“Human Strain” Probiotics
The origin of a strain simply specifies from what source that particular strain - often part of a blend - was first isolated. Its origin is related to establishing intellectual property and a chain of custody, but not to any possible health benefits. There are all kinds of organisms, both desirable and undesirable, in our guts, but microbiologists do not consider the first identified/isolated source to be predictive of the health benefits that any particular strain (substrain) will provide to people.
So touting a “human source” or “soil organism” is actually a marketing game, not a valid scientific argument, and in fact is an anti-scientific message. Just because an organism was obtained from human feces (or rarely, saliva), perhaps because the person actually obtained it by eating fermented foods or even from contact with soil, doesn’t mean that it has probiotic properties…or even different properties than eating it in that yogurt or directly consuming those soil organisms. We all probably have some small quantity of E coli and Salmonella in our bowels; should they therefore be promoted as “human stain” probiotic bacteria? Obviously not…
In the scientific literature the benefits of a probiotic strain (or blend) depends solely on its technical qualities: proper identification of the specific strain (substrain), its stability in a consumer product, its bile and acid resistance, its ability to colonize and persist in the human GI tract, and any specific health effects it provides as measured in both test tube and human clinical trials when given to a human being. None of these qualities depend on its original sourcing. Specific label claims relating to substrains of probiotics depend totally on the body of clinical evidence of how that substrain provides benefits to people.
Look for the addition of a third name to the Latin binomial (2-word Latin name) of a strain to indicate a specific substrain, as in “Lactobacillus acidophilus La-14” or “Bifidobacterium lactis BL-04”.
If a company is touting the origin of their strain(s) rather than their proven clinical health benefits, then they may have no clinically validated strains and are just trying to promote theoretical rather than demonstrated benefits. Why would they promote strains based on irrelevant historical factors related to the strain's discovery rather than providing evidence of their product's demonstrated health benefits if they do have clinically relevant strains?
Smart consumers will look for evidence-based label claims, such as clinical trials utilizing their particular strain to assure that a probiotic product will have some credible evidence of being health promoting.
Wednesday, November 06, 2013
“Human Strain” Probiotics
Tuesday, August 06, 2013
Monday, July 15, 2013
- “This is not a randomised controlled trial but a trial comparing Omega 3 levels in men with prostate cancer with healthy men. The men with prostate cancer had higher levels of Omega 3. But you cannot extrapolate cause and effect from this finding. It is like saying that if the majority of men with prostate cancer played tennis compared to healthy controls then tennis could trigger prostate cancer.”
- In 2009 the Harvard School of Public Health reported that “Omega 3 deficient diets cause up to 96,000 preventable deaths a year in the US. The researchers estimated the number of deaths resulting from 12 preventable causes and Omega 3 deficiency ranked as the sixth highest killer of Americans. A deficiency in these fats was classed as a bigger killer than high intake of trans fats.” 
- “…there are many cultures such as the Japanese who eat high amounts of oily fish containing Omega 3 fatty acids and yet have one of the lowest prostate cancer death rates in the world.”
- “Hundreds of studies over the past two decades have shown omega-3 fatty acids to have positive effects associated with cardiovascular health, perinatal health, inflammation, cognitive function, or cancer. Collectively, this body of research serves as the basis for numerous recommendations from respected organizations, scientific boards and healthcare practitioners that Americans get omega-3 fatty acids in their diets.”
- “While we encourage researchers to continue to study omega-3 fatty acids with an open mind, it is counterproductive when studying nutrition for researchers to promote their study as if it were the only piece of research that counts. In this case in particular, it is especially disingenuous for the researchers to make the kinds of assertions we've seen in the press, given their results are in stark contrast to previous epidemiologic studies that not only demonstrate no correlation between omega-3 consumption through fish and/or supplementation and the risk of prostate cancer, but in many cases also showed a protective effect against prostate cancer.”
