Prayer
Holy Quran said
in
[ Women
verses]
[103]
When ye pass (congregational) prayers, celebrate Allah's praises, standing,
sitting down, or lying down on your sides; but when ye are free from danger, set
up regular prayers: for such prayers are enjoined on Believers at stated times.
Narrated Jabir bin `Abdullah:
The
Prophet used to pray the Zuhr at midday, and the `Asr at a time when the sun was
still bright, the Maghrib after sunset (at its stated time) and the `Isha at a
variable time. Whenever he saw the people assembled (for `Isha' prayer) he would
pray earlier and if the people delayed, he would delay the prayer. And they or
the Prophet used to offer the
Fajr Prayers when it still dark.
1.536:
Narrated Salama:
We used
to pray the Maghrib prayer with the Prophet when the sun disappeared from the
horizon
Narrated Abu Huraira:
Allah's
Apostle said, "The prayer of a person who does Hadath (passes urine, stool or
wind) is not accepted till he performs the ablution." A person from Hadaramout
asked Abu Huraira, "What is 'Hadath'?" Abu
Huraira replied, " 'Hadath' means the passing of wind
1.146:
Narrated Abu Aiyub Al-Ansari:
Allah's
Apostle said, "If anyone of you goes to an open space for
answering the call of nature he should neither face nor turn his back towards
the Qibla; he should either face the east or the west
Holy Quran said
in
[ Women
verses]
[43] O
ye who believe! approach not prayers with a mind befogged, until ye can
understand all that ye say, nor in a state of ceremonial impurity (except when
travelling on the road), until after washing your whole body. If ye are ill, or
on a journey, or one of you cometh from offices of nature, or ye have been in
contact with women, and ye find no water, then take for yourselves clean sand or
earth, and rub therewith your faces and hands. For Allah doth blot out sins and
forgive again and again
3.155:
Narrated Humran:
I saw
`Uthman performing ablution; he washed his hands thrice, rinsed his mouth and
then washed his nose, by putting water in it and then blowing it out, and washed
his face thrice, and then washed his right forearm up to the elbow thrice, and
then the left-forearm up to the elbow thrice, then smeared his head with water,
washed his right foot thrice, and then his left foot thrice and said, "I saw
Allah's Apostle performing ablution similar to my present ablution, and then he
said, 'Whoever performs ablution like my present ablution and then offers two
rak`at in which he does not think of worldly things, all his previous sins will
be forgiven
@Book 4,
Number 1142:
Ibn
'Umar reported: The Messenuer of Allah (may peace be upon him) said: He who eats
of this (offensive) plant must not approach our mosque, till its odour dies:
(plant signifies) garlic .
@Book 4,
Number 1134:
Anas b.
Malik reported the Apostle of Allah (may peace be upon him)
saying: When the supper is brought and the prayer begins, one, should first take
food
: WHEN
FOOD IS BROUGHT BEFORE A MAN AND HE IS INCLINED TO TAKE IT, HE SHOULD NOT SAY
PRAYER BEFORE EATING IT AND UNDESIRABILITY OF PRAYING WHILE FEELING THE CALL OF
NATURE
Book 3,
Number 0662:
Mu'adha
said: I asked 'A'isha: What is the reason that a menstruating woman completes
the fasts (that she abandons during her monthly course). but she does not
complete the prayers? She (Hadrat 'A'isha) said: Are you a Haruriya? I said: I
am not a Haruriya, but I simply want to inquire. She said: We passed through
this (period of menstruation), and we were ordered complete the prayers ..
@Book 4,
Number 1401:
Abu
Musa reported Allah's Messenger (may peace be upon him) as saying: The most
eminent among human beings (as a recipient of)
reward (is one) who lives farthest away, and who has to walk the farthest
distance, and he who waits for the prayer to observe it along with the Imam, his
reward is greater than one who prays (alone) and then goes to sleep. In the
narration of Abu Kuraib (the words are):" (He waits) till he prays along with
the Imam in congregation
[149]
From whencesoever thou startest forth turn thy face in the direction of the
Sacred Mosque; that is indeed the truth from thy Lord. And Allah is not
unmindful of what ye do.
