gall stones and metabolic syndrome [STOOL TALK ALERT!]

[Guest guest]

http://www.ajcn.org/cgi/content/full/80/1/1

isn't that interesting? so this whole liver/gallbladder thing is pretty serious.

yeah, there's always the curezone place to provide us with the

up-close-and-personal views to what may lurk within our tortured bodies.

i heard someone say that they didn't approve of the extreme nature of these

" cleanses " . well, i didn't like the cleanses either, and i remember i was very

productive as an insane vegetarian out of control falling to the majesty of my

higher self (who had to retreat into inhabiting my physical body, the coarsest,

lowest level fo existence). it was those huge intakes of tahini (sesame nut

paste) after the apples... those 2-3 granny smith apples. yes. smith changed me,

i learned something from them. i used those fun, cleansing indian herbs and all

that, the cloves, cardamom, coriander, the raw ginger and cayenne pepper... they

all had some part to play, but it was really all that malic acid and the 5000+

constituents in those raw, blended, sub-acid apple concoctions... those crazy

vegetarian cleansing concoctions... followed by all that fat, so much, really,

very drastic follow-up meal. god bless my starving body's many cries for

methionine... i ended up discharging all sorts of flak during two of those

days... weird, messy poopies. but that was life as a planet-saving vegetarian.

sure is interesting, eh? to imagine people can hold that much weird s__t in

their bodies and not even know it.

Cholesterol gallstones: a fellow traveler with metabolic syndrome?

M Grundy

1 From the Center for Human Nutrition and Departments of Clinical Nutrition and

Internal Medicine, University of Texas Southwestern Medical Center, Dallas

See corresponding article on page 38

2 Reprints not available. Address correspondence to SM Grundy, Center for Human

Nutrition, Department of Clinical Nutrition, University of Texas Southwestern

Medical Center, 5323 Harry Hines Boulevard, Room Y3-206, Dallas, TX 75390-9052.

E-mail: scott.grundy@....

INTRODUCTION

Obesity is accompanied by many medical complications. Foremost among these is

atherosclerotic cardiovascular disease. The term metabolic syndrome is often

used to denote the multiple metabolic risk factors that accompany obesity and

increase the risk of atherosclerotic cardiovascular disease (1). Risk factors

for the metabolic syndrome include atherogenic dyslipidemia, elevated blood

pressure, hyperglycemia, a prothrombotic state, and a proinflammatory state.

Persons with the metabolic syndrome are also at increased risk of developing

type 2 diabetes because most of them have insulin resistance, which is a major

risk factor for diabetes. In addition to atherosclerotic cardiovascular disease

and diabetes, persons with the metabolic syndrome are more likely to have fatty

liver and its complications, nonalcoholic steatohepatitis, and cryptogenic

cirrhosis. Finally, persons with the metabolic syndrome may be susceptible to

yet another complication, namely, cholesterol gallstones.

OBESITY AND CHOLESTEROL GALLSTONES

A relation between obesity and cholesterol gallstones is well recognized. Obese

women are more likely to develop gallstones than are obese men (2). In the past,

our laboratory focused on the mechanisms whereby obesity increases the risk of

developing gallstones (3, 4). The bile in obese persons is more lithogenic than

is that in nonobese persons, ie, the bile of obese persons has a high ratio of

cholesterol to solubilizing lipids (bile acids and phospholipids). This high

ratio predisposes to crystallization of cholesterol and gallstone formation. The

primary reason for lithogenic bile in obese persons is an increase in total body

synthesis of cholesterol. The metabolic basis for this increase remains to be

elucidated. A likely prime mechanism is overloading of tissues with fatty acids,

which provide precursors for cholesterol synthesis. Other adipose tissue-derived

substances, which are produced in excess in obesity, may further contribute to

overproduction of cholesterol. As a result of this overproduction, cholesterol

secretion into bile increases. In many obese persons, the amounts of cholesterol

entering the bile exceed the solubilizing capacity of the bile acids and

phospholipids. Both obese women and obese men synthesize increased amounts of

cholesterol and secrete more cholesterol into bile than do nonobese persons (5).

Obese men generally secrete more bile acids and phospholipids into bile than do

obese women; consequently, the bile of obese men is less lithogenic, and they

have fewer gallstones.

