[Keto Info week 1/1]

CATEGORY: biology/metabolism

TECHNICAL: ****

SUMMARY:

This document gives the rather technical/intimate

details of how someone who is low-carb and ketogenic can

sustain a weightlifting session and have the energy to do so

start through finish.

It's a pretty rough read for those uninterested in

the biomedicine, so I'll give you the short version here.

Your body accomplishes this task by using the "waste products"

of active muscle exercise: lactate (which gives you that

burning feeling) and pyruvate (another precursor to the

glucose generation process) to synthesize new glucose in the

liver. This new sugar is then sent back into the bloodstream

for use by the active muscle.

It's important to realize that amino acids are part

of this process, so be sure to get enough protein in your

diet as well as fats, or you may risk muscle loss (to the

conversion process).

Incidentally, you will also notice (as I have) that

because of this glucose generation process - if you check for

excess ketones in the urine stream (with ketostix) right after

you train - you'll see that you're temporarily non-ketogenic.

That is why it is a good idea to follow up a weight

lifting session with a little easy, short aerobic work. Cycling,

for example, can more rapidly remove the excess lactate from

the working muscle and convert it back to muscle/liver glycogen.

This not only reduces your post-workout soreness, but

also drops your blood sugar and speeds you back into a ketogenic

state. (and primes your muscles with stored glycogen for the

next lifting session)

-------------------------------------------------------------

Subject: The anabolic diet...

Date: Sun, 4 Jun 1995 13:22:37 -0500 (CDT)

Hello!

I finally found the answer I was looking for regarding the anabolic

diet. When people (my adv. nutrition teacher, biochemistry professor

etc.) put me on the spot, I have reluctantly explained the diet based

upon the manuals findings, which I explained were not technical enough,

and had real difficulty convincing them. But now I finally found an

answer that is technical enough, and explains the reasoning behind this

ever so commonly asked question; "since weight training is anaerobic,

where is your energy going to come from when you don't consume enough

carbs, since glycolysis is the major pathway involved in anaerobic

exercise?". Well I finally struck pay dirt. It took an inordinate

amount of time, too much time in fact, and I am going to call Optimum

Training Systems and request that they revise the manual or add an

addendum in which this is explained more in depth. Like I said, you are

going to be hard pressed when someone in the know starts battering away

with technical questions, that the diet doesn't provide. Sure the manual

tells you that dietary and body fat will be the fuel for your workouts

along with the creatine from the red meat, but that doesn't cut it. Which

finally leads me to this answer.

Since anaerobic wt. training HAS to go through glycolysis, I thought

that readdressing that pathway might lead me to an answer, and it did. As

you know the 2 hormones insulin and glucagon work together, when carbs

are present, insulin secretion from the pancreas increases, and times

when carbs are low, glucagon secretion increases to supply carbs for

energy. When going through glycolysis there are 3 regulatory steps, one

of them involves the enzyme PFK-1 (phospofructokinase-1). It is one of

the reactions that are catalyzed early in glycolysis, the third step If I

recall correctly. Anyway, it seems that this enzyme PFK-1 is sensitive

to levels of carbs in the blood. When carbs are low, as in the diet,

glucagon is going to be chronically activated, which in turn will

influence the enzyme PFK-1. When this happens, it tells the metabolic

pathway that glucose just is not available, and therefore the reaction of

glycolysis can not proceed in the normal fashion. THat is why it is a

regulatory step. When this happens, glycolysis basically skips all the

normal steps and proceeds to the end where pyruvate is formed. From

there pyruvate can be converted (broken down) to lactate. Once lactate

is formed from a reaction catalyzed be lactate dehydrogenase, lactate has

no other metabolic fate than reconversion to pyruvate. Hence, lactate is

commonly considered a metabolic dead end. Since lactate formation

catalyzed by lactate dehydrogenase regenerates NAD+ from NADH, the

pathway of glycolysis is complete, with NAD+ becoming available for

glyceraldehyde 3 phosphate dehydrogenase reaction. Thus no net oxidation

or reduction takes place during anaerobic glycolysis to lactate. The

final product, lactate in glycolysis generates 2 mol ATP per mol of

glucose consumed. Oxygen is not required in either case. In most cells,

the majority of ATP is produced by oxidative phosphorylation, which is

strictly an oxygen dependent process. Yet, in the cornea of the eye, for

example, oxygen availability is limited by poor blood circulation.

Anaerobic glycolysis meets the need for ATP in the abscence of sufficient

oxygen for oxidative phosphorylation. When skeletal muscle is active,

lactate and pyruvate are transported out of the muscle cells and carried

via the circulatory system to the liver where lactate is converted to

pyruvate by the action of hepatic lactate dehydrognease. Pyruvate can be

further metabolized in various ways by the liver: a fraction of it is

aerobically oxidized to Co2 via the Krebs cycle (citric acid cycle), and

some of it is transaminated to alanine, which is used in protein

synthesis. Pyruvate in liver cells can also be converted back to free

glucose by gluconeogenesis. Liver is the principal organ responsible for

regulating the supply of blood glucose to other cells of the body,

including skeletal muscle cells. Thus, a portion of the metabolic burden

of muscular contraction is borne by the liver, which metabolizes the

by-products of muscle activity (lactate and pyruvate) and synthesizes

blood glucose. This inter-organ metabolism, in which liver receives

lactate and pyruvate and furnishes glucose for skeletal muscle, where

glucose is glycolytically metabolized to generate ATP, is referred to as

the Cori Cycle.

Hope this reaches all the doubters out there who were not convinced

the first time! Thanks!

Jeffrey P. Krabbe

Pre-Dietetics, Senior

University of Nebraska, Lincoln

:cool: TJ :cool:

[Supplements]

At the Moment I'm dong a sort of spEEdfrEEk's eating Plan & XNikX's Weight Workout (Hello Pain!)

Heh heh heh, it gets easier.. :grin:

I was wondering, what supplements should I take.

1. a good multivitamin without iron

2. a good antioxidant supplement (extra C, E, beta carotine)

3. potassium

4. calcium

5. magnesium

6. zinc

7. iodine

and for immuno enhancement:

8. flax seed oil

9. AFA blue-green algae

Cretaine (get ready for a flame from spEEdfrEEk)

Only if you want to overwork your kidneys and add waterweight

you your frame. The extra weight leaves as soon as you quit

taking the creatine.

Hey spEEdfrEEk, do you have a website yourself with your wisdom on?

Used to. It's been taken down. I have been reposting the messages

here, but took the last few weeks of due to the holidays. (everyone

should eat badly over the holidays )

If you ever want free Webhosting let me know, you & others have helped me heaps!

I'll ask my old web hoster/mistress if she can give me the raw files

for rehosting..

:cool: TJ :cool:

[Factory]

Out of curiosity, what pilot jets does the factory jet kit come

with for the 'Bird?

:cool: TJ :cool:

[conversion?]

I've heard that DynoJet uses a different numbering system

for their jets than Honda does. That true? If so, anyone

know where a conversion chart is located?

I'm working on Jetting a bike and it ain't a Bird :wink:

Thanks!

:cool: TJ :cool:

[This looks even better..]

Better/cheaper.. Gotta sniffer, like dynojet dynos.. :wink:

http://www.aep.bigstep.com/digital.htm

:cool: TJ :cool:

[Calorie King]

I've got the entire USDA nutrient database on CD if anyone

wants it (15MB)

Shoot me an e-mail with your postal address and I'll

mail it to you for x-mas

:cool: TJ :cool:

[Anyone got one of these?]

Seems like they might come in handy for tuning..

:cool: TJ :cool:

http://knpowersports.com/airfuelmonitors.htm

[POLL: What have you had to replace?]

1) Tires

2) My left nut, after having to buy my Corbin BeetleBags brand new

TJ

[Power gain via G-box?]

I was looking at something like this:

http://www.superchips.co.uk/bikes/indexfr.htm

Aparently it gives fine ignition control to your bike --

a seemingly good idea for carby bikes that can

be properly jetted but cannot make use of things

like Power Commanders..

:cool: TJ :cool:

[Keto Info Week 12/8]

CATEGORY: biology/immune_sytem

TECHNICAL: **

SUMMARY:

This document is one that I have made reference, a number

of times, to a few of you about. It is the original paper that

discusses the adverse effects of sugar on the leukocytic index.

As some of you may remember, you are generally not succeptable

to viral attack or tumor growth if your immune rsponse is kept at

high levels (more specifically, the strength and count of your NK

cells). However, when exposed to sugars, the immune state is

weakened considerably. Is it any wonder that we suffer from so

many forms of cancer, and viral infections when the typical american

diet is so high in refined, processed, carbohydrates? Most americans

repeatedly supress their immune systems at regular intervals daily!

-------------------------------------------------------------

Sugar and Immunity

_________________________________________________________________

Leukocytic Index proves the devastating effect of refined carbohydrates on

immunity.

Many people have been asking for a mechanism for the depressed

immunity seen in people who eat sugar and other refined carbohydrates.

Many are known but the Leukocytic Index is an especially helpful one for

many people to begin to take this health risk seriously.

More than 20 years ago a large study was published about the effects

of refined carbohydrates (of which sweets are the worst) on the leukocytic

index. Our white cells are the most important factors in protecting us

from invading organisms. The leukocytic index is a measure of how many

organisms one white blood cell (WBC) can eat in an hour. Therefore an

index of 10 means that that one WBC ate 10 organisms in THAT hour.

The average LI (leukocytic index) in the USA--and remember, average

is not as healthy as one can get--is about 13.9. Within 15 minutes, after

an individual eats the amount of refined carbohydrates normally ingested

in the evening meal --about 100 grams, the leukocytic index drops to about

1.4. Depending on the genetic susceptibility to this problem, it might be

better or worse--this is just an average. Diabetics ALWAYS have a LI of

less than 2.