Narrated Abu Huraira:
Once
the Prophet entered the mosque, a man came in, offered the prayer and
greeted
the Prophet. The Prophet returned his greeting and said to him, "Go back and
pray again for you have not prayed." The man offered the prayer again, came back
and greeted the Prophet. He said to him thrice, "Go back and pray again for you
have not
prayed." The man said, "By Him Who has sent you with the truth! I do not know a
better way of praying. Kindly teach Me how to pray." He said, "When you stand
for the prayer, say Takbir and then recite from the Qur'an what you know and
then bow with calmness till you feel at ease, then rise from bowing till you
stand straight. Afterwards prostrate calmly till you feel at ease and then raise
(your head) and sit with Calmness till you feel at ease and then prostrate with
calmness till you feel at ease in prostration and do the same in the whole of
your prayer."
Consensus Development Conference on Insulin Resistance
The
possibility that there can be defects in the sensitivity of tissues
to insulin action in people with diabetes was first reported nearly 50 years ago
. Since then many investigators have described, with increasing detail, the
pathogenesis and consequences of what has become known as "insulin resistance."
As our understanding of the biology of glucose homeostasis has grown, insulin
resistance has clearly emerged as an important cause of glucose intolerance
leading to type 2 diabetes, and may even play a role in other pathological
conditions. Type 2 diabetes is a heterogeneous disorder, requiring impairment of
both insulin secretion and insulin action (insulin resistance). Medical
nutrition therapy (MNT) and exercise therapy, as well as a number of
pharmacological interventions, have demonstrated that reducing insulin
resistance will improve glucose homeostasis.
Despite the wealth of knowledge that characterizes the nature of insulin
resistance (namely, its impact on health role in disease, its biochemical basis,
and its measurement) many fundamental questions remain. To assess our present
knowledge and understanding and to provide guidance to practitioners, the
American Diabetes Association convened a Consensus Development Conference 5 6 November 1997, on the
subject of insulin resistance.
1. What is the definition of insulin resistance and how should it be measured?
2. What is the mechanism(s) of insulin resistance?
3. Does insulin resistance predict diabetes? Is it a risk factor for
cardiovascular disease?
4. Should insulin resistance be treated for the primary prevention of diabetes
or other diseases?
QUESTION 1: What
is the definition of insulin resistance and how should it be measured?
Insulin resistance is defined as an impaired biological response to either
exogenous or endogenous insulin. The measured biological responses could
reflect, in theory, metabolic processes (changes in carbohydrate, lipid or
protein metabolism) as well as mitogenic processes (alterations in growth,
differentiation, DNA synthesis, regulation of gene transcription). In vivo
biological responses to insulin vary according to insulin concentration,
exposure time, tissue delivery, and pulsatility.
QUESTION 2: What
is the mechanism(s) of insulin resistance?
Understanding the biology of insulin resistance is important to identify
affected causative genes and their products, to facilitate the development of
new therapies, and to optimize current therapies. The aspect of insulin
resistance, which has been most extensively studied in man, animal models of
diabetes, and cell culture, is the defective insulin-mediated uptake and
utilization of glucose. In patients with insulin resistance, this defect is
manifested by a reduction in insulin-stimulated storage of glucose as glycogen
in muscle and liver. In muscle, the primary mechanism responsible appears to be
a block in the glucose transport/phosphorylation step. This defect has both a
primary genetic component and a secondary environmental component.
The primary genetic component is characterized by reduced efficiency of
translocation of the GLUT4 in muscle cells, although nuclear magnetic resonance
(NMR) data in humans suggest that a separate defect in glycogen synthesis may
also exist. In cell culture, several lines of evidence suggest that the
phosphatidylinositol kinase (PI 3-kinase) pathway, one of the two major pathways
activated by insulin receptor phosphorylation of insulin receptor substrate
(IRS)-1, is both necessary and sufficient for stimulating GLUT4 translocation.
In another model, knockout mice, heterozygous for either the insulin receptor or
for IRS-1, are not insulin resistant, yet mice heterozygous for both the insulin
receptor and for IRS-1 are insulin resistant. These observations suggest that a
critical threshold level of IRS-1 activity is necessary in order to maximally
stimulate PI-3 kinase, and further suggest that IRS-1 may play a central role in
insulin-stimulated GLUT4 translocation in the intact animal. Other experiments
with knock-out mice suggest that insulin resistance can be abolished by blocking
the action of endogenous tumor necrosis factor- (TNF-). It is
likely that the molecular basis of insulin resistance is polygenic, and the
relative contribution of individual components may vary among individuals. The
additive effects of several mild alterations of signal transduction pathway
molecules may be sufficient to induce insulin resistance.