INDICATORS OF OBESITY

The precise relation between obesity and gallstones, however, remains undefined.

To understand the relation, an important question must be answered: what is

obesity? A simple definition is an excess of total body fat. One proposed simple

definition is a body fat content of >25% in men and >33% in women (6). Because

the measurement of percentage of body fat requires special methodology, both

clinical evaluation and epidemiologic studies use surrogate indicators (7). One

such indicator is body mass index (BMI), which is weight (in kg) divided by

height (in m) squared. The correlation between BMI and percentage of body fat is

positive but by no means perfect. The correlation is higher in women than in

men. In men, waist circumference appears to be a better indicator of total body

fat than is BMI (7), because waist circumference is strongly determined by fat

in the upper body and because men have a tendency to deposit fat in the upper

body.

BODY FAT DISTRIBUTION IN OBESE PERSONS

Two commonly identified patterns of obesity are lower body obesity and upper

body obesity. In the former, excess fat predominantly accumulates subcutaneously

in the gluteofemoral region; in the latter, fat accumulates predominantly in the

trunk. The adipose tissue in the trunk occurs in several compartments: truncal

subcutaneous, intraperitoneal (visceral), and retroperitoneal (8). When women

first become obese, they generally show the pattern of lower body obesity; as

obesity increases, excess fat also begins to accumulate in the trunk. Less

commonly, women have upper body obesity without excess lower body fat. Most, but

not all, obese men show the pattern of upper body obesity from the start. In

most cases of upper body obesity, excess fat is located predominantly in the

subcutaneous region. In some obese men, however, there can be a disproportionate

accumulation of fat intraperitoneally. The latter has been called visceral

obesity. This term is often misapplied because persons with predominant upper

body subcutaneous obesity are mistakenly said to have visceral obesity (9). The

term upper body obesity, which refers to all the fat in the trunk, is

preferable. An alternative name for upper body obesity is abdominal obesity (7).

The latter name has 2 practical advantages: 1) the presence of excess truncal

fat is more noticeable around the waist than around the chest, and 2) simple

measurement of waist circumference is a good indicator of upper body fat.

UPPER BODY OBESITY AND METABOLIC DISORDERS

Abdominal obesity is a characteristic feature of the metabolic syndrome (1).

Because the presence of abdominal obesity indicates an increase in total body

fat in men and in very obese women, some investigators believe that BMI, which

is another measure of total body fat, provides the same predictive information

for the metabolic complications of obesity that measures of abdominal obesity

provide (10). The consensus view, however, is that waist circumference, which is

an indicator of abdominal fat, provides predictive power for metabolic

complications beyond that provided by BMI (1, 7). Some investigators hypothesize

that the visceral component of abdominal obesity is the major determinant of

metabolic complications. Others contend that total abdominal fat is more telling

than is visceral fat alone (9). Regardless of which view is correct, the

literature seems to suggest that upper body fat is more bioactive than is lower

body fat. This bioactivity includes increased production of nonesterified fatty

acids, inflammatory cytokines, leptin, and prothrombotic factors and decreased

production of adiponectin, a putative protective adipokine. Thus, if upper body

adipose tissue is the predominant source of these bioactive products, then it

may be the major cause of the higher prevalence of metabolic complications in

obese persons than in nonobese persons. The report by Tsai et al (11) in this

issue of the Journal that abdominal obesity is a stronger predictor of

gallstones in men than is BMI is consistent with the concept that upper body

adipose tissue is a major cause of metabolic complications. Still, whether the

greater predictive power of upper body fat relates to unique metabolic features

of this type of adipose tissue or just to the fact that waist circumference in

men is a better indictor of total body fat than is BMI is unclear. In any case,

the association between abdominal obesity and gallstone formation represents an

additional complication that appears to be associated with the metabolic

syndrome. It would be interesting to know how well the incidence of gallstone

disease correlates with other components of the metabolic syndrome.

