Showing posts with label canola oil. Show all posts
Showing posts with label canola oil. Show all posts

Monday, July 5, 2010

Please explain this to Cargill

6 September: As you can see, Monsanto keeps eyeing markets for its genetically modifed soybeans. In a joint venture with Solae, Monsanto wishes to flood the supplement market, and probably Big PhRMA products too, with their oil as a source of omega 3.  As this excerpt notes, ALA is not well converted to active omega 3 by most humans.  Remember that it has just been found that soy bean oil contributes to cataract.  This oil is also used as a "plant sterol" in margarines and many other products that allege they support heart health.

Monsanto and Solae are leading research into genetically modified soybeans containing SDA as a source of omega-3. Soybean oil is not normally a good source of omega-3 because it contains alpha-linolenic acid (ALA), which the body coverts inefficiently to SDA. Read complete article

5 July: While we know this product is highly unlikely to be non-GMO, it's also another example of corporate irresponsibility.

I've posted numerous articles on Natural Health News about the promotion of "plant sterol" products allegedly for heart health.

When doing some digging I found that it is GMO canola and soy oils used to push this agenda, and consumers are mostly unaware.

Flax seeds and flax oil are tremendous health promoting foods, but flax oil is extremely fragile and turns rancid quickly. One has to wonder will Cargill utilize GMO flax seed to make their oil. And what will they use to make it stable for nine months, non-refrigerated?.
What it's got: Flaxseed is a good plant source for a type of omega-3 fatty acid known as alpha-linolenic acid (ALA). It also contains soluble fiber and plant estrogens called lignans..
Why it's super: Flaxseed may improve heart health by lowering blood pressure, inflammation, and blood triglyceride levels and helping to prevent clot formation in arteries. Some studies suggest it may also reduce the risk of some cancers.
The major issue beyond GMO and the liver toxicity relationship to canola oil, is the inability for a vast majority of people to convert these oils from ALA to Omega 3.

Additionally, most commercial oils are produced with toxic hexane and toxic benzene.

I guess you'd better learn to read labels, your life may depend on it.
Cargill To Introduce Industry-First Healthy Oil Innovation, Clear Valley® Omega-3 Oil Made From Canola And Flax Seed, At IFT Food Expo
Revolutionary new oil delivers heart health benefits, allows ALA omega-3 label claim in low-fat, shelf-stable products

Minneapolis, MA /PRNewswire/ - Cargill will introduce a revolutionary new canola/flax seed oil blend at the Institute of Food Technologists (IFT) Food Expo July 18-20 in Chicago. Cargill recently completed a GRAS (Generally Recognized As Safe) self-determination for the ingredient, which will allow food manufacturers to make a "good source of ALA (alpha linolenic acid) omega-3" or "excellent source of ALA omega-3" Nutrient Content Claim(1) on the front of the package. The new oil contains up to 30 percent of ALA omega-3 and provides a minimum of 160 milligrams of ALA in most applications. Clear Valley® Omega-3 Oil, which is patent pending, is now available for product trial testing.

"As heart-health is top of mind for many consumers, Cargill developed Clear Valley®Omega-3 Oil to help manufacturers who want to seamlessly deliver heart-healthy products to this market," said Willie Loh, Ph.D., vice president in Cargill's oils and shortenings business. "This is not a small opportunity for our customers. Seventy-seven percent of consumers have used heart-healthy foods in the past year(2), and 63 percent of consumers are trying to add sources of omega-3 to their diets(3)," said Loh. Loh further discusses the subject of healthy oils innovation on the Cargill Innovation Exchange. Read complete article

Thursday, March 12, 2009

Canola Comments

This update comes via my "Southern Comrade" and fellow health nut. I was throwing words around in my brain about a title for one of his posts. It had to be cleaver because we have this on-upsmanship thing going on.

I thought about a fellow I used to work with 30 years ago who is now a PhD and head of his village corporation in Alaska. He and I share another acquaintance who is an amazing artist and Puffin fan.

Not that any of this makes sense, it all comes back to play on words, so here is a link to more on fat, and 'Puffin PUFAS'.
Canola oil is a too commonly used ingredient in food, especially now that "plant sterols" are plugged into all kinds of things like margarine, vitamins, even aspirin. You'll find it in dog food and even in an ever increasing number of items in the natural food market place.