- “One should also consider whether this study could have simply been measuring a biomarker reflecting recent intake of fish or fish oil supplements in a group of high risk cancer patients that had been told to increase their EPA and DHA levels, as compared to a group of non-cancer patients that had not been told to consume more EPA and DHA. Plasma levels of EPA and DHA reflect very recent intake and are considered a poor biomarker of long term omega-3 intake especially when compared to red blood cell levels, which reflect medium term intake. A single fish oil dose (or hearty serving of fish at lunch) results in >100 percent increase in plasma omega-3 levels. So looking at plasma levels in healthy and sick people may only provide insight into the recent habits of these individuals.”
- “The American Heart Association, the World Health Organization (WHO), the U.S. Institute of Medicine’s Food Nutrition Board (IOM FNB) and the 2010 Dietary Guidelines all have current policies advising Americans to eat more fatty fish to get the benefits of omega-3 fish oils. It is highly unlikely this one study will change that advice. Omega-3s can also be obtained by taking one of the many supplement products on the market. For those consumers who have concerns about prostate cancer or other questions about omega-3 fatty acids, we recommend speaking with your doctor or other healthcare practitioner.”
- Were DHA levels related to diet, supplementation, or both?
- Were fish and/or fish oils perhaps consumed as a deliberate health choice because of prior knowledge of prostate issues, rather than actually causing or aggravating those issues? In other words, could the consumption represent an attempt to improve a pre-existing condition by improving one’s nutritional status and be unrelated to the disease itself? Perhaps even suggested by medical teams as potentially helpful for patients' diet?
- If they had been collected, what would key inflammatory and oxidative markers, that are much likelier to be related to prostate health problems than long-chain omega-3 fatty acids such as DHA, have told us about these men’s state of health and disease?
- Where is the biochemical evidence that DHA itself may negatively contribute to prostate concerns? None is presented, even theoretically.
- “The difference in mean blood plasma phospholipid fatty acids blood level for omega-3s was 4.66% in the combined cancer group versus 4.48% in the control. They are basing their results on just ca. 0.2% difference in omega-3 levels.”
- “Plasma phospholipid fatty acids as measured in this study are not a good index of long term intake and are influenced dramatically by a single meal, or even timing of a fish oil dose. A single fish oil dose massively increases LC omega 3 (typically increasing levels by 100% or more) in about 4-12 hours and then washes out around 48 hours.”
- “The study was not designed to look at omega-3 and confounded with selenium and Vitamin E used in the treatment arms.”
- “The test cohort included sick and healthy people. It is possible that sick people were taking fish oil supplements at a higher rate than the healthy individuals.”
- “A recent meta-analysis of fish consumption and prostate cancer by Szymanski et al. (2010) reported a large reduction in late stage or fatal prostate cancer among cohort studies." 
- "Several population based studies have shown a benefit of increased omega-3 fatty acid intakes to reducing prostate cancer risk.” , 
Tuesday, May 28, 2013
Canola oil has less oleic (omega-9) and more ALA (omega-3) than olive oil and been shown to:
• improve lipid measurements greater than olive oil in human subjects in a randomized, double-blinded trial: http://www.ncbi.nlm.nih.gov/pubmed/8399091
• improve cardiovascular health more than olive oil in a rat model: http://www.ncbi.nlm.nih.gov/pubmed/7722678
Tuesday, May 07, 2013
Recent attention given to the effects of various fish oils on polystyrene (Styrofoam®) cups has led to some misunderstanding of how these products work in terms of nutrition and safety. It is unfortunate that the use of these stunts imply may confuse or even scare people away from taking this natural product which provides constituents that are essential to human health. Don’t be fooled by this trick! If someone tries to use it as a means to push one product over another, challenge them to explain exactly what the test is supposed to mean. Here’s what you need to know about the test, how it works, and what it means:
Styrofoam® (polystyrene) cups can be dissolved by pure fish oils. All fish oils will have this same effect on polystyrene, but some will take much longer than others. Various healthy natural substances, like fresh lemon oil, will also dissolve polystyrene. In the Styrofoam® cup test, the esterified ethyl ester form of fish oil works to dissolve Styrofoam® much faster than the triglyceride form simply because the number of chemical bonds in the two forms of oil are different; with ethyl ester fish oil having its number of bonds closer to that of Styrofoam®. This similar chemical polarity is the same reason why pure lemon oil also works quickly to dissolve Styrofoam®. No solvents are used to produce the fish oils, so none are present in the finished products. This magic trick does not translate into any legitimate safety concerns, despite its obvious visual impact. Fortunately, the human body is not composed of polystyrene and is not negatively affected by fish oils in its commonly available forms.