The environmental component of insulin resistance involves the effects of
increased levels of glucose and free fatty acids. The effects of chronic
hyperglycemia, termed "glucotoxicity," reduce insulin-stimulated glucose uptake
by decreasing GLUT4 translocation in muscle. Two possible mechanisms have been
investigated. One involves increased glucose flux through the glucosamine
pathway. This pathway may induce insulin resistance in muscle when metabolite
flux exceeds demand, so that the metabolites may be shunted to the liver for
conversion to fat. Hyperglycemia may also activate isoforms of protein kinase C,
which in turn may increase serine phosphorylation, decrease activity of the
insulin receptor and/or IRS-1, and thereby decrease their activity. Elevated
plasma levels of free fatty acids also can increase insulin resistance by
decreasing glucose transport and phosphorylation in muscle perhaps by acylating
regulatory proteins, or by giving rise to diacylglycerol, which activates
protein kinase C. The capacity of free fatty acids to inhibit glycolysis also
plays a role in insulin resistance.
The above summary only briefly touches on our knowledge of intracellular
signaling mechanisms and their role in insulin-mediated glucose uptake and
storage. We still, however, need much more information before insulin resistance
is completely understood at the molecular level.
QUESTION 3: Does
insulin resistance predict diabetes? Is it a risk factor for cardiovascular
disease?
Plasma insulin levels whether measured in the fasting state or after a glucose
load are a powerful predictor for the risk of type 2 diabetes, independent of
obesity or waist circumference. This risk is particularly strong for individuals
with a family history of diabetes. It is not known whether the risk relationship
is linear or curvilinear, and the risk gradient is unknown. The insulin
sensitivity index and the acute insulin response are also both very strong
predictors of the risk of diabetes.
It is likely that measures of insulin sensitivity and acute insulin responses
are better predictors of the risk of diabetes than is a fasting insulin level,
although it is not known how much better they are. Given the cost and complexity
of specific testing for insulin sensitivity, including the simpler approaches
previously described, the predictability of these tests for the development of
diabetes would have to be substantially better than that of a fasting insulin
level in order for them to be clinically useful. At present, the comparative
predictability of the fasting insulin level versus the various insulin
sensitivity indexes has not been determined in any randomly selected population
sample followed for a long period of time. However, by using existing data sets
we may be able to compare the predictability of diabetes by various methods of
measuring insulin resistance. Also, by more accurately defining the laboratory
phenotypes of insulin resistance we may improve the success of identifying genes
related to insulin resistance.
QUESTION 4: Should
insulin resistance be treated for the primary prevention of diabetes or other
diseases?
The fact that insulin resistance is associated with so much morbidity and
mortality does not prove that it is the cause of these outcomes, or that
amelioration of insulin resistance will prevent them. Furthermore, lacking a
clinically practical test for insulin resistance or a way to follow it
longitudinally in the clinical setting, it is impossible for the clinician to
know whether a given treatment is specifically alleviating insulin resistance
and preventing its associated conditions.
Nevertheless, there are a series of interventions that do reduce insulin
resistance, including hypocaloric diet, weight reduction, exercise, and the
medications metformin and troglitazone. The effect of a low-calorie diet on
insulin resistance has been known for many years. Insulin resistance is reduced
within a few days of instituting a hypocaloric diet, even before much weight
loss has occurred. Weight reduction, attained over a longer time frame, further
improves insulin sensitivity. Conversely, avoiding excess weight gain may be the
most effective means to prevent insulin resistance and its associated morbidity.
Distribution of dietary calories among carbohydrates and various fat sources
does not appear to be so critical in influencing insulin resistance as is total
caloric intake (i.e., to establish a hypocaloric diet). Reduction of saturated
fat intake is important in improving a high-risk lipid profile.
The effects of exercise are complex. Regular vigorous exercise improves Vo2max
and reduces insulin resistance, even in the elderly. This training effect on
insulin resistance drops off quickly, within 5 days after cessation of the
exercise. Long-term exercise results in little weight reduction unless caloric
intake is controlled. However, a cardiovascular benefit may be obtained with
even modest levels of habitual exercise.
