Re: Exercise aids blood sugar levels

[Guest guest]

Dr. Giarnella:

I read this article with great interest. I was diagnosed last year with type 2

diabetes. Until a week ago my fasting bg was 81 to 84. Then last week it went up

to 100 and the next day 105 and now 121. I know these are low numbers, and after

some research I learned about the effect where the body thinks the bg is too low

so it creates glucose which raises the bg. I understand all that.

One of my rules for losing weight has been to stop eating at least 3 hours

before going to bed. This puts me in a fasting state for about 12 hours. So in

an effort to avoid that morning high, I've added 2 tbsp of all natural peanut

butter before bed.

Okay I said al that to say this: I've been walking on the treadmill 30 minutes a

day, usually around 10:00 am. Now that I have this morning glucose problem, I

thought it might be good to exercise at night. I'm sure I dont' have the energy

to walk 30 minutes twice a day. So here are my questions:

Will 15 or 20 minutes of aerobic activity two times a day work? Does other

exercise, non-aerobic, work as well? If I walked in the morning and did some

other exercise at night--weight training, Tai Chi, Yoga, Isometrics--would this

work?

I realize that every body is different and I might have to experiment, but I was

wondering if you knew of any statistics on the best way to do it. I may be able

to work up to 30 minutes of walking twice a day, but with Fibromyaliga/CFS I

just don't know.

Any input would be appreciated.

Vicki Lockwood

NW Missouri

=================================

Exercise aids blood sugar levels

The following article should be of interest.

Ralph Giarnella MD

Southington Ct USA

***********************************

Exercise aids blood sugar levels

By Nanci Hellmich, USA TODAY

Good news for diabetics: Both aerobic exercise and

strength training improve blood sugar levels. And lots

of both provides the best results, a new study shows.

About 20.8 million people in the USA have diabetes.

Type 2 diabetes - the most common kind - is associated

with obesity, lack of exercise and genetics.

Diabetes is caused by the body's failure to produce

enough insulin or to use it effectively to reduce

blood sugar levels. Over time, high sugar levels

damage large and small blood vessels, leading to heart

disease, stroke, nerve damage, amputations, blindness

and kidney disease.

To test the impact of different types of exercise on

blood sugar control, researchers in Calgary and

Ottawa, Canada, recruited 251 sedentary diabetics,

ages 39 to 70.

Participants were assigned to one of four groups: no

exercise; 45 minutes of aerobic exercise such as

walking or indoor biking three times a week; strength

(resistance or weight) training for 45 minutes three

times a week; aerobics and strength training for 45

minutes each three times a week.

They were given memberships to an exercise facility

and asked to follow their plans for 22 weeks. They

used treadmills and indoor exercise bikes and wore

pedometers to track their activity. Their programs

were periodically supervised by personal trainers.

At three and six months, participants were given a

test that measures hemoglobin A1c, an estimate of the

average blood sugar level over the past three months.

It's expressed in percentages.

A 1 percentage point decrease in this score (for

example, dropping from a 7.5% to a 6.5%) is associated

with a 15% to 20% decrease in the risk of heart

attacks or strokes and a 25% to 40% decrease in risk

of diabetes-related eye or kidney disease.

The American Diabetes Association says people with

diabetes should aim for 7% or less.

The findings in today's ls of Internal Medicine

show:

. The no-exercise group had no change in A1c.

. The aerobic exercise group had an average decrease

of 0.51% in A1c compared with the no-exercise group.

. The strength training group had an average decrease

of 0.38%.

. Participants who did both types of exercise had a

0.97% drop.

. The average A1c for the exercise groups went from

above 7% to at or below 7%; the other group stayed

above 7%.

" This confirms the tremendous value of exercise for

people with type 2 diabetes, and those who want to

maximize the results should do both aerobic exercise

and resistance training, " says lead author

Sigal of an associate professor of medicine, cardiac

sciences and kinesiology at the University of Calgary.

" For people with diabetes, this is spectacular news, "

says Larry Deeb, past president of the American

Diabetes Association. " It shows how important both

kinds of exercise are. Take your pick, and you'll

lower A1c. Exercise can lower blood sugar level almost

as much as any single pill you can take. "

Miriam , an exercise researcher at Tufts

University, says, " If I had type 2 diabetes, I would

be out there doing abundant aerobic activity and

strength training.

***The great thing about aerobic

activity is it burns a lot of calories and improves

the whole vascular system from the heart to the cells.

Strength training makes the muscles stronger and more

sensitive to insulin.***

=======================

[Guest guest]

--- Vicki Lockwood

wrote:

> Dr. Giarnella:

>

> I read this article with great interest. I was

> diagnosed last year with type 2 diabetes. Until a

> week ago my fasting bg was 81 to 84. Then last week

> it went up to 100 and the next day 105 and now 121.

> I know these are low numbers, and after some

> research I learned about the effect where the body

> thinks the bg is too low so it creates glucose which

> raises the bg. I understand all that.