Fish oil naturally comes in a volatile triglyceride (triacylglycerol) form and can be esterified for additional benefits. As soon as a fish is caught the oils begin to degrade and can easily go rancid. Esterification is a process that stabilizes and maintains the freshness of fish oil to prevent rancidity and allows higher concentrations of the essential omega-3 EPA and DHA fatty acids to be available. During this esterification process, the triglycerides are removed, changing the number of molecular bonds in the fish oil. Both the purified ethyl ester form and the triglyceride form must be digested to a simpler fraction, the free fatty acid, to allow bioavailability from the human gut. Ethyl ester and triglyceride forms are equally well digested by lipase and available for absorption as free fatty acids, and the ethyl ester form is at least as bioavailable as the triglyceride form. (1)
There is some evidence that the ethyl ester form will sustain circulating levels of the omega-3 fatty acids EPA and DHA better than the triglyceride form. The ethyl ester form of EPA and DHA is the form that is used in most successful clinical studies evaluating the potential health benefits of supplemental Omega-3 fats. In fact, clinical trials on the ethyl ester form more consistently generate positive results than those done with the triglyceride form. Also EPA and DHA as ethyl esters inhibit platelet aggregability and control serum triglycerides while leaving other serum lipids essentially unaltered. (2) The ethyl ester forms build up body stores, allowing conversion to free fatty acids more consistently than the triglyceride form. (3) Because of their proven benefits and safety, it would be unfortunate if a misunderstood “test” causes some people to reject the use of solvent-free ethyl ester fish oils as part of their diet.
Chemical Polarity plays a role in how compounds react with one another. Polarity refers to the electro-magnetic charges of a molecule, or the attraction between the positively and negatively charged parts of a molecule. Compounds are considered polar due to the unequal sharing or electrons. For example, water is a polar compound. A compound is non-polar when the electric charge is balanced. Edible oils are typically non-polar.
In Chemistry there is a rule to describe how polar and non-polar solvents react with similar solutes: “like dissolves like”. We all know that oil and water do not mix. The reason why is that water, which is polar, will not react (mix) with oil, which is non-polar. “Like dissolves like.”
Two common compounds, sugar and salt, are both polar and in nature they readily mix with water, another polar compound.
With polarity, compounds of differing polarity do not react/mix, while those with like polarity do mix. So a chemical reaction occurs when a non-polar compound comes into contact with another non-polar compound, and more readily when the number of chemical bonds in one substance more closely matches the other.
Polystyrene, a moisture-resistant foam commonly known as Styrofoam®, is formed from a long chain of polymers. This plastic is used in the manufacture of coffee cups and plates as an insulator and as packaging material, and is non-polar. What makes Styrofoam® ideal for keeping most hot beverages hot and cold beverages cold is that as a non-polar compound it will not react with the polar water used to make coffee, tea, and other beverages. This same material will react with any form of edible oil; this can be olive oil, lemon oil, fish oil, etc. This reaction is naturally occurring and its intensity is based solely upon the chemical properties of both compounds and the polarity of each.