That means: the average person loses more than 90% of their immune

function within 15 minutes of indulging in this poisonous substance. This

deficiency lasts for about 2 hours after the stress occurs.

What is routinely given intravenously during surgery? Glucose water!

When Ringer's Lactate (which has no sugar) is used instead, the incidence

of post operative infection is reduced by two thirds. The only reason I

can think of for this kind of persistent ignorance is that there is no

money in changing the thinking of operative routine. There is a lot more

money in treating the infections that are created by the Allopathic

Monopoly.

Since this has been known for more than 20 years, don't you think it

is time for this information to get out to the public?

:cool: TJ :cool:

[Keto Info Week 12/1]

CATEGORY: diets/paleo

TECHNICAL: **

SUMMARY:

This is an interesting little document that I found quite a long

time ago. It attempts to shatter the myth that neolithic humans (in

Europe) were primarily plant eaters. This is significant when one

considers the arguments made by vegans/vegetarians that human beings

are, and have always been, primarily herbivores.

Many on this list know that I staunchly believe that humans

consumed a majority of animal based food and not vegetable foods. This

does not mean I advocate a meat-only diet. It does, however, mean that

I encourage the consumption of mostly fiberous veggies (and herbs, etc.),

and getting a majority of calories from protein and fat sources.

If this research proves to be correct, then it indicates

something that is pretty important from an evolutionary point of view.

Namely, that humans (of european origin/background) may not have had as

much time to adapt to a grain based diet as expected. The previous

estimate was about 20,000 years. This document argues otherwise (4,000 -

2,000 years).

Should that be the case, then it's very unlikely we've had time

to adjust to such a quick change in diet (from animal to grain). And,

that adds fuel to the argument that grains are contributing

significantly to the increase in diseases of degeneration so prominent

today...

-------------------------------------------------------------

British Archaeology, no 12, March 1996: Features

_________________________________________________________________

Bone analysis suggests Neolithic people preferred meat, writes Mike

Richards. `First farmers' with no taste for grain

The Neolithic period is traditionally associated with the beginning

of farming, yet in Britain - by contrast with much of the rest of Europe -

the evidence has always been thin on the ground. Where are the first

farmers' settlements? Where are the fields?

The almost complete absence of this kind of evidence has led some

archaeologists, over recent years, to question the view that people in

Britain actually grew most of their food in the 4th and 3rd millennia BC.

Now, a scientific study of Neolithic human bone seems to point in the same

revisionist direction.

The small-scale study - the first of its kind - of the bones of about

23 Neolithic people from ten sites in central and southern England,

suggests that these `first farmers' relied heavily on animal meat for

food, or on animal by-products such as milk and cheese, and that plant

foods in fact formed little importance in their diet. The bones date from

throughout the Neolithic, c 4100BC - c 2000BC.

The study was based on the idea that our bodies are made up of

organic and inorganic components derived from the foods we have eaten.

There are a number of ways of tracing the original food source of some of

our tissues, and one way is to look at the relative ratios of certain

elements, known as `stable isotopes', in bone protein.

These stable isotopes can tell us a number of things about what a

person's diet has been for most of their life. One particular isotope can

tell us whether humans were getting most of their food from plant or

animal sources. Generally speaking, this is done by comparing human

isotope values to animal isotope values. If the human values are more like

that of a herbivore (eg, horses or cattle) they are eating a great deal of

plant food, and if they are more like carnivores (eg, wolves or foxes),

they are eating more meat.

A number of human bones from the Iron Age and from Romano-British

sites were also tested, and their isotope values were a little higher than

those of herbivores. This is as we might expect, as there is little doubt

that in these periods people practised relatively intense cereal

agriculture, and only supplemented their diet with meat. The Neolithic

results, however, were surprisingly different. They were as high, and

sometimes even higher, than stable isotope values of carnivores. This

suggests the Neolithic people had relatively little plant food in their

diet and instead were consuming large amounts of meat. It could also mean

they were eating a lot of animal by-products, like milk and cheese, as

these are indistinguishable from meat itself using stable isotopes.

So what, then, was the Neolithic economy based on? Animal remains

from Neolithic sites are generally of domestic species (eg, cattle and

pig) rather than wild, and cattle from Neolithic sites such as Hambledon

Hill in Dorset are actually larger than the cattle typically found in the

Iron Age. This evidence may suggest an animal-dependent economy - indeed,

one in which animals were well treated and kept for a long time - and, as

the Neolithic specialist Andrew Sherratt has suggested, the British

Neolithic may have been characterised by a `secondary products

revolution', with animal husbandry and an emphasis on animal milk and

cheese, instead of by an `agricultural revolution' and the growing of

crops.

Grain and agricultural implements have, of course, been found at

Neolithic sites in Britain. The isotope results do not rule out some

limited grain production and consumption; but they suggest it did not form

a significant portion of the diet. The sites where grain has been found

generally seem to have been used mainly for ritual purposes, and it is

possible (as archaeologists such as Richard Bradley and Julian Thomas have

argued) that in Britain, on the edge of Europe, grain was grown, or even

imported from the continent, only for ritual purposes. Agricultural

implements may also have assumed a largely ritual significance.

There are, however, potential difficulties with stable isotope

analysis. The main concern is whether the animal stable isotope data used

as a benchmark are accurate for the specific British Neolithic sites

tested. In the study, we took `average animal values' from a large

database, held at the Oxford Radiocarbon Accelerator Unit, covering all

Europe over the past 10,000 years. It may be that there are regional

variations in plant and animal isotope values of which we are, as yet,

unaware. Research, however, continues - and if our preliminary results are

confirmed, we may be able to scrap the notion of Neolithic

agriculturalists in Britain once and for all.

Mike Richards is a PhD student at the Research Laboratory for Archaeology

in Oxford

:cool: TJ :cool:

[Big bore kit on ebay]

I placed a bid! :grin:  

And I intend on winning it, unless the price gets out of range!

Cool, I hope you win it! That way you can put it in and try it

out and give us a review :grin:

:cool: TJ :cool:

[Good Frickin Bye Ketosis]

I'll hate myself tomorrow when I pee on the strip.

Get ready for your first "sugar hangover". I'm surprised you're

not comatose -- everytime I eat a ton of carbs after being keto

for any period of time I immediately pass out and sleep for a

few hours..

TJ

[Negative crank case pressure - 2 Bhp for nothing!!!!!]

Pictures, pictures??

:cool: TJ :cool:

[Motorcycle ramps]

Sam's club down here was selling a really nice one for

$50.0. I bought two and use them side by side to

tote the 'Bird around. They have a combined capacity

of 1/2 a ton..

:cool: TJ :cool:

[Free online service manuals]

Yep, nuthin there for my XX, my CBR 1000F or even my VTR 1000F

:razz: TJ :razz:

[Disillusioned with DeWalt]

If I hadn't ended up with a ridiculously low price for mine, I'd take it back and get the Ryobi.

Japanese tools are built with the same concepts of quality in

mind as Japanese motorcycles..

Be it Ryobi, Makita, etc.

:cool: TJ :cool:

[Keto Info Week 11/23]

CATEGORY: diets/lowcarb

TECHNICAL: *

SUMMARY:

This document was written by an individual who was on

another health/training list that I was a part of back in 1996.

In this note, he describes (in detail) one of the earliest low-carb

diets ever recorded, "the banting diet". The author does a really

good job documenting the chronology of everything, and even

discusses his own successes using the approach at the end. As you

read through it, you will find suggested diet plans for the banting

approach. Though I agree with low-carb diets in general, I would

make the case that this is not an optimal approach. In my view,

paleo-lowcarb is the only way to go. I will discuss that in the

future as well as provide my exact diet for everyone's scrutiny.

-------------------------------------------------------------

A few days ago I discovered this group while "surfing" and

contributed an opinion in the "Dr. Atkins vs the World" thread.

Basically, it pointed out that Dr. Atkins was a johnny-come-lately in the

low-carbohydrate scheme of things. The low-carbohydrate diet seems to

have originated with "A Letter of Corpulence", published in London in

1864 by a man named William Banting. It was so popular in the U.K. that

one may still find in the Oxford English Dictionary the verb "to bant" as

well as "banting" and "bantingism". My copy of the Oxford English

Dictionary quotes an editor's response to a correspondent:

Pall Mall Gazette - 12 June 1865

"If he is....gouty, obese, and nervous, we strongly recommend him to

bant."

So the low-carbohydrate way of eating predates calorie counting as a

method of weight control, though it does not predate the earlier method,

STARVATION, - poor ol' Henry VIII!

There is a low-carbohydrate diet which works as swiftly as any

proposed by Dr. Atkins, which does not involve placing a human being into

artificial starvation, with the throwing off of ketones, and resultant

straining of the kidneys.

If you want to throw away those ketostix, or use them as coffee stirrers,

read on.

Dr. William D. Howe was a well-known medical doctor and a member of

the Canadian parliament in Ottawa, representing the riding of

Hamilton-South for the NDP (Socialist) party. In March of 1965 a column

was written in "The Ottawa Journal" mentioning that fact that many

formerly obese members of parliament were looking slim- and-trim these

days, thanks to a method of weight control devised by Dr. Howe, and the

diet was given. This casual mention brought a flood of mail. In two

months Dr. Howe had mailed out 1500 copies, the Ottawa Journal's files

had been stripped of clippings, and the national radio (C.B.C.) had done

a 15 minute report on it. On Monday, May 3, 1965 and Tuesday, May 4th,

the Ottawa Journal reprinted the diet along with a number of articles

concerning it. Since I have the clippings (and would never part with

them) I am excerpting the relevant material here:

<<OPEN QUOTE - Ottawa Journal, May 3, 1965>>

You May Eat:

Meat, even fat meat

Milk and cream

Fish, cheese and eggs

Butter and margarine

Leafy vegetables such as lettuce, cabbage, spinach

Stem vegetables such as asparagus, celery, broccoli

Coffee & tea with cream and saccharin/sweetener

You Must Eat:

Vitamin C - 100 mg daily in unsweetened tablet form

(inexpensive at drug store).

