetes and the incidence of Alzheimer’s disease. The elevated glucose levels typical of diabetes lead to the overproduction of reactive oxygen species, resulting in oxidative stress, which is a common factor in both diabetes and Alzheimer’s disease. Other research has shown cinnamon’s beneficial effects in managing blood glucose and other problems associated with diabetes.

“Since tau is vulnerable to oxidative stress, this study then asks whether Alzheimer’s disease could benefit from cinnamon, especially looking at the potential of small compounds,” said George.

Although this research shows promise, Graves said, they are “still a long way from knowing whether this will work in human beings.” The researchers caution against ingesting more than the typical amounts of cinnamon already used in cooking.

If cinnamon and its compounds do live up to their promise, it could be a significant step in the ongoing battle against Alzheimer’s.

Confessions of a Wheat Addict – 2 Years Later

Monday, May 5th, 2014

Gluten makes up 80% of the protein in wheat, rye, and barley grains. Gluten sabotages the gut, reducing its surface area and impairing digestion. Gluten is directly toxic to intestinal cells by inhibiting cell proliferation, increasing cellular oxidation products, and changing membrane structure. In the body, gluten changes the structure of the intestine by reducing height of villi, decreasing depth of crypts, and decreasing enterocyte surfaces.

As all toxins do, gluten inspires an immune response. This immune response is intended to clear the gluten from the intestine and preventing a build-up of toxins, however, in the process it inflames the intestine.

A little known, but important point to remember: wheat triggers gut inflammation in nearly everyone.

This reaction varies from 1) observable gut inflammation in ~83% of the population, to 2) anti-wheat-gluten antibodies developing locally in the intestine (~30% of the population), to 3) developing systemic antibodies to wheat gluten (~11% of the population), and finally 4) developing celiac disease where systemic antibodies attack human cells in the intestine, thyroid, pancreas, and elsewhere (~4% of the population).

After reading this information in “Perfect Health Diet” by Jaminet and Jaminet (2010), I came to terms with the reality that consuming wheat and other grains isn’t an option for me because of my history of digestive disorders – unless they are in sprouted form (which neutralizes the gluten).

Up until February, 2012 I was a pasta junkie for the better part of my life. Pasta was quick to make, filling, and gave me the calories I needed for extended periods of exercise or work. I ate pasta probably 3-4 times per week. I call myself a pasta junkie because wheat is a source of opiates.  When I first read this, I was skeptical – it seemed exaggerated and a little out there; I struggled with taking the information seriously.

Then I quit eating pasta cold turkey.

Nausea, muscle tension in my TMJ, lightheadness, fatigue. I had wheat withdrawal for 2 weeks.

Wheat-derived opioids? Those are real. If you don’t believe me, try Googling “wheat withdrawl” and see what comes up. Many people experience this short-term setback for the long-term benefit of eliminating wheat from their diets.  Like celiacs or others with leaky gut, I craved the food that made me predisposed to illness: wheat.

Uncovering my mild narcotic addiction to wheat was surprising, but even more so was the subsequent and dramatic relief from “brain fog” that I couldn’t put my finger on and seemed to be getting worse with time. The mental clarity I experienced – and continue to experience – from quitting wheat is priceless. I learned through direct experience brain fog is an indicator of inflammation – usually and almost always in the gut. Eliminate gut inflammation and you will be surprised at how many other ailments clear up on their own.

Do I miss pasta? Not anymore – especially when I have discovered far more satisfying replacements, like spaghetti squash in this fabulous Bolognese sauce recipe!!!

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