All edible oils, which like Styrofoam® are non-polar, are made up of fatty acids; and these fatty acids are made up of a long chain of hydrocarbon molecules. With Fish Oils, some contain triglycerides and some contain ethyl esters. Both the triglyceride form and the ethyl ester form first need to be digested and broken down to a free fatty acid for absorption from the GI tract. After uptake, the free fatty acid is then converted to a triglyceride form in the liver by the addition of already available triglycerides obtained from circulating lipids (fats).
In the example of fish oils, ALL will react with Styrofoam over time; the length of time is determined by the number of chemical bonds in each type of fish oil relevant to the number of chemical bonds in Styrofoam®. Triglycerides will take longer to react with the cup, while oils bonded to ethyl esters, which have more chemical bonds, will naturally penetrate the cup wall faster.
- Krokan HE, Bjerve KS, Mørk E. The enteral bioavailability of eicosapentaenoic acid and docosahexaenoic acid is as good from ethyl esters as from glyceryl esters in spite of lower hydrolytic rates by pancreatic lipase in vitro. Biochim Biophys Acta. 1993 May 20;1168(1):59-67. PMID: 8504143
- von Schacky C. A review of omega-3 ethyl esters for cardiovascular prevention and treatment of increased blood triglyceride levels. Vasc Health Risk Manag. 2006;2(3):251-62. Review. PMID: 17326331
- Rupp H, et al. Risk stratification by the "EPA+DHA level" and the "EPA/AA ratio" focus on anti-inflammatory and antiarrhythmogenic effects of long-chain omega-3 fatty acids. Herz. 2004 Nov;29(7):673-85. Review. Erratum in: Herz. 2004 Dec;29(8):805. PMID: 15580322
Monday, March 25, 2013
The rape plant (Brassica napus) is related to mustard, turnip, cabbage, radish, and horseradish plants. Its oil has been used for centuries as a cooking oil in Europe and Asia (India and the Far East).
Both rapeseed oil and mustard seed oil contain relatively high levels of a fatty acid called erucic acid. As with some other oils, when heated to high temperatures unrefined rapeseed oil can release fumes which have been theorized to be associated with an increased lung cancer risk. These fumes have been blamed on its high erucic acid content; perhaps undeservedly since refined rapeseed oil did not seem to share this characteristic and since mustard seed oil is still a staple cooking oil in South and East Asia.
In any case, rapeseed oil was not sold as a food in the United States for many years, and this is why a low-erucic acid version was developed by traditional cross-breeding of varieties that had lower than usual levels. Originally developed in Canada in 1974, it was dubbed “Canola” oil to distinguish it from traditional rapeseed oil; the name implies its Canadian origin. This oil is often sold in Europe under its more commonly known “rapeseed” rather than the “Canola” name, even if the low erucic acid type is used.
Canola (low erucic acid rapeseed) oil received GRAS status in 1985, allowing it to be sold as a food or food additive in the United States.
These dates are long before the first commercial GMO crops were approved by the U.S. government in the mid-1990s. Since Canola’s breeding history actually goes back decades before that, it clearly was originally developed without the use of genetic engineering (GE, or biotechnology). Today, most of the canola grown in North America is GMO (from GE seeds); though there are still some Identity Preserved (IP) canola crops, from which is produced non-GMO canola oil.
The history of the use of rapeseed oil in food in the US is well summarized in the preamble of the final rule which affirmed the GRAS status of low erucic acid rapeseed (LEAR) oil (Federal Register, 1985: 21 CFR 184.1555 (c)(4)).
Thursday, February 21, 2013
Why do people buy vitamins at health food stores instead of drug stores in the first place? Many people reject some of the pharmaceutical ingredients that are commonly used in products sold in that channel but which are not used in vitamin products sold in the natural channel. These questionable ingredients include petroleum and coal tar derivatives, talc, hydrogenated oil, artificial colors/flavors/sweeteners, crospovidone, butylated hydroxytoluene, and hypromellose.