My suggestion is that you read this following definition of canola oil, understand it is toxic to the liver, it is a trans fat as a result of processing, and consider keeping out of your diet.
"Canola Oil contains 5% saturated fat, 57% oleic acid, 23% omega-6 and 10%-15% omega-3.

This oil was developed from the rape seed, a member of the mustard family. Rape seed is unsuited to human consumption because it contains a very-long-chain fatty acid called erucic acid, which under some circumstances is associated with fibrotic heart lesions. Canola oil was bred to contain little if any erucic acid and has drawn the attention of nutritionists because of its high oleic acid content.

But there are some indications that canola oil presents dangers of its own. It has a high sulphur content and goes rancid easily. Baked goods made with canola oil develop mold very quickly. During the deodorizing process, the omega-3 fatty acids of processed canola oil are transformed into trans fatty acids, similar to those in margarine and possibly more dangerous.

A recent study indicates that "heart healthy" canola oil actually creates a deficiency of vitamin E, a vitamin required for a healthy cardiovascular system. Other studies indicate that even low-erucic-acid canola oil causes heart lesions, particularly when the diet is low in saturated fat."

Tuesday, November 11, 2008

What's In Your Oil

Once again -

If you follow Natural Health News you know that I am against the use of canola oil in any way, shape or form. You know as well that I have written about the "plant sterol" fiasco that is sweeping the aisles of OTC products that include Centrum Cardio and Bayer's Heart Advantage.

You'll find canola oil in Promise and their "super shots" as well.

Canola is also generally GMO in the market place and it is toxic to your liver.

One expert on fats and oils classes canola oil as "too monounsaturated for health".

Here is a chart and some comments from another natural health advocate that might enlighten you.
7.4% Saturated - 61.6% Monounsaturated - 31.0% Polyunsaturated

Although Canola Oil contains a high percentage of relatively stable monounsaturated fatty acids, canola oil goes rancid quite easily, and relative to olive oil, forms high concentrations of trans fatty acids.

Canola oil consumption has also been linked to vitamin E deficiency and heart disease, especially when a person is not getting enough saturated fatty acids in his or her diet.

I recommend staying away from canola oil whenever possible.

Monday, July 14, 2008

Canola and Soy oil not worth the risk

UPDATE: 1 September 2010: Vegetable oils can lead to cataract and macular degeneration -
Professor Paul Beaumont explained: “The oils that you eat become part of your eye, but normally they’re used and flushed out. Researchers believe the eye finds it particularly difficult to biodegrade vegetable oils. They end up blocking the eye’s cells and causing macular degeneration”. Complete article

Original post: The following article is from a series I receive related to my requirement for continuing legal education, written for healthcare professionals.

The issue of necessary omega 3 in the diet is one I beleive in.

What I do not support is the following excerpt from this report.ALA intake has increased during the past several decades, however, mainly through the consumption of vegetable oils such as soybean, canola, and flaxseed oil.

Soy, and the oil, is a very unhealthy substance. Soy is more likely than not to be genetically modified (GMO), as it is in the supplement and food additvie CoroWise found in Centrum Cardio vitamins and some of the cholesterol lowering supermarket products and margarines. Soy is a highly allergenic food. Commercially prepared soy oil is usually processed with hexane and/or benzene, both toxic solvents. Plastic bottles that leach xenoestrogens into the oil when exposed to bright light as on supermarket shelves lead to more toxins in the oil.

Canola is in the same GMO category and is effected by the same type processing and packaging. Canola oil is toxic to the liver, which I have pointed out in other articles in this blog. Canola, by the processing, becomes a trans fat.

I suppose I wish more doctors would read my comments. Getting some dieticians to read them too would be progress. The same holds for readers. There is always more research you can do to learn what the facts are in deference to some proclamation from a double blind study, often funded by the product manufacturer.

If you want to find out more about soy and canola oil, look for information from Mary Enig. She probably knows more about oils than anyone in a scientific field today.