Some form of vegetable oil such as corn, taken straight

or splashed on salads. (1 tbsp)

You Must not Eat:

Bread

Any dessert

Seed vegetables such as peas & beans

Root vegetables such as beets, parsnips, turnips, potatoes

Or anything containing sugar, starch, or flour.

Dr. Howe: "In 2 months I cut from 220 to 172 and trimmed my waist 11

inches"

Murdo Martin (NDP MP for Timmins): "Down I came in 10 weeks from 268 to

227, with 7 inches and 7 notches off my belt line."

Eric Winkler (Conservative MP): "I pared down from 226 pounds to 193 in

6 weeks."

It is important to realize with this diet that quantity is not the,

or even a factor. The diet eliminates almost all carbohydrates, which

most of us eat in large proportions. Carbohydrates come in the form of

sugar, starch and flour.

The logic of this diet is that our bodies are unable to use surplus

carbohydrates and therefore they are converted to fat and stored --

usually around the waist.

We lose the fat and the fat only, while building up muscle, blood

and other tissues with no loss of energy, no failure of drive or a

lessening of zest for living.

The diet is self limiting -- when the fat is gone, you stop losing

weight and remain constant at your natural and correct level.

"I tell you", says Martin enthusiastically, "this diet works.

What's more, you feel like a million bucks on it - lots of energy, drive

to burn - and you don't go around, as on most diets, feeling like a

grizzly bear."

"I swear on it," says Mr. Winkler with conviction, "this diet does

it, not only painlessly but pleasantly. The only fault I found with it,

I went down so fast I couldn't get my suits taken in quickly enough to

match the belt-line

Dr. Howe's "Eat & Drink Up Diet" is so short, so simple, some people

suspect there must be more to it.

There really isn't.

It's all there under 3 headings:

You May Eat

You Must Eat

You Must Not Eat

It covers broadly all foods.

<<CLOSED QUOTE - The Ottawa Journal, May 3, 1965>>

The following day, responding to requests for suggested menus, the

following was published:

<<OPEN QUOTE - The Ottawa Journal, May 4, 1965>>

Breakfast:

Tomato Juice, liquid or jellied consomme, sauerkraut juice or avocado.

Bacon or ham and eggs, all you can eat. Coffee, tea or milk.

Lunch:

Martini or Scotch & water, etc. *if desired*. Any cold meat: Beef, ham,

turkey, lamb, chicken, pork, salami, bologna, veal, tongue, liver, lean

or fat it doesn't matter. Salad with an oil & vinegar dressing or blue

cheese (*not* Thousand Island Dressing). Lettuce, cress, parsley, green

& red peppers, shredded cabbage, kale, dandelion greens, tomatoes,

asparagus... (any leafy vegetable).

Dinner:

Shrimp or lobster cocktail. Avocado or tomato stuffed with fish or fowl.

Any soup, including cream soups, so long as no rice, barley or macaroni.

Any stem or leafy vegetable - asparagus, brussels sprouts, cabbage,

cauliflower, celery, collards, endive, kale, lettuce, mushrooms, parsley,

peppers, sauerkraut, spinach, squash, tomatoes, turnip/beet greens.

Cheese of any kind. *Sugarless* ice cream, sherbets or gelatins. Coffee

or tea with cream. Milk.

Dr. Howe emphasizes that this diet is for healthy people only. You

don't have to stint, but don't go overboard either. Eat & drink enough

for comfort and health, but no more. "If you're healthy, you won't

anyway" says Dr. Howe.

Dr. Howe stresses that if a person is under medical or psychiatric

care, the diet is for his own personal physician and not Dr. Howe to

prescribe.

Dr. Howe's "Eat & Drink Up Diet" has been criticized by some as

having something of a resemblance to one which has been published in

California as "The Drinking Man's Diet", and this has been criticized as

a diet which will leave you fat and drunk. Dr. Howe points out that the

Drinking Man's Diet permits fruit and even seed vegetables. Dr. Howe

rules these out as being too heavily loaded with fat making

carbohydrates.

<<CLOSED QUOTE - The Ottawa Journal, May 4, 1965>>

Notes: Dr. Howe allows one to have a can of cream soup, or tomato

soup, when desired, so long as they contain NO rice, pasta, potatoes, etc.

There is some carbohydrate in these soups, but nowhere near enough to

sabotage the diet.

You may use unsugared strawberries in desserts.

You may use sugar-free soda pop.

Milk has 12 gms. of carbohydrate per glass - scientifically speaking.

Almost none of these carbohydrate are usuable by the vast majority of

humans as they are in the form of lactose, milk sugar, which very few

people can metabolize well, if at all. Hence, drink up.

Try not to use a lot of yogurt, or acidophilus milk, or any dairy

product which has been treated with a bacteria which breaks lactose down

into a "digestible" form. Yogurt is not off the menu, just don't eat more

than a cup a day or so. Sour cream is not a problem, as it is made from

full- fat cream and thus is low in lactose to begin with.

Do NOT use "Calorie-wise" dressings, or anything labelled "light".

Use full-fat dressings such as Ranch, Blue Cheese, Caesar, etc. Look on

the bottle, if they have a carbohydrate count of 1 gm/serving. or less,

use with abandon. If you do so, you will have fulfilled your oil

requirement in the "You Must Eat" category.

Whisky and hard liquor are allowed. Dry red or white wine may be

taken with meals - be sure is has a sugar count of 3 or less (or says

"dry" or "very dry" on the label.

LASTLY: And MOST important. Do NOT mix apples and oranges so to

speak. Do NOT take a part of this diet and a part of that diet. Low-

carbohydrate diets are not as "forgiving" as low-calorie diets. Do THIS

diet or DON'T do it. Don't mix and match, it is too confusing. If you

follow this diet you will lose a pound a day or so, if you add a chocolate

bar, a bran muffin, or a potato to the menu ALL THOSE FAT GRAMS become

AVAILABLE to the body for metabolization. One slip can ruin your whole

day. It isn't worth it: nothing tastes as good as thin feels.

My Personal Story:

In 1965 I was 17. I was 323 lbs. of misery. 6'1". I was so

desperate to lose weight and "fit in" that I used to take the bus to the

last stop on the line and try to walk the 10 or 15 miles back to my home.

I was never able to make it. I had been told, without solicitation, that

I should "turn the fat into muscle by exercise" by a wafer-thin cousin...

On Saturday, May 1st, 1965 I read on the front page of the newspaper

that "Dr. Howe's Diet" would be reprinted on Monday. When I read the diet

it seemed to be doable. The first week I lost an impressive amount of

weight (I don't remember exactly how much). By October I remember that I

was down 100 pounds.

It took about 5 or 6 months until I finally hit 190 lbs., largely

because my social life had improved to the point where I was "out with the

gang" instead of watching television. A teenager eats frenchfries,

burgers and pizza when in company, even in 1965.

31 years later I am still at 190 lbs. Once one has been overweight,

it is a lifelong struggle, no matter WHICH diet one chooses. I have

gained as much as 30 lbs. back before dieting. I have done Weight

Watchers and bought the Susan Powter tapes. I did this largely because I

was constantly told by thin friends (some of whom have since passed on)

that a high-fat, low-carb diet was dangerous.

I am the healthiest person I know.

No diet is suitable for all people. If you think you'd like to try this

diet, go to it!

P.S.: As far as desserts go... try a Bavarian Cream using an

envelope of sugar-free gelatine, made and removed from the refrigerator

when partially set. Mix in a cup of cream which has been whipped

separately and sweetened with Sweet & Low. Return to refrigerator until

fully set. Each it all in one sitting if you like. Yum! Orange Jello

Bavarian is my favourite.

Or, how about baking an egg custard? Use artificial sweetener and

chill. Cover with freshly whipped cream if liked. Use full-fat milk for

the custard, I find cream too cloying.

:cool: TJ :cool:

[Well... shit. My cholesterol's through the roof]

I've seen some have increased total cholesterol numbers on

low-carb diets. However, it's mostly because HDL (good)

increases.. Not because of LDL (bad). Get your blood work

numbers from your doc. I wanna see 'em.

To be honest though, the triglyceride is a better indicator of

heart disease.

One, predominant, reason for this kind of action is reduced

fiber in low-carb diets. You need to make sure you eat enough

raw veggies and raw/unsalted nuts to keep fiber intake up.

That's the only way we get rid of excess cholesterol (via

bile acids..)

Also, make sure you're getting plenty of antioxidant vitamins.

This includes vit. C, E, and beta carotene. I usually take 2-3g

of C daily..

:cool: TJ :cool:

[Well... shit. My cholesterol's through the roof]

Cholesterol is _NOT_ and indicator for heart disease.

There are many people with high cholesterol who never

develop heart disease and also people with very low

cholesterol who have it. (long story)

What was your triglyceride count? What is your

blood pressure?

:cool: TJ :cool:

[Carb Blocker pills (?)]

Used two times a month, let's say for example, you think there could be long term effects?

Probably not.. My guess is that you may get a little bit of

gastro-intestinal distress the next day, though. Specially if you've

been low-carb for a while. Generally these things work by

inhibiting enzyme production..

But hey, you could prolly get some wicked farts that way --

if you've got someone you want to offend for fun

:cool: TJ :cool:

[Carb Blocker pills (?)]

Do any of you have experience with any of the pills on the market to help block carb absorption? Say perhaps for Thanksgiving dinner or other binge inducing occasions? :?:

To be honest, I would avoid these like the plague. They allow sugars

to pass the entire length of the intestine without being properly handled

by the correct enzymes. The net effect is that bacteria in the digestive

tract have a large amount of substrate to feed on, etc.

