Conjugated Linoleic Acid - Conjugated or Compromised?

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Conjugated Linoleic Acid - Conjugated or Compromised?

JoAnn Guest

Dec 14, 2003 21:35 PST

 

Conjugated Linoleic Acid - Conjugated or Compromised?

• Full Length 6-part Document with Scientific References

 

 

EXPANDED VERSION: CLA –

Conjugated Linoleic Acid - Conjugated or Compromised?

 

Conjugated linoleic acid, or CLA, has attracted a lot of attention

over

the past few years. Many claims for benefits have been made—from

" enhancing " weight loss and providing antioxidant protection to

treating

diabetes and cardiovascular disease.

 

What is CLA?

Conjugated linoleic acid is one or more of 8 possible *twisted*

" trans-fatty " acids created from linoleic acid, also known as n-6

essential fatty acid. In nature, the conversion of linoleic acid

into

CLA occurs naturally in the stomachs of cows, goats, sheep and other

cud-chewing animals; accordingly,

 

CLA is found in the meat and milk fat of these species. Butter, for

example, normally contains about 5 mg of CLA per gram of fat.

Let's Run Some Numbers--

Cream, nature's richest natural source of CLA, contains 5mg/gram

(0.5%)

of fat. The dairy isomer of CLA is mostly c9,t11-18:2.That much is

apparently safe and desirable for calves. At

0.5% CLA, a tablespoon (14 grams) of butter provides about 70mg of

CLA.

 

To get 3 grams of CLA from butter,one would need to eat more than 40

tablespoons of it,which is 560 grams of 1.25 pounds of butter.

That's a

lot more saturated fat than can be recommended.

 

CLA is sold in supplement form.To achieve this, n-6 fatty acids are

treated by a process called *hydrogenation*, during which the

original

molecular structure of the fat is *twisted* into a different shape.

The result is called a " trans fat " , and as more and more people are

becoming aware, transfats do not have the same desirable effects on

health as essential fatty acids.

 

CLA * interferes*with the conversion of EFAs (both n-6s and n-3s) to

derivatives

*necessary*for hormone production!!

 

CLA is not *essential*- Unlike n-3s and n-6s, without which we

cannot

live, we could live healthfully on a CLA-free diet our entire life.

The

body has no requirement for CLA. But the body has an absolute

requirement for EFAs, which should not be *interfered* with.

 

Research Review-

While CLA is 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. Some animal studies suggest that CLA can

perform antioxidant functions and might have anti-cancer,

anti-inflammatory, anti-diabetic, and cardio-protective properties.

Other studies suggest that CLA actually increases *oxidation* of

cell

membranes,which is not good and carries a warning

about the possible *worsening* of cardiovascular and degenerative

conditions.

 

If one wants antioxidant protection, there are hundreds of

substances

with antioxidant activity equal to or better than CLA, including

vitamin A, beta-carotene and vitamin E.

In addition, about half of all edible green plants contain hundreds

of

different

anti-cancer, cardio-protective, anti-diabetic, anti-inflammatory

ingredients.

At the CLA doses used in human studies, the research results are

quite

disappointing.

 

Human studies find *no* benefits for the degenerative conditions for

which CLA is recommended: weight loss, impaired immune and

antioxidant

function, and cardiovascular problems.

 

What Should be Our Focus? Instead of considering CLA, we need to

focus

on getting enough EFAs. It is important to obtain our EFAs in the

most

beneficial ratio, which we find to be approximately two n-3s to each

n-6.

 

If the diet is lacking in a balance of EFAs, saturated fats will

take

the place of EFAs within cell membranes,reducing membrane fluidity

and

efficiency, thereby elevating cholesterol levels,homocysteine and

C-Reactive Protein and starting a process of premature *aging* and

disease development.

 

Getting the omega-6 and omega-3 fatty acids in the right proportions

will reduce C-Reactive protein,homocysteine, LDL cholesterol and

raise

good HDL cholesterol as well.