I am in support of flax oil, especially the high lignan kind. Of course this oil should be properly processed, stored only in refrigerated black, light resistant bottles, and used 4-6 weeks of opening the bottle. This oil is very fragile and becomes rancid quickly. Our office sells only a single source of flax oil, perhaps the finest in the market place. We are also very fond of hemp seed oil and use it almost exclusively now because of the high protein content.
From Heartwire — a professional news service of WebMD

July 11, 2008 — The consumption of a diet containing vegetable oils rich in alpha-linolenic acid (ALA) is associated with significant reductions in the risk of nonfatal myocardial infarction (MI), a new study has shown [1]. Investigators say the protective effect of ALA is evident among individuals with low intakes, suggesting the greatest benefit might be in developing countries, where fatty-acid consumption is limited.

"The potential for benefit is great when the baseline intake is low," said lead investigator Dr Hannia Campos (Harvard Medical School, Boston, MA). "In countries where people eat very little fish — and some of these countries have almost no sources of omega-3 fatty acids because they cook with corn or sunflower oils — the consumption of vegetable oils with ALA could have a major impact on heart disease."

In an editorial accompanying the published study [2], Dr William Harris (University of South Dakota, Sioux Falls) said that the data are suggestive and would be good news for individuals who will not or cannot eat fish, but more studies are still needed. "If ALA were able to do the same 'heavy lifting' that [eicosapentaenoic acid] EPA and [docosahexaenoic acid] DHA do, this would be welcomed news, because the capacity to produce ALA is essentially limitless, whereas there are only so many fish in the sea," he writes.

The results of the study and editorial are published online July 8, 2008 in Circulation.

Benefit is great when the baseline levels are low

ALA is an intermediate-chain n-3 polyunsaturated fatty acid that is often overshadowed by the more famous long-chain members of the n-3 family, namely EPA and DHA acids that are found in fish oils. ALA intake has increased during the past several decades, however, mainly through the consumption of vegetable oils such as soybean, canola, and flaxseed oil. Speaking with heartwire, Campos said some studies have shown that low ALA intake was associated with a risk of coronary heart disease and sudden cardiac death, and others, although not all, have suggested an inverse association between ALA consumption and risk of MI.

In this study, 1819 patients who survived an MI provided samples of adipose tissue for analysis of fatty-acid stores and completed a validated food questionnaire, with 1817 matching controls doing the same. ALA in the adipose tissues ranged from 0.36% in the lowest decile to 1.04% in the highest decile. The corresponding median levels for ALA intake were 1.11 g/day to 2.35 g/day.

In a multivariate model that included smoking, physical activity, history of diabetes, hypertension, fat intake, and waist-to-hip ratio, among others, there was an observed inverse relationship between adipose tissue ALA and dietary ALA intake and risk of nonfatal MI.

Deciles of adipose tissue, ALA intake, and risk of MI Decile 1 2 3 4 5 6 7 8 9 10
ALA intake, g/day 1.11 1.25 1.38 1.38 1.52 1.62 1.79 1.83 2.08 2.35
Median, % ALA in adipose tissue 0.36 0.45 0.5 0.55 0.6 0.64 0.7 0.77 0.88 1.04
Relative risk of MI (95% CI) - 0.94 (0.66 - 1.34) 0.85 (0.59 - 1.24) 0.59 (0.40 - 0.87) 0.52 (0.34 - 0.78) 0.51 (0.34 - 0.79) 0.43 (0.30 - 0.67) 0.45 (0.28 - 0.71) 0.37 (0.23 - 0.59) 0.41 (0.25 - 0.67)


"The relationship between ALA and myocardial infarction was nonlinear," said Campos. "We see a dose effect, but only up to about 0.7% of adipose tissue, which corresponds to about 1.8 g/day. Increasing intake further was not associated with increased protection. This is why we hypothesized that if we were to conduct a study in a population already within this range, you're not likely to see an effect."

Campos said modest intakes of ALA appear to convey benefit, with small amounts of flaxseed oil, even just half a teaspoon, or one to two teaspoons of soybean oil, sufficient to increase ALA intake to 1.8 g/day. More commonly, salad dressings using canola or soybean oil would be enough to increase intakes to cardioprotective levels.