I think that those pills could lead to things like intestinal cancer, chrone's

disease, IBS, etc. if used over any significant period of time.

Just my $0.02

:cool: TJ :cool:

[Keto Info Week 11/17]

CATEGORY: diets/ketogenic

TECHNICAL: ***

SUMMARY:

This document is part one of a lengthy technical document

on Cyclical Ketogenic Diets (CKD's). It was written by a friend

of mine who, at the time, was a member on

another mailing list of people (mostly athletes) who used CKD's

for fat-loss, or to increase muscle gain in the gym.

This work is sort of like a treatise on the whole topic

of CKD's. It discusses what ketones are, what ketosis is, and the

effects that they have on your body. It's a fairly technical

document but a good read none the less.

If you read through it, you'll get an overall picture of

how your hormones respond to low-carb diets, and why low-carb diets

aid in fat loss. He's also very complete, and gives both positives

and negatives (as he sees them).

Bear in mind, though, that there have since been many

new studies that prove the efficacy of ketogenic diets. I just

wanted to show you this because it sort of lays it out in a fairly

easy to understand manner. I don't exactly agree with everything

he states here, but the jist is on target.

-------------------------------------------------------------

Surviving and Thriving on a Low Carb Diet

Beyond Atkins, Di Pasquale and Duchaine

by David Greenwalt B.Sc.

There is currently a great debate over which diet is best with

special emphasis on high fat/low carb or high carb/low fat. Each group

makes "spot" claims and neither really covers the issues which really

matter. What are these issues?

1. What is your goal? A. Fat loss? B. Muscle hypertrophy? C. Endurance

improvements? D. Longevity?

2. What foods do you like? A. Are you a vegetarian? B. Do you rarely eat

fresh fruits and vegetables? C. Do you like fish? D. Do you like to cook?

E. Are you married or single and does your spouse like to cook?

3. Do you plan on staying on this diet forever?

4. Are you going to use the diet temporarily for any number of reasons?

Many of the arguments which begin between rigid dieting rivals are

ghost-like, in that neither side knows, or cares, what the goals are of

the other. I, speaking personally, do not know a very large, muscular

vegetarian. An argument can be made that vegetarianism is healthiest,

however, from purely an observational perspective, I don't want to look

like any vegetarian I know or have ever seen. My goals, as a bodybuilder,

are to be as big and lean as I can be genetically and naturally. At this

point, a vegetarian and I are most likely polar opposites.

We must define our goals if we are to intelligently discuss diets

because simply talking about calories in, calories out or arguing over

diets which are supported in scientific literature as health-giving versus

diets purported to be more anabolic is assanine. It's almost like saying

"I like apples. Well, I like Ferrari automobiles." One has little to do

with the other.

There are so many diets for sale it can be bewildering to most

people. While all of these diets cause dietitians to shake their heads in

most cases, the personal bioindividuality isn't taken into consideration.

Take a recent example in which a relative of mine was counseled on a

weight problem by a physician (M.D.). My relative was told to eat low fat,

high carb, fruits and veges and eat fish at least twice a week because of

the benefits of the essential fatty acids in the fish. This advice is

patented medical standard protocol for anyone overweight and might be very

good for a majority of the population. Problem: My relative hates fish and

so do I for that matter. It is because of our individual likes and

dislikes that so many diets are made available. Most are effective in

their own right but many are imbalanced and do not include a wide variety

of foods. The Registered Dietitians (RD) of America push the Food Guide

Pyramid. The Atkins followers push the low carbohydrate diet. Others push

high protein or low protein, fasting, grapefruit only, soup only, no

fruits, etc. etc.. All may serve a purpose and all may be valid but until

we know about goals and individual sensitivities like intolerance to

certain foods, allergies, medical conditions and personal likes and

dislikes, there can be no intelligent discussion about which diet is

better.

This paper is an attempt to clear up the disinformation which exists

regarding the low carbohydrate diet which causes ketonuria and ketonemia.

Whether we're talking about an Atkins (low carb everyday) or Di Pasquale

(low carb 5 1/2 days, med. carb 1 1/2 days) they both cause considerable

ketosis.

There are those who follow a low carb diet and have done so for more

than a year. Atkins' book gives several examples of individuals who have

chosen to make low carb a part of their life style (5). A certain, small

percentage of epileptic children who suffer from intractable seizures and

don't respond well to drug therapy are purposely placed and medically

supervised on a low carb (herein called Ketogenic Diet) for periods of two

years or more (1). A key difference between an epileptic child and a

healthy bodybuilder consuming similar foods is fluid intake. A ketogenic

diet is closely monitored for an epileptic child because water intake is

restricted. This is because the ketone bodies, which are synthesized in

high quantities on a ketogenic diet, are actually the medicine for the

child. Epileptic children wouldn't respond as well if the "medicine" was

being flushed down the toilet in large quantities as the kidneys filtered

them with super consumption of water.

A non-epileptic, otherwise healthy adult does not have the same goal

as the epileptic child. Ketones are not medicine. They are an energy

source but not medicine to the healthy bodybuilder. They are a byproduct

of the diet which we want to excrete if in excess (We'll cover some

biochemistry later).

There are those who believe that the world nearly stops when benign

dietary ketosis is caused with a ketogenic diet. Scare tactics such as

"The Kreb's cycle collapses due to insufficient carbohydrate intake",

there will be more "bruising" of blood vessels because of higher fat

traffic on a ketogenic diet, increased risks of morbid obesity and

increased coronary heart disease lipid factors, and finally the great myth

that we must have hundreds of grams of carbohydrates per day to fuel the

brain and other tissues which require glucose for energy. Some of these

claims are simply false and others are completely unsubstantiated in

current medical journals. What must be taken into consideration, before

wild claims are made, are the ratios of the nutrients consumed and making

sure that whether it's an epidemiological study or small 10 person study,

were the study participants consuming a diet which is the same as those

following a typical ketogenic diet consisting of 70% fat, 20% protein and

5% carbohydrate? In nearly any case which examines fat intake and

increased risks of CHD and obesity, the fat intake is coupled, arm-in-arm

with high dietary carbohydrate ingestion or at least substantially higher

than the ketogenic 5% we're discussing in this paper.

The scare tactics, like the ones above, are used by the ill-advised

and ignorant who feel their diet is best. There is no cookie cutter

"best". There is no "one size fits all." For these reasons we can only

discuss physiology, biochemistry and scientific literature reviews which

are pertinent to humans following identical diets. Rat studies may be

better than nothing but not much better. In-vitro studies are only a place

for scientists to start, not a place for pragmatists to review.

In this paper I'll cover how a ketogenic diet works to support life

and activity and I'll also discuss how a ketogenic diet may even be

beneficial for some individuals. The research I have conducted for this

paper has led me to recommend a ketogenic diet for the following

individuals under the following circumstances:

1). Medically supervised epileptic children who don't respond to standard

drug therapy;

2). Dieting bodybuilders in precontest dieting phases, up to 12 weeks in

duration;

3). Strength phase athletes who want to incorporate more meat without a

large weight increase or any weight increase;

4). Type II diabetics (non-insulin dependent) 6-12 weeks, with

carbohydrates brought back in slowly and in measured quantities;

5). Anyone, who is otherwise healthy, but overweight and not happy with

the mirror may want to consider giving this diet a try for 6-12 weeks then

bring back in carbohydrates slowly and in reduced/measured quantities.

Yes, every class is temporary and it is believed, by this writer,

that a low carbohydrate, non-ketogenic diet would be the goal, eventually,

for anyone following a current ketogenic diet because ketosis is not a

normal, everyday, physiological state and was not intended to be from a

physiology standpoint. With all of this said let's begin.

What is a ketogenic diet and why would anyone want to modify their

current eating regimen to adapt to and follow a ketogenic diet?

First, let me say that the ketogenic diet dates back to biblical

times and in more modern times of the 20th century, the ketogenic diet has

been studied extensively with more research warranted even so (1).

The word ketogenic reveals the basic identity of the metabolic

process in humans of ketone (keto) production (genic). So we've produced

ketones. What does this mean and how are ketones used as ready substrates

to fuel anabolic and catabolic reactions, or better stated, how are

ketones used to fuel metabolism?

Ketones are a byproduct of fatty acid catabolism and this process of

breaking down triglycerides into glycerol and fatty acids is known as

lipolysis. Lipolysis is a normal physiological event occurring at times

when the body is utilizing fat as a fuel source and thus, breaking down

stored triglycerides and mobilizing free fatty acids and glycerol for

further catabolism into our body's absolute source of energy, ATP.

Lipolysis is activated during normal calorie-restrictive dieting

conditions and partially explains the reason we lose body fat during

hypocaloric periods or when we've created a net calorie deficiency when

activity, such as exercise, coupled with our basal metabolic rate creates

a greater need for calories than we are providing through our diet.

Ketone production is an indicator that lipolysis has been activated

and you are now, at least partially, burning fats for fuel. A ketogenic

diet, as you might expect, is a diet which promotes lipolysis as a chief

energy source, in preference to dietary glucose, the principal

carbohydrate utilized by the body after breaking down polysaccharides into

the monosaccharide glucose.

If lipolysis is the goal of a ketogenic diet for otherwise healthy

individuals, what is the best way to accomplish this? To give ourselves a

reference point and provide the baseline for comparison, I present the

highly touted pyramid of healthy eating.

The food guide pyramid, as many of you have seen, is representative

of what mainstream dietetics in 1996 want the majority of the American

population to consume on a daily basis for health, vigor and longevity.