 

There are three families of EFAs: Omega-3,omega-6 and omega-9 fatty

acids.

 

Experimental studies confirm that a balanced combination of these

three

families is essential for maximal effect in lowering blood pressure

and

improving the serum lipid profile

while reducing C-Reactive Protein and cholesterol as well.

 

When dietary omega-6 and omega-3 oils were in combination in a study

on

the regression of experimental atherosclerosis in rabbits,

C-Reactive Protein & cholesterol levels decreased faster in the

group

fed the combination oils.

 

In this group there was also a three-fold reduction of

*atherosclerotic*

plaques in the aorta compared to untreated animals

(Khalilov et al., 1997).

 

The results indicate that a combination of omega-6 and omega-3

(in this case, GLA and EPA), in a proportion ranging from 2:1 to 4:1

(two to four parts of omega-6 to one part of omega-3), is the ideal

combination to reduce bad LDL cholesterol, raise good HDL

cholesterol

and thus

improve the LDL/HDL cholesterol ratio (van Jaarsveld et al., 1997).

 

 

Olive Oil, rich in omega-9s is beneficial for sugar balancing-

Essential

Fatty Acid (EFA) Deficiency- Lowering LDL Cholesterol – and Vascular

disease.

 

Olive oil is most noted for it's heart-smart value as an important

component of the Mediterranean diet that prevents vascular disease.

 

Being very rich in oleic acid, a monounsaturated 'omega-9' fatty

acid,

olive oil is resistant to the formation of trans fatty acids

and other free radical compounds that cause inflammation and cell

damage. Olive oil also lowers high blood pressure as well. A

Stanford

Medical School study of seventy-six middle-aged men found that

taking

the equivalent of three tablespoons of olive oil daily lowered

systolic

pressure about nine points and diastolic pressure about six points.

A

study done at the University of Kentucky found that a mere two-

thirds of

a tablespoon of olive oil daily could do almost as well.

 

Because eating oxidized fat triggers the release of insulin and the

buildup of glucose in the blood, it is recommended that people use

olive

oil as the main dietary oil (or other foods rich in monosaturated

fats

like avocadoes, almonds, macademia and other nuts).

 

Consuming oils rich in " omega-6 " fatty acids, like corn, sunflower

and

safflower oils,

can cause the blood to be *infused* with free radical *peroxides*.

 

If the body doesn't have enough antioxidants to mop them up, these

radicals shut down an enzyme that *metabolizes* sugar

and then glucose levels build up in the blood and this stimulates

insulin secretion.

 

High blood sugar and blood insulin damages the vascular system.

 

In a clinical trial with humans, olive oil prevented these effects,

whereas sunflower oil, rich in linoleic acid, did not.

 

Active Ingredients: Olive oil contains (per 100g): Vitamin E (ATE),

12.4mg; Tocopherol (alpha), 11.9mg;

Lipids: Fatty acids, total saturated, 13.5g; 16:0=11.0g; 18:0=2.2g;

Fatty acids, total monounsaturated 73.7g; 16:1=0.8g; oleic acid or

18:1=72.5g; 20:1=0.3g;

Fatty acids, total polyunsaturated=8.4g; linoleic acid or 18:2=7.9g;

linolenic acid or 18:3=0.6g;

Phytosterols 221mg/100g. (National Agriculture Library's USDA

Nutrient

Database for Standard Reference at http://www.nal.usda.gov).

Another source lists Extra Virgin Olive Oil as:

14% Saturated fat; 77% monosaturated fat; 8% omega-6 fat and 1%

omega-3

fat.

 

---

----

 

 

All the benefits touted for CLA (and more) are more effectively

provided

by the right combination of EFAs.

 

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

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

 

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 in 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!

 

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).

 

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.

Commercially, CLA is made by *hydrogenation* or, alternatively, by

the

action of certain kinds of bacteria fed diets containing the n-6

EFA,

LA.

