Transfats Disguised in Supplements

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Transfats Disguised in Supplement

CLA: conjugated linoleic acid, a trans- fatty acid made from the n-6

essential linoleic acid by bacterial or by industrial partial

hydrogenation. CLA, made by a bond shift and a twist of the molecule, is

not a nutrient that is ‘essential’ for health.

 

EFA: essential fatty acid, one of two fatty acids (n-6 and n-3) that are

‘essential’ to the body, which means that:

The body cannot make them;

It must have them for health to be possible; and

The body must therefore obtain ‘essential’ fatty acids from foods or

supplements.

 

In addition to the 2 EFAs, 20 minerals, 13 vitamins, and 8 amino acids

from proteins are also ‘essential’ for health by the above definition.

N-6: omega-6, the name by which all members of one family of essential

fatty acids is identified. The members include linoleic acid (LA),

gamma-linolenic acid (GLA), dihomogamma-linolenic acid (DGLA), and

arachidonic acid (AA). LA: linoleic acid, the n-6 essential fatty acid,

from which the body makes several derivatives with important functions,

including GLA, DGLA, and AA. DGLA and AA are the starting points for

making hormone-like Series 1 and Series 2 eicosanoids (formerly called

‘series 1 and series 2 prostaglandins’). AA is also required for the

development and function of the brain. N-3: omega-3, the name by which

all members of the other family of essential fatty acids is identified.

The members of the n-3 family include alpha-linolenic or ALA or LNA),

stearidonic acid (SDA), eicosapentenoic acid (EPA), and docosahexaenoic

acid (DHA).ALA: alpha-linolenic acid, the n-3 essential fatty acid, from

which the body makes several derivatives with important functions,

including SDA, EPA, and DHA. EPA is the starting point for making

hormone-like Series 3 eicosanoids (formerly called ‘series 3

prostaglandins’). DHA is required for brain development and brain

function.

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CLA has attracted a lot of attention over the past few years, some

through the media, but far more through health and fitness magazines.

Many claims for benefits have been made for CLA, from weight loss, to

antioxidant, anti-cancer and, more recently, to diabetes and

cardiovascular disease as well. Is CLA all it’s been cracked up to be?

This article addresses that question.

 

Research Studies Of 139 references pulled off the Internet in June of

2001, 29 were published in 2001; 65 in 2000; 33 in 1999; and 15 in 1998.

Of these 139 references, the following is a breakdown of topics:

10 were production-oriented studies.

6 were reviews, (i.e., these are not studies).

14 were studies about how to get CLA into different foods. One of these

came to the brilliant conclusion that cows eating grass (their natural

food) contained a better fatty acid (n3: n-6) profile and more CLA than

cows fed concentrates from bags. Wow! What a stunning discovery!1

2 were molecular studies.

24 were studies using cell cultures.

69 were studies performed on animals.

14 studies were carried out on humans.

Of these research studies, those carried out in living animals and

humans (in vivo) are more likely than studies carried out in various

normal and abnormal animal and human tissue cultures (in vitro studies)

to show how CLA actually affects human health and disease. And, it is

important to note that, while CLA is being touted for many human

problems, there are relatively few human studies to draw on.

Unfortunately, a substantial number of these studies indicate that CLA

does not do in human studies what it appears to do in animal studies.

 

 

What is CLA?

 

 

Conjugated linoleic acid (CLA) is a mixture of 8 (and perhaps even more)

different forms (or isomers)2 of an 18-carbon fatty acid made by

hydrogenation from linoleic acid (LA), the omega-6 (n-6) essential fatty

acid (EFA). In nature, this is accomplished by bacteria in the stomach

of beef, goats, sheep and other cud-chewing animals (which include deer,

moose, caribou, elk, buffalo, yak, musk ox), and CLA is found in meat

and milk fat of these species. Each of its eight different isomers has a

different spatial structure and each therefore has different action in

the body, with different effects on health. The isomer found in dairy

products is mainly the (delta)9c,11t-18:2 isomer.3Butter normally

contains about 5mg of CLA per gram of fat, but this can be increased to

40mg per gram by feeding cows sunflower oil.4 Milk chocolate contained

0.3mg of CLA per gram chocolate in a study.5 Commercially, CLA is made

by hydrogenation6 or, alternatively, by the action of certain kinds of

bacteria fed diets containing the n-6 EFA, LA.7

 

 

 

How is LA Changed to CLA?