REFERENCES

1.. National Cholesterol Education Program (NCEP) Expert Panel on Detection,

Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment

Panel III). Third Report of the National Cholesterol Education Program (NCEP)

Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol

in Adults (Adult Treatment Panel III) final report. Circulation

2002;106:3143-421.[Free Full Text]

2.. Kern F Jr, Erfling W, Braverman D. Why more women than men have

cholesterol gallstones: studies of biliary lipids in pregnancy. Trans Am Clin

Climatol Assoc 1979;90:71-5.[Medline]

3.. Grundy SM, Metzger AL, Adler RD. Mechanisms of lithogenic bile formation

in American Indian women with cholesterol gallstones. J Clin Invest

1972;51:3026-43.[Medline]

4.. Grundy SM, Duane WC, Adler RD, Aron JM, Metzger AL. Biliary lipid outputs

in young women with cholesterol gallstones. Metabolism 1974;23:67-73.[Medline]

5.. Bennion LJ, Grundy SM. Effects of obesity and caloric intake on biliary

lipid metabolism in man. J Clin Invest 1975;56:996-1011.[Medline]

6.. Bray GA. Contemporary diagnosis and management of obesity. Newton, PA:

Handbooks in Healthcare, 1998.

7.. Clinical Guidelines on the Identification, Evaluation, and Treatment of

Overweight and Obesity in Adults-The Evidence Report. National Institutes of

Health. Obes Res 1998;6(suppl):51S-209S. (Published erratum appears in Obes Res

1998;6:464.)[Medline]

8.. Abate N, Burns D, Peshock RM, Garg A, Grundy SM. Estimation of adipose

tissue mass by magnetic resonance imaging: validation against dissection in

human cadavers. J Lipid Res 1994;35:1490-6.[Abstract]

9.. Abate N, Garg A, Peshock RM, Stray-Gundersen J, Grundy SM. Relationships

of generalized and regional adiposity to insulin sensitivity in men. J Clin

Invest 1995;96:88-98.[Medline]

10.. Abbasi F, Brown BW Jr, Lamendola C, McLaughlin T, Reaven GM. Relationship

between obesity, insulin resistance, and coronary heart disease risk. J Am Coll

Cardiol 2002;40:937-43.[Medline]

11.. Tsai C-J, Leitzmann MF, Willett WC, Giovannucci EL. Prospective study of

abdominal adiposity and gallstone disease in US men. Am J Clin Nutr

2004;80:38-44.[Abstract/Free Full Text]

[Guest guest]

I was probably the chicken about extreme cleanses. I don't know if I

meant approve, I just won't do them myself. If I had serious

digestive issues I'd probably change my mind. I actually finished a

mini 3-day detox yesterday. I can't say I feel incredibly better,

but I was surprised that I wasn't hungry with the reduction in normal

food intake. I only had 2 tbsp. of oil per day, still much more than

I normally consume.

> http://www.ajcn.org/cgi/content/full/80/1/1

>

> isn't that interesting? so this whole liver/gallbladder thing is

pretty serious. yeah, there's always the curezone place to provide us

with the up-close-and-personal views to what may lurk within our

tortured bodies.

>

> i heard someone say that they didn't approve of the extreme nature

of these " cleanses " . well, i didn't like the cleanses either, and i

remember i was very productive as an insane vegetarian out of control

falling to the majesty of my higher self (who had to retreat into

inhabiting my physical body, the coarsest, lowest level fo

existence). it was those huge intakes of tahini (sesame nut paste)

after the apples... those 2-3 granny smith apples. yes. smith changed

me, i learned something from them. i used those fun, cleansing indian

herbs and all that, the cloves, cardamom, coriander, the raw ginger

and cayenne pepper... they all had some part to play, but it was

really all that malic acid and the 5000+ constituents in those raw,

blended, sub-acid apple concoctions... those crazy vegetarian

cleansing concoctions... followed by all that fat, so much, really,

very drastic follow-up meal. god bless my starving body's many cries

for methionine... i ended up discharging all sorts of flak during two

of those days... weird, messy poopies. but that was life as a planet-

saving vegetarian.

>

> sure is interesting, eh? to imagine people can hold that much weird

s__t in their bodies and not even know it.

>

> Cholesterol gallstones: a fellow traveler with metabolic syndrome?