The base and foundation of the pyramid suggests 6-11 servings of bread,

cereal, rice and pasta with the following other food groups and servings

providing the remaining calories in a given day: vegetables 3-5 servings,

fruits 2-4 servings, milk, yogurt and cheese 2-3 servings, meat, poultry,

fish, dry beans, eggs and nuts 2-3 servings, and last but not least fats,

oils and sweets are to be used sparingly. Upon visual observation of the

actual pyramid represented you can see the food groups are arranged with

the foods which should be consumed in greater quantities at the bottom,

and which are representative of a strong, solid foundation on which to

build (2).

When you are eating a ketogenic diet we turn everything upside down,

except that turning the pyramid upside down only provides an unstable

pivot point which the pyramid couldn't possibly be supported by. What we

really must do to represent the ketogenic diet appropriately is move the

food groups and provide for a solid base, consisting of fats and oils as

the foundation to build upon.

With a ketogenic diet, fats and oils are indeed representative of the

greatest proportion of the macronutrient organic molecules; lipids,

proteins, carbohydrates and nucleic acids eaten on a daily basis.

There's a good chance, as you sit there right now that you're in a

serious state of denial and many walls have already been put up doubting

the efficacy of this diet. I mean, after all, isn't it fat that makes us

fat? How could we possibly even maintain our current weight, let alone

lose weight with a diet which works off a structure of fats first, protein

second and carbohydrates third? Fat has been portrayed as an evil villain.

I mean, remember the traditional pyramid? Fats and oils are to be used

sparingly! Fat-free this and fat-free that. It's all good. It's all O.K.

if it's fat-free. Not true and even potentially dangerous for some people

who don't metabolize sugars properly.

In spite of the plethora of enzymes and metabolites in each cell,

metabolism is not random. Rather, it is highly regulated. If each of the

possible metabolic reactions were to occur at a fixed rate all of the

time, organisms would be incapable of reacting to changes in their

environment. For example, the intake of energy may be sporadic (e.g.

meals), yet organisms expend energy continuously. Metabolism must

therefore be regulated so that an organism can respond efficiently to the

availability of energy or food. When there is no intake of food but a

continued need for energy expenditure, metabolic fuels are mobilized from

storage depots at a rate sufficient to supply cells with oxidizable

substrates. Humans, for example, can survive periods of starvation as long

as five to six weeks when provided with water. A very obese adult could

probably endure a fast of more than a year, but physiological damage and

even death could result from the accompanying extreme ketosis after this

amount of time (7) (Remember, we're not starving, we're eating everyday).

Keep in mind that any organism responds not only to external demands but

also to genetically programmed instructions. The responses of organisms to

changing demands may involve alterations in many pathways or only a few

and may occur on a time scale ranging from less than a second to hours or

longer. Briefly, and very simplified, this is what occurs when a normal,

otherwise healthy person eats a typical meal consisting of 55%

carbohydrates, 30% fats, 15% protein- in other words, the "ideal diet".

Lipids are catabolized into fatty acids, carbohydrates to monosaccharides

and proteins are broken down into amino acids. Absorption of

macromolecules is primarily achieved in the small intestine and the

macromolecules are used to fuel glycolysis, the kreb's cycle and the

electron transport system, with carbohydrates being burned preferentially

to fats and proteins as an energy source. As long as glucose is plentiful

and insulin is present, glucose fuels the human machine and fats are

burned primarily as a fuel source only when carbohydrates are insufficient

or the body perceives an insufficiency, as is the case in diabetes

mellitus.

A ketogenic diet has been compared to a fasting/starvation diet

because in many ways, the metabolic pathways responsible for energy

production are similar in both. There is one striking difference which

should be very obvious, however, between a fasting/starvation diet and the

diet presented here. FOOD! We are neither fasting nor starving with a

ketogenic diet and in fact we are consuming, in some degree, all three of

the major energy-producing organic macromolecules which are, once again,

lipids, proteins and carbohydrates. To better illustrate how the body

could possibly survive and even thrive on such a diet it should be

understood that individuals who may benefit the greatest from a diet of

this type are individuals who don't process sugars properly, as is the

case in Type II, Noninsulin dependent, Adult-Onset Diabetes, and

individuals who are at greater risk for coronary heart disease due to

complications associated with morbid obesity.

Briefly, Noninsulin dependent diabetes is usually associated with

obesity and insulin secretion may be normal. Circulating levels of insulin

may even be elevated, thus the problem is not a shortage of insulin, but

insulin resistance resulting from decreased sensitivity, poor

responsiveness, or both. Chronic hyperglycemia (high blood sugar) is the

result. A drop in insulin production is often observed in individuals as

time passes and currently there is strong evidence to support a tiring of

the pancreas from chronic insulin output. A drop in insulin production is

often observed in individuals with NIDDM as time passes. NIDDM affects

about 5% of the population or approximately 12,500,000 people nationwide.

Chronic hyperglycemia can lead to a number of complications including

cataracts, sclerotic lesions in blood vessel walls, and general ill health

associated with obesity The aim of all regimens for the management of

diabetes is control of blood glucose levels. Dietary modifications are

often sufficient to control NIDDM and this type of diabetes may even

disappear with moderate weight loss and a program of exercise (3).

If obesity begets NIDDM and NIDDM begets obesity then we can begin to

realize the seriousness which surrounds a diet which may help control

blood glucose levels and which promotes the dissolving of fat. The health

risks of overfatness are so many that it has been declared a disease:

obesity. Besides diabetes and hypertension, other risks threaten obese

adults. Among them are high blood lipids, cardiovascular disease, sleep

apnea, osteoarthritis, abdominal hernias, some cancers, varicose veins,

gout, gallbladder disease, respiratory problems, liver malfunction,

complications in pregnancy and surgery, flat feet and even a high accident

rate. Moreover, after the effects of diagnosed diseases are taken into

account, the risk of death from other causes remains twice as high for

people with lifelong obesity as for others. An estimated 25 percent of

U.S. adults are overweight to a degree that incurs such risks (2).

As I stated before, a ketogenic diet is compared to a fasting diet

because of similar metabolic reactions for utilizing fatty acids and

protein as principle energy substrates when glucose levels are low. So, in

very simplified form, this is what happens when we change from a typical

"fed state" in which carbohydrates are plentiful and the fasting or

ketogenic state in which carbohydrates are restricted.

In the absorptive phase, lasting from 2-4 hours after a meal, the

level of glucose in the blood rises. Glucose is rapidly taken up by the

liver, skeletal muscle and the brain. If the level of glucose in the blood

rises above the ability of the kidney to reabsorb filtered glucose, the

excess is lost to the urine, as is the case with hyperglycemia and

diabetes.

High blood glucose triggers the release of insulin, which has many

physiological effects including stimulation of glycolysis (utilization of

glucose to form 2 ATP and 2 pyruvic acid molecules), fatty acid synthesis

and protein synthesis as well as inhibition of glycogenolysis (breaking

down glycogen to glucose), gluconeogenesis (conversion of noncarbohydrate

sources to glucose), fatty acid oxidation (cleaving long chain fatty acids

2 carbons at a time into shorter fatty acids), ketogenesis (producing

ketones) and proteolysis (breaking down proteins). Glucagon, which acts

only on liver, has effects that are in general, opposite those of insulin.

Insulin levels are high in the fed state (a state generally associated

with food consumption containing carbohydrates); glucagon levels are high

in the fasted state (or states in which glucose levels are low such as the

ketogenic diet).

Lipids entering the body during the absorptive phase are packaged in

chylomicrons (a transporter for lipids). Triglycerides in chylomicrons are

delivered to peripheral tissues (peripheral tissues are defined as any

tissue which is not the liver, indicating the liver's central role in

metabolism and filtration of toxins). Triglycerides are hydrolyzed outside

the cell and fatty acids are taken up, esterified (relinked with glycerol)

and stored (3). Stored lipid represents the body's most plentiful source

of potential energy. Relative to other nutrients, the quantity of lipid

available for energy is almost unlimited. The actual lipid fuel reserves

in a typical young adult male amount to about 90,000 to 110,000 kcal

(23,800kJ) of energy. In contrast, the carbohydrate energy reserve is

about 2% of this total, or approximately 2000 kcal (8400kJ) (6).

Dietary amino acids arrive at the liver during the absorptive phase.

These amino acids are either catabolized, used for protein synthesis or

permitted to pass unaltered to peripheral tissues. Oxidation of the amino

acids in liver generates a large amount of ATP, much of which is

immediately consumed by the pathways of gluconeogenesis and urea

synthesis, which remove the carbon and ammonia, respectively, generated by

amino acid catabolism.

In the transition into early starvation or initial ketogenic dieting,

the absorption of dietary glucose slows, the levels of insulin drops and

the level of glucagon rises. The liver responds to the hormonal changes by

breaking down glycogen and releasing glucose. Low levels of insulin are

also accompanied by an increase in the rate of lipolysis in adipose tissue

and an increase in the release of free fatty acids into circulation.

In addition to gluconeogenesis there is another revelation that may

come as a shock to some of you. When choice is available, most tissues use

fatty acids as fuels before ketone bodies, and BOTH BEFORE GLUCOSE (3).

This means that glucose is used only when it is abundant and other fuels

are scarce. Fatty acids are used in preference to glucose even though the

concentration of circulating glucose is always much higher than the

concentration of free fatty acids. The glucose-fatty acid cycle, first

proposed by Philip Randle, explains how the preference for glucose or

fatty acids is determined by metabolic conditions. Operation of the

glucose-fatty acid cycle requires that low concentrations of glucose

correspond to greater fatty acid availability. As I've stated earlier, low

availability of glucose results in decreased levels of insulin. Less

insulin means that lipolysis inhibition in adipose tissue has been lifted

and the availability of free fatty acids rises. The glucose-fatty acid

cycle contributes to the maintenance of blood glucose levels by sparing

the oxidation of glucose in peripheral tissues. This pattern of fuel use

is usually observed only when the availability of glucose is low, such as

after liver glycogen stores are exhausted, but the cycle predicts that any

rise in the level of circulating fatty acids will decrease glucose use.