 

CLA is made from LA, the n-6 EFA, by flipping one of the double bonds in

the LA molecule one carbon closer to the other one. This changes the

‘methylene-interrupted’ double bonds present in EFAs (double bonds start

3 carbons apart) into ‘conjugated’ double bonds (double bonds start 2

carbons apart). At the same time, one of the double bonds found in the

cis- configuration in an EFA (hydrogen atoms on the carbons involved in

the double bond are on the same side of the molecule) twists 180°. The

hydrogen atoms are now in a more stable, but biologically less desirable

trans- configuration (hydrogen atoms on the carbons involved in the

double bond are on opposite sides of the molecule). Trans- means

‘across’. Hence the name trans- fatty acid.

 

 

Is CLA an Essential Nutrient?

 

CLA is not an essential nutrient. It is, like monounsaturated (n-9) and

saturated fatty acids, a non-essential fatty acid. It is not required

for human health. This means that, unlike the n-6 and n-3 EFAs, which we

cannot live without, we can live on a CLA-free diet a whole life time

and continue to be healthy. CLA is also a trans- fatty acid. To be fair,

the 9c,11t-18:2 isomer of CLA found in milk fat and beef appears to be

one of the more easily digested trans- fatty acids, and is therefore

less toxic than the types of trans- fatty acids found in margarine,

shortening, and partially hydrogenated vegetable oils. However, CLA

interferes with the conversion of EFAs (especially n-6) to derivatives

from which the body makes the eicosanoid (prostaglandin) hormones.8 This

should concern low fat dieters, who already get too little n-6 EFA, LA.

It should also concern those who use flax oil exclusively, because they

get too much n-3 in comparison to their intake of n-6, and CLA will make

their low n-6 status even worse.

 

 

Conjugated Double Bonds

 

Conjugated double bond systems have antioxidant activity, and some

studies suggest that CLA can perform antioxidant functions. Other

studies suggest that CLA increases oxidation, which is not so good.

However, there are hundreds of molecules with antioxidant activity equal

to or better than that of CLA. Among those that, like CLA, are

oil-soluble there are vitamin A, carotene, vitamin E, and many complex

molecules with aromatic carbon rings.3.9g/day of CLA for 63 days did not

show benefits regarding the prevention of atherosclerosis; blood

cholesterol and lipoprotein levels did not change;42

 

 

3.9g/day of CLA for 63 days did not show benefits regarding blood

coagulation and platelet function;43

 

 

Increasing CLA in the fetus correlated with decreased length of

gestation;44

 

 

3.9g/day of CLA for 63 days did not show benefits regarding immune

function in human females;45

 

 

4.2g/day of CLA increased lipid peroxidation in men with abdominal

obesity after one month of use;46

 

 

In patients with chronic renal failure, CLA did not help;47

 

 

At 3 g/day, CLA resulted in no fat loss, no change in appetite, no

change in blood glucose, but increased insulin and produced a transient

decrease in leptin; CLA did not affect these parameters in a manner that

promotes fat loss;48

 

 

At 3 g/day, CLA provided no change in body composition, energy

expenditure, fat oxidation, or respiratory exchange ratio;49

 

 

4.2 g/day of CLA increased lipid peroxidation, apparently by both

enzymatic and non-enzymatic processes;50

The negative changes induced by CLA include:

Alteration of egg yolk and egg white pH, distribution of minerals in

yolk and white, and decrease egg quality and hatchability of chicks;31

At 2% of food, CLA accelerates the decomposition of storage lipids,

resulting in lipid peroxidation and morphological change in the liver;32

 