Again congratulations on your persistence with your

exercise program. Re-active hypoglycemia is rather

unusual unless you are using Insulin injections or a

class of medications known as sulfonylureas

(glyburide, glipizide etc).

Reactive hypoglycemia may also occur in situations

where your blood sugar rises to very high levels (

200-300) and your pancreas over reacts causing in turn

your blood glucose to bottom out (below 60) which then

causes a rush of glucagon, adrenaline and cortisol

which will cause your blood sugar to rise again.

The key is to eat frequent small meals with a lower

glycemic index and lower glycemic load.

Sometimes an elevated fasting glucose in the morning

is a result of a very large meal in the evening which

may take 3-6+ hours to digest.

> One of my rules for losing weight has been to stop

> eating at least 3 hours before going to bed. This

> puts me in a fasting state for about 12 hours. So in

> an effort to avoid that morning high, I've added 2

> tbsp of all natural peanut butter before bed.

I don't think that an evening snack is necessary

unless you are taking Insulin or a sulfonylurea

medication.

> Okay I said al that to say this: I've been walking

> on the treadmill 30 minutes a day, usually around

> 10:00 am. Now that I have this morning glucose

> problem, I thought it might be good to exercise at

> night. I'm sure I dont' have the energy to walk 30

> minutes twice a day. So here are my questions:

I would recommend that you continue to exercise in the

morning (as early as you can- even before breakfast).

This will lower your morning glucose level.

> Will 15 or 20 minutes of aerobic activity two times

> a day work? Does other exercise, non-aerobic, work

> as well? If I walked in the morning and did some

> other exercise at night--weight training, Tai Chi,

> Yoga, Isometrics--would this work?

Studies have been cited in this forum in the past

which have shown that 10-15 minutes of exercise 2-3

times daily is as good if not better than one

continuous bout of exercise of 30-45 minutes.

Any exercise that you enjoy doing will work. An after

supper walk in the park even at a leisurely pace would

be very helpful. I would avoid excessively intense

exercise in the hour prior to bedtime since this may

make it more difficult to sleep.

> I realize that every body is different and I might

> have to experiment, but I was wondering if you knew

> of any statistics on the best way to do it. I may

> be able to work up to 30 minutes of walking twice a

> day, but with Fibromyaliga/CFS I just don't know.

> Any input would be appreciated.

Exercise of moderate intensity will help with you with

fibromyalgia/CFS.

I think that it is important to realize that

Fibromyalgia and CFS are neurological diseases and not

muscular diseases.

> Vicki Lockwood

> NW Missouri

Best of luck and keep on exercising.

Ralph Giarnella MD

Southington Ct USA

[Guest guest]

Ralph,

Here is some further information on this topic.

http://www.cumc.columbia.edu/news/press_releases/karsenty_cell_osteocalcin_endoc\

rine.html

<<<NEW YORK – Bones are typically thought of as calcified, inert structures, but

researchers at Columbia University Medical Center have now identified a

surprising and critically important novel function of the skeleton. They’ve

shown for the first time that the skeleton is an endocrine organ that helps

control our sugar metabolism and weight and, as such, is a major determinant of

the development of type 2 diabetes.

The research, published in the August 10 issue of Cell, demonstrates that bone

cells release a hormone called osteocalcin, which controls the regulation of

blood sugar (glucose) and fat deposition through synergistic mechanisms

previously not recognized. Usually, an increase in insulin secretion is

accompanied by a decrease in insulin sensitivity. Osteocalcin, however,

increases both the secretion and sensitivity of insulin, in addition to boosting

the number of insulin-producing cells and reducing stores of fat.

In this published research, authors show that an increase in osteocalcin

activity prevents the development of type 2 diabetes and obesity in mice. This

discovery potentially opens the door for novel therapeutic avenues for the

prevention and treatment of type 2 diabetes.

“The discovery that our bones are responsible for regulating blood sugar in ways

that were not known before completely changes our understanding of the function

of the skeleton and uncovers a crucial aspect of energy metabolism,” said Gerard

Karsenty, M.D., Ph.D., chair of the department of Genetics and Development at

Columbia University Medical Center, Marks Professor in the Basic Sciences,

and senior author of the paper. “These results uncover an important aspect of

endocrinology that was unappreciated until now.”

Karsenty and his colleagues had previously shown that leptin, a hormone released

by fat cells, acts upon and ultimately controls bone mass. They reasoned that

bones must in turn communicate with fat, so they searched bone-forming cells for

molecules that could potentially send signals back to fat cells.

The researchers found that osteocalcin, a protein made only by bone-forming

cells (osteoblasts), was not a mere structural protein, but rather a hormone

with totally unanticipated and crucial functions. Osteocalcin directs the

pancreas’ beta cells, which produce the body’s supply of insulin, to produce

more insulin. At the same time, osteocalcin directs fat cells to release a

hormone called adiponectin, which improves insulin sensitivity. This discovery

showed for the first time that one hormone has a synergistic function in

regulating insulin secretion and insulin sensitivity, and that this coordinating

signal comes from the skeleton. Additionally, osteocalcin enhances the

production of insulin-producing beta cells, which is considered one of the best,

but currently unattainable, strategies to treat diabetes.