Mechanisms at work

In terms of underlying mechanisms, some have speculated that the protective benefit is mediated by converting ALA to EPA, but Campos said the data from this study do not support that hypothesis, as ALA correlated poorly with adipose and erythrocyte EPA. There are data supporting ALA in reducing low-density lipoprotein (LDL)-cholesterol and triglyceride levels, but ALA is thought to reduce the expression of inflammatory markers, although the data at this point are still inconclusive, she said.

In an unrelated study published online July 7, 2008 in Hypertension, Japanese investigators, led by Dr Katsuyuki Miura (Shiga University of Medical Science, Otsu, Japan), observed an independent inverse correlation between dietary linoleic acid and systolic and diastolic blood pressure [3]. Among individuals with higher linoleic acid consumption — in this study, as high as 9 g/day — the effect on systolic and diastolic blood pressure was a reduction of approximately 1.4 mm Hg and 0.9 mm Hg, respectively.

In his editorial, Harris notes that the findings by Campos and colleagues are at odds with other studies, particularly a recent meta-analysis of six studies showing no significant difference between coronary heart disease patients and controls in adipose linoleic acid. The best bet for discovering the true effect of linoleic acid on coronary heart disease risk is the Alpha-Omega Study, a 4800-patient study in which subjects are randomized to 400 mg of EPA plus DHA, 2 g of linoleic acid, both, or neither. The primary end point is cardiac mortality, and results are expected in 2009.

The study by Campos and colleagues was supported by the National Institutes of Health. The study authors have disclosed no relevant financial relationships.

The study by Miura and colleagues is supported by the National Heart, Lung, and Blood Institute, National Institutes of Health, and the National Institutes of Health Office on Dietary Supplements (Bethesda, Maryland); the Chicago Health Research Foundation; and by national agencies in China, Japan (the Ministry of Education, Science, Sports, and Culture, Grant-in-Aid for Scientific Research), and the United Kingdom. The study authors have disclosed no relevant financial relationships.

Sources

Campos H, Baylin A, Willett WC. Alpha-linolenic acid and risk of nonfatal acute myocardial infarction. Circulation. 2008;DOI:10.1161/CIRCULATIONAHA.107.762419. Available at: http://circ.ahajournals.org.
Harris WS. Cardiovascular risk and alpha-linolenic acid. Circulation. 2008;DOI: 10.1161/CIRCULATIONAHA.108.791467. Available at: http://circ.ahajournals.org.
Miura K, Stamler J, Nakagawa H, et al. Relationship of dietary linoleic acid to blood pressure. Hypertension. 2008;52:DOI:10.1161/HYPERTENSIONAHA.108.112383. Available at: http://hyper.ahajournals.org.

The complete contents of Heartwire, a professional news service of WebMD, can be found at www.theheart.org, a Web site for cardiovascular healthcare professionals.

Describe the association between linoleic acid intake and blood pressure in the International Study of Macro-Micronutrients and Blood Pressure.
Clinical Context
In many countries worldwide, there is low intake of long-chain n-3 fatty acids found in fish, namely EPA and DHA, which have been linked to a lower risk for all-cause mortality, cardiac and sudden death, and stroke. ALA could be a viable cardioprotective alternative to these fatty acids in these countries. The hypothesis of this case-control study conducted in a Costa Rican population by Campos and colleagues was that ALA is associated with lower risk for MI, that the maximal benefit of ALA is obtained within a specific range of intake, and that the association between ALA and MI is independent of fish intake.

Observational and interventional studies of the association of dietary linoleic acid with blood pressure have been inconsistent. The population-based International Study of Macro-Micronutrients and Blood Pressure (INTERMAP) conducted by Miura and colleagues attempted to resolve these inconsistencies by collecting standardized, high-quality data on large samples of diverse populations. The hypothesis of INTERMAP was that dietary linoleic acid intake of individuals is inversely related to their blood pressure.