> M Grundy

> 1 From the Center for Human Nutrition and Departments of Clinical

Nutrition and Internal Medicine, University of Texas Southwestern

Medical Center, Dallas

>

> See corresponding article on page 38

>

> 2 Reprints not available. Address correspondence to SM Grundy,

Center for Human Nutrition, Department of Clinical Nutrition,

University of Texas Southwestern Medical Center, 5323 Harry Hines

Boulevard, Room Y3-206, Dallas, TX 75390-9052. E-mail:

scott.grundy@u...

>

>

> INTRODUCTION

>

> Obesity is accompanied by many medical complications. Foremost

among these is atherosclerotic cardiovascular disease. The term

metabolic syndrome is often used to denote the multiple metabolic

risk factors that accompany obesity and increase the risk of

atherosclerotic cardiovascular disease (1). Risk factors for the

metabolic syndrome include atherogenic dyslipidemia, elevated blood

pressure, hyperglycemia, a prothrombotic state, and a proinflammatory

state. Persons with the metabolic syndrome are also at increased risk

of developing type 2 diabetes because most of them have insulin

resistance, which is a major risk factor for diabetes. In addition to

atherosclerotic cardiovascular disease and diabetes, persons with the

metabolic syndrome are more likely to have fatty liver and its

complications, nonalcoholic steatohepatitis, and cryptogenic

cirrhosis. Finally, persons with the metabolic syndrome may be

susceptible to yet another complication, namely, cholesterol

gallstones.

>

> OBESITY AND CHOLESTEROL GALLSTONES

>

> A relation between obesity and cholesterol gallstones is well

recognized. Obese women are more likely to develop gallstones than

are obese men (2). In the past, our laboratory focused on the

mechanisms whereby obesity increases the risk of developing

gallstones (3, 4). The bile in obese persons is more lithogenic than

is that in nonobese persons, ie, the bile of obese persons has a high

ratio of cholesterol to solubilizing lipids (bile acids and

phospholipids). This high ratio predisposes to crystallization of

cholesterol and gallstone formation. The primary reason for

lithogenic bile in obese persons is an increase in total body

synthesis of cholesterol. The metabolic basis for this increase

remains to be elucidated. A likely prime mechanism is overloading of

tissues with fatty acids, which provide precursors for cholesterol

synthesis. Other adipose tissue-derived substances, which are

produced in excess in obesity, may further contribute to

overproduction of cholesterol. As a result of this overproduction,

cholesterol secretion into bile increases. In many obese persons, the

amounts of cholesterol entering the bile exceed the solubilizing

capacity of the bile acids and phospholipids. Both obese women and

obese men synthesize increased amounts of cholesterol and secrete

more cholesterol into bile than do nonobese persons (5). Obese men

generally secrete more bile acids and phospholipids into bile than do

obese women; consequently, the bile of obese men is less lithogenic,

and they have fewer gallstones.

>

> INDICATORS OF OBESITY

>

> The precise relation between obesity and gallstones, however,

remains undefined. To understand the relation, an important question

must be answered: what is obesity? A simple definition is an excess

of total body fat. One proposed simple definition is a body fat

content of >25% in men and >33% in women (6). Because the measurement

of percentage of body fat requires special methodology, both clinical

evaluation and epidemiologic studies use surrogate indicators (7).

One such indicator is body mass index (BMI), which is weight (in kg)

divided by height (in m) squared. The correlation between BMI and

percentage of body fat is positive but by no means perfect. The

correlation is higher in women than in men. In men, waist

circumference appears to be a better indicator of total body fat than

is BMI (7), because waist circumference is strongly determined by fat

in the upper body and because men have a tendency to deposit fat in

the upper body.

>

> BODY FAT DISTRIBUTION IN OBESE PERSONS

>

> Two commonly identified patterns of obesity are lower body obesity

and upper body obesity. In the former, excess fat predominantly

accumulates subcutaneously in the gluteofemoral region; in the

latter, fat accumulates predominantly in the trunk. The adipose

tissue in the trunk occurs in several compartments: truncal

subcutaneous, intraperitoneal (visceral), and retroperitoneal (8).