People with type 2 diabetes have been shown to have low osteocalcin levels,

suggesting that altering the activity of this molecule could be an effective

therapy. That hypothesis is supported by the Columbia research, which showed

that mice with high levels of osteocalcin activity were prevented from gaining

weight or becoming diabetic even when they ate a high fat diet. Analysis of mice

lacking the osteocalcin protein showed that they had type 2 diabetes, increased

fat mass, a decrease in insulin and adiponectin expression, and decreased

beta-cell proliferation.

This research was supported by the National Institutes of Health, the American

Diabetes Association, the Japan Society for the Promotion of Science, and the

Pennsylvania Department of Health.

The researchers are now examining the role of osteocalcin in the regulation of

blood sugar in humans and are continuing investigations into the relationship

between osteocalcin and the appearance of type 2 diabetes and obesity.>>>

================

Sharah

Sydney Australia

[Guest guest]

Fascinating. So perhaps exercise in some measure helps (undoubtedly

along with many other positive factors) stimulate the production of

osteocalcin. It's one thing to know that exercise helps with certain

conditions, but it is wonderful finding out the mechanisms behind it,

not to mention their complexity.

Burns

Vancouver, Canada

>

> Ralph,

>

> Here is some further information on this topic.

>

>

http://www.cumc.columbia.edu/news/press_releases/karsenty_cell_osteocalcin_endoc\

rine.html

>

> <<<NEW YORK – Bones are typically thought of as calcified, inert

structures, but researchers at Columbia University Medical Center have

now identified a surprising and critically important novel function of

the skeleton. They've shown for the first time that the skeleton is an

endocrine organ that helps control our sugar metabolism and weight

and, as such, is a major determinant of the development of type 2

diabetes.

> The research, published in the August 10 issue of Cell, demonstrates

that bone cells release a hormone called osteocalcin, which controls

the regulation of blood sugar (glucose) and fat deposition through

synergistic mechanisms previously not recognized. Usually, an increase

in insulin secretion is accompanied by a decrease in insulin

sensitivity. Osteocalcin, however, increases both the secretion and

sensitivity of insulin, in addition to boosting the number of

insulin-producing cells and reducing stores of fat.

> In this published research, authors show that an increase in

osteocalcin activity prevents the development of type 2 diabetes and

obesity in mice. This discovery potentially opens the door for novel

therapeutic avenues for the prevention and treatment of type 2 diabetes.

> " The discovery that our bones are responsible for regulating blood

sugar in ways that were not known before completely changes our

understanding of the function of the skeleton and uncovers a crucial

aspect of energy metabolism, " said Gerard Karsenty, M.D., Ph.D., chair

of the department of Genetics and Development at Columbia University

Medical Center, Marks Professor in the Basic Sciences, and senior

author of the paper. " These results uncover an important aspect of

endocrinology that was unappreciated until now. "

>

> Karsenty and his colleagues had previously shown that leptin, a

hormone released by fat cells, acts upon and ultimately controls bone

mass. They reasoned that bones must in turn communicate with fat, so

they searched bone-forming cells for molecules that could potentially

send signals back to fat cells.

> The researchers found that osteocalcin, a protein made only by

bone-forming cells (osteoblasts), was not a mere structural protein,

but rather a hormone with totally unanticipated and crucial functions.

Osteocalcin directs the pancreas' beta cells, which produce the body's

supply of insulin, to produce more insulin. At the same time,

osteocalcin directs fat cells to release a hormone called adiponectin,

which improves insulin sensitivity. This discovery showed for the

first time that one hormone has a synergistic function in regulating

insulin secretion and insulin sensitivity, and that this coordinating

signal comes from the skeleton. Additionally, osteocalcin enhances the

production of insulin-producing beta cells, which is considered one of

the best, but currently unattainable, strategies to treat diabetes.

> People with type 2 diabetes have been shown to have low osteocalcin

levels, suggesting that altering the activity of this molecule could

be an effective therapy. That hypothesis is supported by the Columbia

research, which showed that mice with high levels of osteocalcin

activity were prevented from gaining weight or becoming diabetic even

when they ate a high fat diet. Analysis of mice lacking the

osteocalcin protein showed that they had type 2 diabetes, increased

fat mass, a decrease in insulin and adiponectin expression, and

decreased beta-cell proliferation.

> This research was supported by the National Institutes of Health,

the American Diabetes Association, the Japan Society for the Promotion

of Science, and the Pennsylvania Department of Health.

> The researchers are now examining the role of osteocalcin in the

regulation of blood sugar in humans and are continuing investigations

into the relationship between osteocalcin and the appearance of type 2

diabetes and obesity.>>>

>

> ================

> Sharah

> Sydney Australia

>