Study Highlights
Campos and Colleagues
The first study evaluated the association of ALA and the risk for nonfatal acute MI in 1819 participants living in Costa Rica with a first nonfatal acute MI and in 1819 population-based control subjects matched for age, sex, and area of residence.
Fatty acids were evaluated with gas chromatography of adipose tissue samples and with a validated food frequency questionnaire (FFQ) specifically designed for this population.
Multivariate conditional logistic regression models calculated odds ratios (ORs) and 95% confidence intervals (CIs).
In adipose tissue, ALA ranged from 0.36% in the lowest decile (0.42% of energy intake) to 1.04% in the highest decile (0.86% of energy intake).
Whether evaluated in adipose tissue or by FFQ, greater ALA was associated with a lower risk for MI.
For the highest vs the lowest decile, ORs for nonfatal MI were 0.41 (95% CI, 0.25 - 0.67) for ALA in adipose tissue and 0.61 (95% CI, 0.42 - 0.88) for dietary ALA.
There was a nonlinear relationship between ALA and MI in that risk did not decrease further with intakes of more than approximately 0.65% energy (1.79 g/day).
At the levels found in this population, intake of fish, EPA, and DHA did not modify the observed association.
The investigators concluded that intake of vegetable oils rich in ALA could provide important cardiovascular protection and that the apparent protective effect is strongest among subjects with low intakes.
The main limitation of this study is the retrospective case-control design.
Miura and colleagues
INTERMAP is a cross-sectional epidemiologic study in which investigators looked at associations of linoleic acid intake in individuals with their blood pressure.
The study cohort consisted of 4680 men and women, aged 40 to 59 years, from 17 population samples in China, Japan, United Kingdom, and the United States.
For each participant, nutrient intake data were based on 4 in-depth, multipass 24-hour dietary recalls and 2 timed 24-hour urine collections.
At 4 visits, systolic and diastolic blood pressures were measured a total of 8 times per participant.
Several models controlled for possible dietary or other confounders.
For all of the participants, there was a nonsignificant inverse relationship of linoleic acid intake (percent kilocalories) to systolic and diastolic blood pressures according to linear regression analyses.
In a subgroup of 2238 individuals not following a special diet or consuming nutritional supplements, without diagnosed cardiovascular disease or diabetes, and not taking antihypertensive medication, the relationship was stronger.
For this "nonintervened" subgroup, estimated systolic and diastolic blood pressure differences with 2 SD higher linoleic acid intake (3.77% kcal) were –1.42/–0.91 mm Hg (P < .05 for both), after adjustment for 14 variables. With 2 SD higher intake (4.04% kcal) of total polyunsaturated fatty acid intake, blood pressure differences were –1.42/–0.98 mm Hg (P < .05 for both). The investigators concluded that dietary linoleic acid intake may help prevent and control adverse blood pressure levels in general populations. Limitations of this study include cross-sectional design, underestimation of effect size because of limited reliability in nutrient measurement, and limited ability to fully control for higher-order collinearity. Pearls for Practice In the case-control study by Campos and colleagues, greater ALA was associated with a lower risk for MI, whether evaluated in adipose tissue or by FFQ. There was a nonlinear relationship between ALA and MI in that the risk did not decrease further with intakes of more than approximately 0.65% energy (1.79 g/day). In the INTERMAP study conducted by Miura and colleagues, there was a nonsignificant inverse relationship of linoleic acid intake to systolic and diastolic blood pressures. In a subgroup of individuals not following a special diet or consuming nutritional supplements, without diagnosed cardiovascular disease or diabetes, and not taking antihypertensive medication, the relationship was stronger. According to the Costa Rican case-control study by Campos and colleagues, which of the following statements about the association of ALA with the risk for MI is not correct? Greater ALA in adipose tissue or by FFQ was associated with a lower risk for MI The apparent cardiovascular protective effect is strongest among subjects with low ALA intakes The relationship between ALA and MI was linear Intake of fish, EPA, and DHA did not modify the observed association According to the INTERMAP study conducted by Miura and colleagues, which of the following statements about the relationship of linoleic acid intake to blood pressure is correct? For all of the participants, linoleic acid intake was significantly inversely related to systolic blood pressure For all of the participants, linoleic acid intake was significantly inversely related to diastolic blood pressure For the "nonintervened" subgroup, estimated systolic/diastolic blood pressure differences with 2 SD higher linoleic acid intake were –1.42/–0.91 mm Hg after adjustment The investigators concluded that dietary linoleic acid intake does not affect blood pressure. Target Audience - This article is intended for primary care clinicians, cardiovascular specialists, nutritionists, and other specialists offering dietary advice to patients who may be at risk for cardiovascular disease.

 
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