The glucose-fatty acid mechanism suppresses the use of glucose when fatty

acids are available; when glucose is low, insulin is low, release and

catabolism of fatty acids is high, and products of fatty acid catabolism

(NADH, acetyl CoA and citrate) inhibit glucose degradation and spare the

use of glucose.

Other cycles of metabolism which assist in sparing glucose when

glucose levels are low include the Cori cycle which regenerates ATP from

lactate produced in muscle tissue. The lactate generated is returned to

liver for conversion back to glucose. The glucose-alanine cycle

interconverts glucose to alanine in muscle and then back to glucose once

again in liver.

Amino acids are the major gluconeogenic precursors initially and one

key difference between starvation or fasting and an eucaloric ketogenic

diet is that during starvation the use of endogenous amino acids requires

degradation of body proteins and accompanying loss of protein function.

With a ketogenic diet copious amounts of dietary proteins are being

consumed everyday. As you will see, the body strives to maintain protein

homeostasis and particularly, the precious intracellular proteins. When

given the choice, it is the belief of this writer that the body will

utilize dietary proteins during this initial gluconeogenic activity,

although some body proteins may initially be sacrificed through the

actions of various hormones until adaptation has occurred.

Protein turnover is continuous and the two processes comprising

turnover, synthesis and degradation, approximately balance one another in

the healthy adult. Whole-body turnover in humans is correlated to ones'

metabolic mass. Daily turnover of protein is calculated to be

approximately 4.6g/kg body weight. For the average 70-kg male, turnover of

whole-body protein would approximate 320 g daily (7). Individual body

proteins, however, vary in their turnover rate; the half-life of a protein

can range from only a few minutes to several months. Furthermore, neither

the turnover rate of an individual protein nor that of total body protein

remains constant. The rate of synthesis and degradation can be influenced

by a variety of factors related to nutrition, including immediate food

intake, previous diet, and overall nutrition status. Some have postulated

that during a ketogenic diet we will continuously show accelerated

proteolysis of intracellular proteins and muscle for gluconeogenesis which

is the opposite of what any athletic individual wants to do. During the

initial stages of a ketogenic diet the catabolism of muscle tissue may

occur for a brief period until the body has adapted to the diet and the

use of fatty acids and ketones as primary fuel substrates. Protein

degradation rates decrease concurrently so that even in chronic

starvation, which the low carb diet is not, daily losses of nitrogen

become quite small. For example, a person fully adapted to starvation can

survive at a cost of 3 to 4 g of his or her body protein per day. This new

priority is justified by the vital physiological importance of body

proteins. Proteins that must obviously be conserved for life to continue

include antibodies, needed to fight infection, enzymes, which catalyze

life-sustaining reactions and hemoglobin for the transport of oxygen to

tissues. The protein sparing shift at this point is from gluconeogenesis

to lipolysis, as the fat stores, and if following a ketogenic diet,

dietary fats, become the major supplier of energy. This shift to fat

breakdown also releases a large amount of glycerol, which becomes the

major gluconeogenic precursor, rather than amino acids (7). The principal

mechanism of adjustment to starvation is a change in hormone balance.

Decreased insulin activity, coupled with increased synthesis of

counterregulatory hormones such as glucagon, epinephrine and

norepinephrine promotes fatty acid mobilization from adipose tissue,

production of ketones and the availability of amino acids for

gluconeogenesis. Initially, in starvation or fasting and possibly

preadjustment to a ketogenic diet, glucocorticoids are important in

gluconeogenesis because they promote catabolism of muscle protein to

provide substrates for gluconeogenesis. We must remember that proteolysis

of muscle tissue may occur on a ketogenic diet in the early preadjustment

stages, however, ketogenic dieters are not starving and the initial

increased catabolism of body proteins will not continue for longer than as

little as a few days or perhaps up to a few weeks. Ketogenic dieters are

still consuming lipids, proteins and carbohydrates on a daily basis and

are not starving. An increased adjustment to starvation (or a ketogenic

diet) is characterized by a decrease in the secretion of glucocorticoids,

however (7). As fasting or starvation (or a ketogenic diet) continues,

tissues continue to use fatty acids and glucose for energy, but also begin

to use ketones formed in the liver from fatty acid oxidation. A decrease

in protein catabolism and gluconeogenesis occurs concurrently with the

brain's and other tissues' adaptation to ketones as a source of energy.

Glutamine metabolism in the kidney increases as starvation continues and

acidosis occurs. Within the kidney, glutamine catabolism generates

ammonia, which serves to help correct the potential for acidosis (7). Once

again, a difference between the ketogenic diet and starvation is acidosis.

Acidosis is well regulated in individuals who are not starving and even in

those who are, however, a discussion of protein and amino acid turnover

should include renal glutamine metabolism which is also a regulator of

blood pH.

As carbohydrates continue to remain low and the body is forced to use

fatty acids, proteins and glycerol via gluconeogenesis for fuels, fatty

acids are converted to ketone bodies, which, unlike fatty acids, can cross

the blood-brain barrier and serve as fuel for the brain, further sparing

the use of glucose. Less use of glucose at this state means less

What we've clearly shown thus far, is that the body is adaptive and

utilizes many complex mechanisms to not only spare glucose for organs

which absolutely require it like the kidney medulla, the retina, red blood

cells and parts of the brain, but also regenerates necessary glucose from

non carbohydrate sources.

If further evidence is necessary to convince any doubters that a low

carbohydrate diet can not only sustain life but provide a great abundance

of energy for daily activities, exercise and even intense exercise, I'll

provide the following scenario:

In humans, in the fed state (which as I mentioned before is generally

associated with carbohydrate ingestion), the brain requires about 120

grams of glucose per day and all other glycolytic tissues require about 60

grams per day. Total glucose necessary per day during intermediate

starvation is reduced to approximately 110-120 grams per day (3). The

body, at this stage, is already making adjustments for reduced

carbohydrate availability. As ketone bodies become more readily available,

they can substitute as an energy source in tissues which would normally

otherwise utilize glucose as a fuel source. What tissues can utilize

ketone bodies for energy?

(1) The brain (2) Muscle (3) The Kidneys (4) Small intestine

The sparing effect of ketone bodies on glucose when a eucaloric diet

is still being utilized, ensures that peripheral tissues will have the

glucose they need to function efficiently. During intermediate starvation

and potentially, during initial ketogenic dieting, about 40-50 grams of

the 110-120 grams of glucose used per day are accounted for by the

activity of the Cori cycle (if you'll think back, the Cori cycle was a

cycle of glucose regeneration from glucose to lactate in muscle and then

back to glucose again in the liver). In starvation, lipolysis of adipose

tissue will contribute between 15 and 20 grams of glucose per day and

remains fairly constant during starvation. We can conclude that lipolysis

of adipose tissue as well as fatty acid oxidation of dietary lipids with a

ketogenic diet will produce glucose in at least as great a concentration

as starvation.

So far we've created approximately 70 grams of glucose via the Cori

cycle and lipolysis with another 40-50 grams of glucose needed to fill the

bank and provide peripheral tissues with glucose to operate effectively.

How do we get the remaining glucose we absolutely must have during

intermediate starvation or preadjustment ketogenic dieting?

Gluconeogenesis from amino acids is quite high, even in the absorptive

phase when carbohydrates are present. During starvation, proteolysis of

peripheral tissues increases to provide gluconeogenic precursors at the

liver. During the ketogenic diet protein is consumed in copious amounts,

thus thwarting the debilitating effects of losing precious cellular

proteins and muscle protein. The production of 100 grams of glucose

requires the breakdown of about 175 grams of amino acids. During

starvation this cannot last long as even a small amount of lost protein to

provide energy is accompanied by loss of functional capacity (3). Once

again, we're not starving, we're eating generous portions of lipids,

proteins and minimal carbohydrates. A typical 180 pound bodybuilder, for

instance, will consume approximately 180-360 grams of protein per day

depending on training philosophy and ideas about the benefits in general

of consuming additional protein as a bodybuilder. There is even stronger

evidence to suggest that endurance athletes may benefit from increased

protein consumption (even more so than bodybuilders) and they may in fact

be consuming large amounts of protein from their diet as well. I cannot

speak for them, however (4).

We've already exceeded the minimal necessary amounts of glucose to

keep peripheral tissues functioning efficiently and we haven't even eaten

any carbohydrates yet. Let's not forget that most ketogenic diets don't

advocate abstinence from carbohydrates completely and that most

bodybuilders or dieting individuals following a ketogenic diet will

consume between 30 and 50 grams of carbohydrates per day. We've already

shown that glucose will be plentiful and available to fuel tissues which

require it but let's review thus far how it was accomplished. (1) A

reduction in carbohydrate intake has reduced insulin production, although

insulin in normal, healthy individuals is present at all times in blood,

albeit, in lower concentrations during low carbohydrate ingestion. (2) A

lowering of insulin has lifted the inhibition on lipolysis and lipolysis

is now stimulated. If calories are insufficient to maintain BMR plus

activity then adipose tissue and dietary fatty acids will effectively be

used to generate energy via the beta oxidation of free fatty acids and

gluconeogenesis of glycerol, the back bone of stored triglycerides. In

either case, hypocaloric or eucaloric dieting, lipolysis will be enhanced

and the choice of fuels will be determined by calories consumed with

preference given to dietary lipids first and adipose tissue second. (3)

The glucose-fatty acid cycle dictates that when carbohydrate is low, fatty

acids can serve as a preferred fuel source, thus, lowering the need for

glucose. (4) The Cori cycle recycles glucose by converting glucose into

lactate within muscle and then a reconversion of lactate in the liver back

to glucose takes place, thus completing the cycle. (5) The glucose-Alanine

cycle is similar to the Cori cycle except that glucose is converted into

pyruvate within muscle once again and then to Alanine, also within muscle,

which is transported to the liver for reconversion into glucose. (6) The

body has adapted to the reduction in glucose and is ready and willing to

utilize ketone bodies as a fuel source in certain tissues. (7) We are

still eating some carbohydrates every day!