When women first become obese, they generally show the pattern of

lower body obesity; as obesity increases, excess fat also begins to

accumulate in the trunk. Less commonly, women have upper body obesity

without excess lower body fat. Most, but not all, obese men show the

pattern of upper body obesity from the start. In most cases of upper

body obesity, excess fat is located predominantly in the subcutaneous

region. In some obese men, however, there can be a disproportionate

accumulation of fat intraperitoneally. The latter has been called

visceral obesity. This term is often misapplied because persons with

predominant upper body subcutaneous obesity are mistakenly said to

have visceral obesity (9). The term upper body obesity, which refers

to all the fat in the trunk, is preferable. An alternative name for

upper body obesity is abdominal obesity (7). The latter name has 2

practical advantages: 1) the presence of excess truncal fat is more

noticeable around the waist than around the chest, and 2) simple

measurement of waist circumference is a good indicator of upper body

fat.

>

> UPPER BODY OBESITY AND METABOLIC DISORDERS

>

> Abdominal obesity is a characteristic feature of the metabolic

syndrome (1). Because the presence of abdominal obesity indicates an

increase in total body fat in men and in very obese women, some

investigators believe that BMI, which is another measure of total

body fat, provides the same predictive information for the metabolic

complications of obesity that measures of abdominal obesity provide

(10). The consensus view, however, is that waist circumference, which

is an indicator of abdominal fat, provides predictive power for

metabolic complications beyond that provided by BMI (1, 7). Some

investigators hypothesize that the visceral component of abdominal

obesity is the major determinant of metabolic complications. Others

contend that total abdominal fat is more telling than is visceral fat

alone (9). Regardless of which view is correct, the literature seems

to suggest that upper body fat is more bioactive than is lower body

fat. This bioactivity includes increased production of nonesterified

fatty acids, inflammatory cytokines, leptin, and prothrombotic

factors and decreased production of adiponectin, a putative

protective adipokine. Thus, if upper body adipose tissue is the

predominant source of these bioactive products, then it may be the

major cause of the higher prevalence of metabolic complications in

obese persons than in nonobese persons. The report by Tsai et al (11)

in this issue of the Journal that abdominal obesity is a stronger

predictor of gallstones in men than is BMI is consistent with the

concept that upper body adipose tissue is a major cause of metabolic

complications. Still, whether the greater predictive power of upper

body fat relates to unique metabolic features of this type of adipose

tissue or just to the fact that waist circumference in men is a

better indictor of total body fat than is BMI is unclear. In any

case, the association between abdominal obesity and gallstone

formation represents an additional complication that appears to be

associated with the metabolic syndrome. It would be interesting to

know how well the incidence of gallstone disease correlates with

other components of the metabolic syndrome.

>

> REFERENCES

>

>

> 1.. National Cholesterol Education Program (NCEP) Expert Panel on

Detection, Evaluation, and Treatment of High Blood Cholesterol in

Adults (Adult Treatment Panel III). Third Report of the National

Cholesterol Education Program (NCEP) Expert Panel on Detection,

Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult

Treatment Panel III) final report. Circulation 2002;106:3143-421.

[Free Full Text]

> 2.. Kern F Jr, Erfling W, Braverman D. Why more women than men

have cholesterol gallstones: studies of biliary lipids in pregnancy.

Trans Am Clin Climatol Assoc 1979;90:71-5.[Medline]

> 3.. Grundy SM, Metzger AL, Adler RD. Mechanisms of lithogenic

bile formation in American Indian women with cholesterol gallstones.

J Clin Invest 1972;51:3026-43.[Medline]

> 4.. Grundy SM, Duane WC, Adler RD, Aron JM, Metzger AL. Biliary

lipid outputs in young women with cholesterol gallstones. Metabolism

1974;23:67-73.[Medline]

> 5.. Bennion LJ, Grundy SM. Effects of obesity and caloric intake

on biliary lipid metabolism in man. J Clin Invest 1975;56:996-1011.

[Medline]

> 6.. Bray GA. Contemporary diagnosis and management of obesity.

Newton, PA: Handbooks in Healthcare, 1998.

> 7.. Clinical Guidelines on the Identification, Evaluation, and

Treatment of Overweight and Obesity in Adults-The Evidence Report.

National Institutes of Health. Obes Res 1998;6(suppl):51S-209S.