In hens, 2.5% CLA reduced level of n-6 and increased level of n-3 fatty

acids;33

At 1% of feed in mice, CLA increased TNFa (tumor necrosis factor alpha,

an inflammatory factor) by 12 times, and uncoupling protein UCP-2 (a

thermogenic factor) by 6 times; there was liver swelling, increased

insulin resistance, and leptin depletion;34

Given 1g of CLA every second day, chicks showed altered fat

metabolism;35

Given to rats at 3 to 5%, CLA changes the membrane lipids, increasing

some and decreasing others, increases antioxidant enzymes in liver, and

reduces both LDL and HDL cholesterol;36

At 6.6g/kg (0.66%) of food, CLA increased liver weight by increasing

cell size (hypertrophy) but not fat levels in hamsters;37

In rats given 180mg/day of mixed isomers, CLA was found to compete for

enzymes used to elongate and desaturate EFAs, thereby decreasing the

production of EFA derivatives important to health;38

At 10g/kg (1%), CLA reduced rate of bone formation in rats, while EFAs

enhanced bone growth;39

In mice fed an atherogenic diet containing 5g/kg (0.5%) of CLA, CLA

increased the development of fatty streaks, one of the atherogenic

markers;40

At 3% of food, CLA was ineffective in mice tumor multiplicity ,

whereas SDA and EPA decreased TM by 50%;41

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In summary, while CLA has shown promises of improving degenerative

condition in animal studies, the promises come with contradictory

findings and warnings of worsening of some conditions.

 

 

3.4 g/day of CLA reduced body fat mass; more than 3.4 g/day did not

provide any additional benefit;51

16 g/day of n-6 LA from safflower oil did not result in any increase in

CLA in the body, i.e. the human body does not make CLA from LA;52

 

 

CLA at high doses *competes* with EFAs and crowds *them* and their

derivatives out of *enzyme* spaces.

 

This is cause for serious great concern.

 

This point, conveniently overlooked by manufacturers, is unknown to most

consumers. To effectively treat human diseases, for which CLA showed

benefits in animals, larger doses would be needed. Instead of 3

grams/day, on which we based out calculations above, and which is

already very high when compared to what butter (the richest natural

source) could supply, CLA doses would need to be even higher.

 

 

The body has no requirement for CLA. But it has an absolute requirement

for EFAs, which should not be interfered with. Recall that EFAs cannot

be made by the body, must be present for the normal (healthy)

functioning of every cell, tissue, gland, and organ, and must therefore

be provided by foods. Since EFAs are easily destroyed by light, oxygen,

and heat, oils containing them should be made and stored under

protection from these destructive influences, and should not be used for

high heat applications in the home.

 

While they can be used in hot soup or on steamed vegetables, they should

not be fried, deep-fried, or even sautéed. They can be used in all kinds

of foods—cold, warm, and boiling water-hot foods. EFAs come in two

varieties: n-3 and n-6. Both are essential. Both are sensitive to

destruction. N-3 is too low for good health in most people’s diet. Low

and no fat diets are too low in n-3 and n-6. N-6 is too low in people

who use flax oil exclusively as the source of EFAs in their diet (these

are primarily people who have been misled, by research on the benefits

of n-3s and problems caused by n-6s, to seek to remove n-6s from their

diet.

 

It is important to obtain both EFAs in the most beneficial ratio, which

we find to be 2 n-3s to each n-6. It is also important that our EFAs

come from oils that retain their ‘minor ingredients’, which include

antioxidants, phytosterols, lecithin, and other oil-soluble molecules

present in seeds and nuts. These ‘minor ingredients’ have major health

benefits. When colorless, odorless, tasteless, shelf-stable oils are

made, the ‘minor ingredients’ are removed from oils for the sake of

longer shelf life. In addition, some of the fatty acid molecules present

in the oil are changed from natural to toxic. The toxicity blamed on n-6

oils like corn and safflower result primarily from the removal of ‘minor

ingredients’ and damage to fatty acids due to careless processing.

 

 

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Summary and Recommendations: Bottom Line

 

 

Instead of using CLA, we need in our diet EFAs made with health in mind,

in an optimal n-3: n-6 ratio, pressed from organically grown seeds, and

retaining their natural antioxidants, phytosterols, and other ‘minor

ingredients’. Being far less expensive than CLA, such oils can be taken

in the 30 to 150 gram/day range over the long term, and confer all of

the health benefits hyped for but not delivered by CLA.