As starvation or the ketogenic diet continues, lipolysis continues to

release considerable amounts of fatty acids, which are taken up by the

liver. Fatty acids enter the mitochondria, where they are partially

oxidized. The citric acid cycle in liver can absorb only a fraction of the

acetyl CoA produced by beta oxidation, and most is converted to the ketone

bodies beta-hydroxybutyrate and acetoacetate. Ketone bodies that are taken

up and metabolized by tissues spare the use of glucose, just as glucose is

spared by the operation of the glucose-fatty acid cycle.

As ketone bodies initially become available, they provide up to 50%

of the energy requirement of skeletal muscle. The most important overall

effect, however, of the use of fatty acids and ketone bodies as

alternatives to glucose, is that, as I stated in previous pages, less

demand for glucose means that less proteolysis of muscle protein is

required to supply the gluconeogenic pathway. Ketone bodies are acidic,

water soluble short chain fats and if left to accumulate in an

uncontrolled fashion could have devastating effects on our central nervous

system. Excess ketones are filtered and diluted ( as they are water

soluble) and excreted in urine. Our body also has very capable buffering

systems in place, (one previously mentioned is the use of renal glutamine

metabolism to create ammonia) to accept the extra hydrogen ions released

in the blood which prevent wild fluctuations in blood pH.

An excellent example of buffer capacity is found in the blood plasma

of mammals, which has a remarkable constant pH of 7.4. Consider the

results of an experiment that compares the addition of an aliquot of

strong acid to a volume of blood plasma with a similar addition of either

physiological saline or water. When 1.0ml of 10 M HCL (hydrochloric acid)

is added to 1000ml of physiological saline or water that is initially at

pH 7.0, the pH is lowered to 2.0. However, when 1.0 ml of 10 M HCL is

added to 1000 ml of blood plasma at pH 7.4, the pH is again lowered, but

only to 7.2- impressive evidence for the effectiveness of physiological

buffering (3).

The pH of the blood is primarily regulated by the carbon

dioxide(CO2)-carbonic acid(H2CO3)-bicarbonate(HCO3) buffer system. The

buffer capacity of blood depends upon equilibria between gaseous carbon

dioxide(which is present in the air spaces of the lungs), aqueous carbon

dioxide(which is produced by respiring tissues and dissolved in blood),

carbonic acid, and bicarbonate. When the pH of blood falls due to a

metabolic process that produces excess hydrogen ions, the concentration of

carbonic acid increases momentarily, but carbonic acid rapidly loses water

to form dissolved carbon dioxide(aqueous), which enters the gaseous phase

in the lungs and is expired as carbon dioxide (gaseous). An increase in

the partial pressure of carbon dioxide in the air expired from the lungs

thus compensates for the increased hydrogen ions. This system of pH

regulation effectively neutralizes the excess hydrogen ions, however, it

does so at the cost of depleting the blood bicarbonate. A bicarbonate

repletion mechanism exists in the kidney and requires the amino acid

glutamine (3). Conversely, if the pH of the blood rises, the concentration

of bicarbonate increases transiently, but the pH is rapidly restored as

the breathing rate changes and the reservoir of carbon dioxide(gaseous) in

the lungs is converted to carbon dioxide (aqueous) and then to carbonic

acid in the capillaries of the lungs. Again, the equilibrium of the blood

buffer system is rapidly restored by changing the partial pressure of

carbon dioxide in the lungs (3).

One point which must be addressed when discussing the effects of

buffering systems and the acidic nature of ketone bodies is the

incorrectly assumed potential for ketoacidosis in individuals who still

have the ability to secrete normal amounts of insulin from the pancreas.

In diabetics, who are vivid negative examples of what can go wrong with

the integration of metabolism and metabolic regulation (homeostasis) for

the continuance of life, ketoacidosis and metabolic acidosis are very real

and serious problems which must be taken into consideration by those

individuals. In diabetics, who are already at risk for chronic

hyperglycemia, diuresis leads to a dehydration compounded by increased

insensible water loss due to hypernea of metabolic acidosis. Metabolic

acidosis results from the excessive ketogenesis occurring in the liver.

Peripheral circulatory failure, a consequence of severe hemoconcentration

leads to tissue hypoxia with a consequent shift of the tissues to

anaerobic metabolism. Anaerobic metabolism raises the concentration of

lactic acid in the blood, thereby worsening the metabolic acidosis. The

ketonuria along with glucosuria associated with acidosis causes an

excessive loss of sodium from the body; loss of this extracellular cation

further compromises body water balance. A net loss of potassium, the chief

intracellular cation, accompanies increased protein catabolism and

cellular dehydration, both of which characterize uncontrolled diabetes

(7).

In non-insulin dependent diabetics or the overweight but healthy

individuals who are utilizing a ketogenic diet this cascade of events,

which eventually may lead to coma or death, does not occur. If it did,

we'd have a lot of very sick or dead dieters to deal with and in all

actuality we wouldn't be writing this paper because the diet would not be

as "trendy" as it has become. Why then, don't type II diabetics or normal

but overweight individuals succumb to the hazards of ketoacidosis or

metabolic acidosis? The answer lies in the body's innate ability to

maintain homeostasis. With a ketogenic diet we are mobilizing large

amounts of free fatty acids which are producing ketone bodies in large

quantities. Ketone bodies are acidic. If we agree thus far in this

paragraph then let's elucidate the reason we aren't all dropping like

flies. When plasma ketone concentrations reach 4-6mmol, insulin release

from the pancreas is stimulated. This blunts (but does not normalize)

lipolytic activity in the fat cell such that plasma free fatty acid (FFA)

levels are fixed at about .7-1.0mmol - sufficient to allow moderate

production of aceto-acetate and 3-hydroxybutyrate by the liver, but

insufficient to allow maximum rates of production required to develop

ketoacidosis. In type I diabetics subjects the protective ketone-insulin

feedback loop cannot operate because of beta-cell failure in the Islets of

Langerhans. As a consequence, plasma FFA reach much higher concentrations,

driving ketone production to maximal rates, thereby leading to the

ketoacidotic state (8). Another, perhaps more obvious advantage, is our

ability as human beings to utilize common sense. Since the kidneys are

going to help us flush unused ketones then we can help our kidneys do

their job by drinking a lot of distilled water everyday. At least one

gallon of distilled water should be consumed everyday when individuals are

following a ketogenic diet or any diet for that matter.

I've spent a lot of time covering the basic metabolic pathways

associated with a ketogenic diet consisting of 75% lipids, 20% proteins

and 5% or less carbohydrate. There are those who profess to have all the

answers and shriek at a diet which promotes such a high fat consumption

and, in the beginning, nearly excludes certain food groups. There are

great differences between this type of diet and someone who is ill with

Insulin Dependent Diabetes Mellitus. A normal person produces insulin but

may not regulate blood glucose levels and uptake very efficiently due to

many factors. An Insulin Dependent Diabetic does not produce insulin, or

very much, and has lost much of the control that healthy, but overweight

individuals possess.

You may be curious about exactly what foods are acceptable for this

diet. In general: All meat, all fish, all fowl, all shellfish, all eggs,

almost all cheeses, vegetables of 10% carbohydrate or less, cauliflower,

tomatoes, spinach, sauerkraut, broccoli, brussels sprouts, spices, sugar

free beverages, fats and oils, nuts and seeds in moderation, peanut butter

in moderation and water as the principle dietary solvent (5).

Final recommendations and general guidelines for anyone following a

ketogenic diet: Generally speaking, when individuals are strictly

following the initial dieting changes which accompany this diet they are

lacking in various vitamins, minerals and fiber. While there is great

controversy over whether fiber is of vital importance for life-long health

and cancer prevention, this writer believes fiber should be sought and not

avoided. Because I have made initial recommendations that anyone following

this diet will not be on it in its strict form for more than 12 weeks

there are some simple ideas which I think are important; (1) Drink at

least one gallon of distilled water every day, (2) While carbohydrate

intake will most likely be limited to 30-50 grams per day it is important

to make the carbohydrates you do eat of a fibrous nature. Vegetables which

are high in fiber and nuts can help balance the carbohydrate/fiber issue.

They are also a rich source of vitamins and minerals. I suggest not eating

any carbohydrate that contains greater than a 3:1 ratio of carbs to fiber

grams. In other words, if the package of nuts you're eating has 6 grams of

carbs, it should also contain 2 grams of fiber or more. Assuming the eggs

and other products you're going to be eating that contain trace amounts of

carbs equals no more than 6 grams of carbs per day, you will have between

24 and 44 grams of carbs left to consume. In these carbs you should strive

to eat those which contain the 3:1 ratio of carbs to fiber. In this way

you'll get between 8 and 15 grams of fiber everyday. You may also want to

take a carbohydrate-free fiber supplement, available at any health food

store, if your fiber intake is less than the range above. Additionally, if

your bowel movements are less than one per day, after two weeks of

adaptation to the diet, you may want to consider adding in a fiber

supplement as well. (3) Take a complete multi-vitamin and mineral

supplement everyday to prevent any possibility of vitamin and mineral

deficiencies, (4) Optionally, take free-form glutamine in supplemental

form for optimal intestinal, skeletal muscle and renal functioning.