 

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 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 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. –Like *all* " trans-fatty " acids,

CLA

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

derivatives from which the body makes the eicosanoid (prostaglandin)

hormones. Unfortunately, the average American diet is high in

refined

vegetable oils which provide an excess of linoleic acid, that is

generally metabolized into 'pro-inflammatory' substances,

and an insufficient amount of those fatty acids that are needed to

make

anti-inflammatory substances.

 

The omega-3 family-- includes alpha-linolenic acid, eicosapentaenoic

acid, and docoahexaenoic acid.

 

In certain plants, omega-3 fatty acids are found in the form of

alpha-linolenic acid. In the body, this fatty acid is converted into

EPA, which is then converted into DHA.

 

The oils of certain fish contain " preformed " EPA and DHA,which are

the

most active and desirable forms of the omega-3 family. It is this

final

'conversion' to prostaglandins that is responsible for omega-3s

" therapeutic " effects.

 

The omega-6 family-- includes cis-linoleic acid, linoleic acid, and

gamma-linolenic acid.

 

(GLA). Cis-linoleic acid is found in certain plants and vegetable

oils.

Linoleic acid is found in most plants and vegetable oils.

However, it should be noted that cis-linoleic acid and linoleic acid

can also be

converted into pro-inflammatory prostaglandins. which is generally

metabolized into pro-inflammatory substances, and an insufficient

amount

of those fatty acids that are needed to make anti-inflammatory

substances.

 

" Evening Primrose Oil--

An ideal therapeutic balance of 9% GLA, 72% omega-6 and 9% omega-9

essential fatty acids.Clinical studies on EPO suggest it reduces

inflammation and alleviates some forms of hormonal stress. This

nutritional property, in conjunction with the presence of other

phyto

(or plant-based) nutrients, makes EPO an attractive source of

hormone builders.

 

EPO also contains other nutritional lipids such as phospholipids,

sterols, and other active phyto-compounds. Independent medical

research

indicates these compounds are significant immune system and cell

builders " .

http://www.spectrumnaturals.com

 

 

Definitions:

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-----------

 

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; and the body must therefore obtain `essential'

fatty

acids from foods or supplements.

 

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'). " Prostaglandin E3 has

similar functions as prostaglandin E1. It also has a powerful effect

of

preventing the release of arachidonic acid stored in cell membranes

and

its conversion to prostaglandin E2 " .

Omega-3 fatty acids are the source of this beneficial prostaglandin.

 

DHA is required for brain development and brain function.

 

 

 

Conjugated Double Bonds-

 

..9g/day of CLA for 63 days did not show benefits regarding the

" prevention " of atherosclerosis; blood cholesterol and lipoprotein

levels did not change;

 

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

coagulation and platelet function;

 

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

function in human females;

 

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

obesity after one month of use

 

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

expenditure, fat oxidation, or respiratory exchange ratio;

 

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

enzymatic and non-enzymatic processes;

 

The negative changes induced by CLA include:

 

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

resulting in lipid peroxidation and morphological change in the

liver;

 

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

fatty

acids; 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;

 

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 (bad) and HDL (good) Cholesterol.

 

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

cell size (hypertrophy)

but not fat levels in hamsters;

 

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;

 

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

while

EFAs

*enhanced* bone growth;

 

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.

 

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

whereas SDA

and EPA decreased TM by 50%;

 

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-----------

 

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

derivatives out of *enzyme* spaces. This is cause for " serious "

concern.

 

 

This point, " conveniently " overlooked by manufacturers, is " unknown "

to

most consumers!.

 

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

requirement

for EFAs, which should not be *interfered* with.

 

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. .

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.

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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.

 

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 (EFAs)

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(EFA)s as opposed to saturates!

 

CLA is used almost exclusively in Weight Loss Supplements.

Think about it! What is the purpose behind this?

We just MAY be defeating our purpose if we use many of these

unhealthy fats.

 

Best Regards,

 

JoAnn Guest

mrsjo-

DietaryTi-

http://www.geocities.com/mrsjoguest/Transfats.html

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