 

We recommend this approach as part of the ‘The Right Fat Diet®’, a food

program emphasizes green vegetables, the right fat rich in both EFAs in

the right ratio and made, packaged, stored and used right (carefully

with health in mind), and proteins as the foundation for good health. To

make sure that digestion works effectively, we recommend that digestive

enzymes be taken with meals. The Right Fat Diet® lowers most

cardiovascular risk factors, provides the EFAs essential for insulin

function, inhibits fat production and enhances fat burning, promotes

healthy fat loss, increases thermogenesis, and improves insulin

sensitivity.

 

The Right Fat Diet® also improves brain function and mood, inhibits

cancer, enhances bone mineral retention, improves protein retention, has

anti-catabolic benefits, improves skin beauty, increases energy,

stamina, performance, recovery, and healing of injuries, and improves

thyroid, adrenal, and reproductive gland functions. Further, The Right

Fat Diet® decreases inflammation, improves digestion, reduces allergy

symptoms, and decreases the problems of autoimmune conditions.

 

Finally, The Right Fat Diet® enhances food flavors, suppresses appetite,

and improves the absorption from food of oil-soluble phytonutrients with

health benefits. All of the benefits touted for CLA (and more) are more

effectively provided by good old EFAs.

J Nutr 2002 Nov;132(11):3272-9

 

Conjugated linoleic Acid differentially modifies Fatty Acid composition

in subcellular fractions of muscle and adipose tissue but not adiposity

of post-weanling pigs.

 

Demaree SR, Gilbert CD, Mersmann HJ, Smith SB.

 

Department of Animal Science, Texas A & M University, College Station, TX

77843 and. U.S. Department of Agriculture/ARS Children's Nutrition

Research Center, Baylor College of Medicine, Houston, TX 77030.

 

This study examined the interaction between conjugated linoleic acid

(CLA) and dietary fat type on the enrichment of subcellular fractions,

the Delta-9-desaturase index and adiposity in pigs. Early weaned piglets

(n = 6/group) were fed for 35 d diets supplemented with 15 g/100 g diet

beef tallow or corn oil, or 12 g/100 g tallow or corn oil plus 3 g CLA.

There were no effects of dietary fat or CLA on the mass of dissected

skin, bone, muscle or adipose tissue of the 7th to 9th thoracic rib

sections. Medial subcutaneous adipose tissue of pigs fed tallow had

smaller adipocytes than that of pigs fed corn oil. The lateral

subcutaneous site was unaffected by dietary fat type.

 

Microsomes accumulated <50% the concentration of trans-10,cis-12,

cis-11,trans-13, and cis-9,trans-11 CLA as membrane and non-membrane

fractions of adipose tissue and longissimus muscle. There was no

evidence of preferential incorporation of any CLA isomer into any of the

subcellular fractions. Addition of CLA to the diets reduced adipose

tissue non-membrane monounsaturated fatty acids (MUFA; g/100 g total

fatty acids) by 15% in corn oil-fed pigs and by 19% in tallow-fed pigs.

 

Total saturated fatty acids (SFA) were increased by CLA commensurately

in this lipid fraction. This resulted in a reduced Delta(9) desaturase

index [MUFA/(SFA + MUFA)] in the non-membrane lipid fraction of pigs fed

either the corn oil or tallow diets. Thus, in spite of marked effects on

fatty acid composition and the Delta(9) desaturase index, CLA had no

effect on adiposity in early weaned piglets fed high fat diets.

 

PMID: 12421839 [PubMed - in process]

 

 

 

Comment by Oscar Umahro Cadogan: Notice that there is no reduction in

fat mass, and it’s not clear what the lowered d9d index means. Could

that be due to an impairment in the unsaturation of saturates or that it

causes a preferential beta-oxidation of unsaturates, which would

decrease membrane fluidity and thus contribute to insulin-resistance…and

most likely diminished sensitivity to any other signalling substance

interacting with cell membrane bound receptors as well? We know that CLA

engages PPAR-gamma, but as mentioned in a previous mail, only activating

PPAR-gamma seems to do exactly this:

Make the body burn unsaturates as opposed to saturates.

 

 

 

 

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