The walk-away message from this paper is an understanding that

lipolysis is the process of dissolving fat and there is "no lipolysis

without ketosis and no ketosis without lipolysis" (5) and how this diet

differs substantially from a starvation diet and doesn't cause metabolic

acidosis in normal insulin producing individuals. We aren't going to die

by placing our bodies in a state of benign dietary ketosis while we get

our blood sugar under control and lose excess weight in the process. In

fact, we may actually see an improvement in energy, health and mental

stability in the absence of wild fluctuations in blood sugar. Eventually,

you will want to bring in other food groups and carbohydrates, however, if

you're carbohydrate sensitive, you will want to bring them in slowly and

in measured quantities, not exceeding the carbohydrate levels which your

body can efficiently process without laying down fat and without causing

wild fluctuations in blood sugar. In the meantime, many people will enjoy

a reduction in bodyfat with an exceptionally little amount of lean mass

lost in the process, as well as an increase in perceived energy and

perhaps, for the first time in many years, a stabilization of blood sugar.

References:

1. Spalding, K, Amorde, MS RD, (J Am Diet Assoc, Nov. 96, pp.1134)

2. Cataldo, Debruyne, Whitney, "Nutrition and Diet Therapy", 1995

3. Moran, Scrimgeour, Horton, Ochs, Rawn "Biochemistry" 2nd Ed., 1994

4. Wolinsky, Ira, Hickson, James "Nutrition in Exercise and Sport", 2nd

Ed., 1994

5. Atkins, Robert MD "Dr. Atkins New Diet Revolution", 1995

6. Mcardle, Katch, Katch "Exercise Physiology", 1996

7. Groff, J, Sareen, G, Hunt, S "Advanced Nutrition and Human Metabolism",

2nd Ed, 1995

8. Rifkin, Porte "Diabetes Mellitus: Theory and Practice", 1990

MORE READING ON KETOGENIC DIETS

Wing RR; Vazquez JA; Ryan CM Cognitive effects of ketogenic

weight-reducing diets Int J Obes Relat Metab Disord, 19:11, 1995 Nov,

811-6

Gumbiner B, etal Effects of diet composition and ketosis on glycemia

during very-low-energy-diet therapy in obese patients with

non-insulin-dependent diabetes mellitus Am J Clin Nutr, 1996 Jan

Amari A, et al Achieving and maintaining compliance with the ketogenic

diet J Appl Behav Anal, 1995 Fall

Nebeling LC, et al Effects of a ketogenic diet on tumor metabolism and

nutritional status in pediatric oncology patients: two case reports. J Am

Coll Nutr, 1995 Apr

Nebeling LC, et al Implementing a ketogenic diet based on medium-chain

triglyceride oil in pediatric patients with cancer. J Am Diet Assoc, 1995

June

Baron JA, et al A randomized controlled trial of low carbohydrate and low

fat/high fiber diets for weight loss Am J Public Health, (1986 Nov)

76(11):1293-6

Alford BB et al The effects of variations in carbohydrate, protein, and

fat content of the diet upon weight loss, blood values, and nutrient

intake of adult obese women. J Am Diet Assoc (1990 Apr) 90(4):534-40

Rabast U, et al Loss of weight, sodium and water in obese persons

consuming a high or low carbohydrate diet. Ann Nutr Metab (1981)

25(6):341-9

Lambert EV, et al Enhanced endurance in trained cyclists during moderate

intensity exercise following 2 weeks adaptation to a high fat diet. Eur J

Appl Physiol (1994) 69(4):287-293

McCargar LJ, et al Dietary carbohydrate-to-fat ratio: Influence on

while-body nitrogen retention, substrate utilization, and hormone response

in healthy male subjects. Am J Clin Nutr (1989 Jun) 49(6):1169-78

Lopez A, et al Some interesting relationships between dietary

carbohydrates and serum cholesterol. Am J Clin Nutr (1966 Feb)

18(2):149-153

Kasper H, et al Letter: Behavior of body weight under a low carbohydrate,

high fat diet. Am J Clin Nutr (1975 Aug) 28(8): 800-1

Kasper H, et al Response of body weight to a low carbohydrate, high fat

diet in normal and obese subjects. Am J Clin Nutr (1973 Feb) 26(2):197-204

Young CM, et al Effect of body composition and other parameters in obese

young men of carbohydrate level of reduction diet. Am J clin Nutr (1971

Mar) 24(3):290-6

Hodges RE, et al Dietary carbohydrates and low cholesterol diets: effects

on serum lipids on man. Am J Clin Nutr (1967 Feb) 20(2):198-208

Krehl WA, et al Some metabolic changes induced by low carbohydrate diets.

Am J Clin Nutr (1967 Feb) 20(2):139-148

Rosen JC, et al Mood and appetite during minimal-carbohydrate and

carbohydrate-supplemented hypocaloric diets. Am J Clin Nutr (1985 Sep)

42(3):371-9

Tremblay A, et al Diet composition and postexercise energy balance Am J

Clin Nutr (1994 May) 59(5):975-9

Phinney SD, et al Capacity for moderate exercise in obese subjects after

adaptation to a hypocaloric, ketogenic diet. J Clin Invest (1980 Nov)

66(5):1152-61

Yang MU, et al Composition of weight lost during short-term weight

reduction. Metabolic responses of obese subject to starvation and

low-calorie ketogenic and nonketogenic diets. J Clin Invest (1976 Sep)

58(3):722-30

Council on Foods and Nutrition A critiquie of low-carbohydrate ketogenic

weight reduction regimens. A review of Dr. Atkins' diet revolution. JAMA

(1973 Jun 4) 224(10):1415-9

Vazquez JA, et al Protein sparing during treatment of obesity: ketogenic

versus nonketogenic very low calorie diet. Metabolism (1992 Apr)

41(4):406-14

Newbold HL Reducing the serum cholesterol level with a diet high in animal

fat. South Med J (1988 Jan) 81(1):61-3

Kuroshima A, et al Effect of a high-fat diet on metabolic responses to

exercise. Jpn J Physiol (1975) 25(5):575-84

Rabast U, et al Comparative studies in obese subjects fed

carbohydrate-restricted and high carbohydrate 1,000 calorie formula diets.

Nutr Metab (1978) 22(5):269-77

Golay A, et al Similar weight loss with low or high carbohydrate diets. Am

J Clin Nutr (1996 Feb) 63(2):174-8

Kundu SK, Judilla Am Novel solid-phase assay of ketone bodies in urine.

Clin Chem (1991 Sep) 37(9):1565-9

Fery F, et al Hormonal and metabolic changes induced by an isocaloric

isoproteinic ketogenic diet in healthy subjects. Diabete Metab (1982 Dec)

8(4):299-305

Kather H, et al Influences of variation in total energy intake and dietary

consumption on regulation of fat cell lipolysis in ideal weight subjects.

J Clin Invest (1987) 80(2):556-72

Giorski J. Muscle triglyceride metabolism during exercise. Can J Phys

Pharm (1992) 70(1):123-31

Symons JD, et al High-intensity exercise performance is not impaired by

low intramuscular glycogen. Med Sci Sports Exerc (1989) 21(5):550-7

Evans WJ, et al Dietary carbohydrates and endurance exercise. Am J Clin

Nutr (1985) 41(5):1146-54

Mitchell GA, et al Medical aspects of ketone body metabolism. Clin Invest

Med (1995) 18(3):193-216 Rabast U, et al Dietetic treatment of obesity

with low and high carbohydrate diets. Intl J Obesity (1979) 3(3):201-211

Liu VJ, et al Chromium and insulin in young subjects with normal glucose

tolerance. Am J Clin Nutr (1982) 25(4):661-67

Rickman F, et al Changes in serum cholesterol during the Stillman diet.

JAMA (1974) 228:54

Fontbonne A, et al Coronary heart disease mortality risk: plasma insulin

level is a more sensitive marker than hypertension or abnormal glucose

tolerance in overweight males: the Paris prospective study. Intl J Obesity

(1988) 12:557-65

Coulston AM, et al Deleterious metabolic effects of high-carbohydrate,

sucrose-containing diets in patients with non-insulin dependent diabetes

mellitus. Am J Med (1987) 82:213-20

Coulston AM, et al Original articles: persistence of hypertriglyceridemic

effect of low-fat high-carbohydrate diets in NIDDM patients Diabetes Care

1989 12(2):94-101

Stout, RW. Hyperinsulinaemia- a possible risk factor for cardiovascular

disease in diabetes mellitus. Horm Met Res (1985) 15:37-41

Tremblay A, et al Nutritional determinants of the increase in energy

intake associated with a high-fat diet Am J Clin Nutr (1991) 53:1134-37

McGill HC The relationship of dietary cholesterol to serum cholesterol

concentration and to atherosclerosis in man. Am J Clin Nutr (1979)

32:2664-2702

Willett WC, et al Relation of meat, fat and fiber to the risk of colon

cancer in a prospective study among women. NEJM (1990) 323(24):1664-72

Willett WC, et al Original article: dietary fat and the risk of breast

cancer. NEJM (1987) 316(1):22-28 Macquart-Moulin G, et al Case control

study on colorectal cancer and diet in Marseilles. Intl J Cancer (1986)

38(2):183-91

Haenszel W, et al A case-control study of large bowel cancer in Japan. J

National Cancer Institute (1980) 64(1):17-22

Tuyns AJ, et al Colorectal cancer and the intake of nutrients:

oligosaccarides are a risk factor, fats are not. A case-control study in

Belgium. Nutrition and Cancer (1987) 10(4):181-96

:cool: TJ :cool:

[Bathroom is done]

Damn it, now I'm going to have that song running through my head all day.

MUUUUUUAAAAAHHH HA HA HA HA!!

Then my work here is done..

:wink: TJ :wink:

[Bathroom is done]

Ding Bathroom's done

Ding Bathroom's done

DING Bathroom's done

DING Bathrooooooom's doooooooone....

TJ