(Published erratum appears in Obes Res 1998;6:464.)[Medline]

> 8.. Abate N, Burns D, Peshock RM, Garg A, Grundy SM. Estimation

of adipose tissue mass by magnetic resonance imaging: validation

against dissection in human cadavers. J Lipid Res 1994;35:1490-6.

[Abstract]

> 9.. Abate N, Garg A, Peshock RM, Stray-Gundersen J, Grundy SM.

Relationships of generalized and regional adiposity to insulin

sensitivity in men. J Clin Invest 1995;96:88-98.[Medline]

> 10.. Abbasi F, Brown BW Jr, Lamendola C, McLaughlin T, Reaven GM.

Relationship between obesity, insulin resistance, and coronary heart

disease risk. J Am Coll Cardiol 2002;40:937-43.[Medline]

> 11.. Tsai C-J, Leitzmann MF, Willett WC, Giovannucci EL.

Prospective study of abdominal adiposity and gallstone disease in US

men. Am J Clin Nutr 2004;80:38-44.[Abstract/Free Full Text]

>

>

>

>

[Guest guest]

In a message dated 7/22/2004 11:17:50 AM Eastern Daylight Time,

cherylhcmba@... writes:

I was probably the chicken about extreme cleanses. I don't know if I

meant approve, I just won't do them myself.

I'm leaning the same way. I've taken an expensive naturopath's cleanse that

turned my intestines into an open sore (better that TV. It had all of my

attention!) and I've done the liver cleanse that resulted in very few stones. I

actually didn't feel better either and it took me a couple of days to recover

in each case. Strict adherence to the BTD will cleanse the body slowly and

naturally. I think cleanses are good for people who are really sick and need to

immediately flush their systems but as a preventative I feel like they do

nothing for me. Your thoughts?

[Guest guest]

I at least agree. I mainly did this baby detox to get myself back on

track. I modified it so there was nothing incompatible with BTD.

With all the controversy around the Gittleman books, I did her 3-day

summer detox for women. No harm done, but I spent $16 for pure

organic cranberry juice alone, which is only a neutral for me. 2

glasses a day with some kind of green powder, I used Kyo-green and a

fiber supplement, I used Konsyl. In the future I'd use harmonia and

larch, but this was kind of an impulse thing so couldn't get those in

a hurry. 1 tbsp. each of flaxseed oil and olive oil per day, 8 0z.

lean protein, some protein powder or eggs with breakfast, I used O

protein, 3 fruit servings, veggies fill out most of the food. 8 cups

of filtered water, rose hips tea, hawthorn berry tea and licorice tea

filled out the plan. I had one green tea per day, not on her plan,

but OK. She's big on sauerkraut which I didn't use. It was supposed

to be a source of L. plantarum which is not even beneficial for O's.

I think it's in the A probiotic. I would probably use the O

probiotic instead if I did this again. This particular detox was

supposed to target the heart and small intestines which she said are

stressed during the summer, based on traditional chinese medicine.

The summer detox emphasizes " cooling " foods which we also do not

really need. I missed out on many of the beneficials that I would

normally have.

I did drop a lot of fluid from my recent wheat indulgences, but just

getting back to BTD would have done the same thing. I only did this

because it was conservative with a good amount of food and protein.

I was so glad to have back my ghee, salt, green teas and nuts today.

It was however probably the cleanest I've eaten, so maybe it will

improve my BTD compliance.

I will try the D'Adamo detox sometime, supplements and saunas,

wouldn't that be great.

> In a message dated 7/22/2004 11:17:50 AM Eastern Daylight Time,

> cherylhcmba@y... writes:

> I was probably the chicken about extreme cleanses. I don't know if

I

> meant approve, I just won't do them myself.

>

> I'm leaning the same way. I've taken an expensive naturopath's

cleanse that

> turned my intestines into an open sore (better that TV. It had all

of my

> attention!) and I've done the liver cleanse that resulted in very

few stones. I

> actually didn't feel better either and it took me a couple of days

to recover

> in each case. Strict adherence to the BTD will cleanse the body

slowly and

> naturally. I think cleanses are good for people who are really

sick and need to

> immediately flush their systems but as a preventative I feel like

they do

> nothing for me. Your thoughts?

>

>

>