While lifestyle changes approaches do reduce insulin resistance and may put
people in a lower risk category for diseases associated with insulin resistance,
there is little evidence that morbidity is actually prevented. The most direct
link of insulin resistance to morbidity and mortality is by way of type 2
diabetes . People with insulin resistance, measured rigorously by the euglycemic
insulin clamp or the minimal model are at greatly increased risk of developing
impaired glucose tolerance and type 2 diabetes. Since the pathophysiology of
type 2 diabetes virtually always includes significant insulin resistance, there
is good reason to hypothesize that the treatment of insulin resistance could
prevent or delay the onset of type 2 diabetes.
A major National Institutes of Health study, the Diabetes Prevention Program
(DPP), is designed to determine which, if any, of these treatments is most
effective in the primary prevention of type 2 diabetes in people with impaired
glucose tolerance, over a 5-year period. A control group and three treatment
arms are being studied: intensive lifestyle changes designed to effect a 7%
reduction in body weight through caloric reduction and exercise, or the use of
troglitazone or metformin. Each of the treatments could be considered to be
reducing insulin resistance.
Pending the outcome of the DPP, it is reasonable for the clinician to offer
nonpharmacological treatments designed to reduce insulin resistance in the hope
of preventing diabetes, recognizing that it will be impossible to prove or
disprove efficacy in the individual patient. People at risk include those who
are overweight, particularly with central obesity, those with a strong family
history of diabetes, a history of gestational diabetes, impaired fasting plasma
glucose (i.e., between 110 and 125 mg/dl), or other reasons to suspect insulin
resistance (e.g., hypertension and dyslipidemia). Given our current state of
knowledge, and until we have the results of the DPP, troglitazone and metformin
are not recommended for the prevention of type 2 diabetes.
It is unclear whether insulin resistance causes or is simply associated with
many frequently accompanying other high-risk conditions such as hypertension,
dyslipidemia, and accelerated atherosclerosis. Given the lack of definitive
information on causality, there is inadequate rationale for the pharmacological
treatment of insulin resistance itself in the hope of preventing any of these
disorders.
Exercise
Reduces Diabetes by Reducing Insulin Resistance
It has been
shown numerous times that exercise may prevent certain diseases such as heart
disease and diabetes, although the exact mechanism of this effect is often
disputed. This study found that one of these mechanisms is that physical
activity causes a reduction in insulin resistance.
·
The study included 5159 men
aged 40 to 59 years with no history of coronary heart disease, type 2 diabetes,
or stroke.
·
During an average follow-up
period of 16.8 years, there were 616 cases of major coronary heart disease
events (fatal and nonfatal) and 196 incident cases of type 2 diabetes.
·
Physical activity was
inversely related to coronary heart disease rates, with the lowest rates in the
men undertaking moderate physical activity and with no further benefit
thereafter.
·
For type 2 diabetes, risk
decreased progressively with increasing levels of physical activity.
·
Physical activity was
associated with serum insulin level and with factors associated with insulin,
ie, heart rate, hyperuricemia (elevated uric acid in the urine), diastolic blood
pressure, and high-density lipoprotein cholesterol level, and with
-glutamyltransferase level, a possible marker of insulin resistance in the
liver.
The authors
maintain that insulin resistance definitely plays an important role in the
development of diabetes, although they were not able to come to the same
conclusion in regards to heart disease. They feel that the majority of the risk
reduction for heart disease induced by exercise must be obtained through a
different mechanism.
A fifth
of the adult population is obese
The
number of people who are obese has tripled over the last 20 years, and is still
rising say experts.
Figures
to be presented to Parliament in a National Audit Office (NAO) report on
Thursday, show most adults in England are overweight, and one in five is obese.
The
report 'Tackling Obesity In England', showed obesity caused 30,000 premature
deaths in 1998 alone.
The NHS
spends at least £500m a year on treating obesity, which could also be costing
the economy over £2bn a year.
If the
rise continues, it could cost the economy £3.5bn a year by 2010.
Heart
disease, diabetes, high blood pressure and osteoarthritis are all conditions
linked to obesity.
It
estimated that each person whose death is directly linked to an obesity related
condition, loses nine years of life.
Launching the report, the head of the NAO Sir John Bourn, said: "Nearly two
thirds of men and over half of women in England are now overweight or obese.
"And
the problem here is increasing faster than in most other European countries.
"If
prevalence continues to rise at the current rate, more than one in four adults
will be obese by 2010."
He said
such a rise would increase the incidence of diseases like coronary heart
disease.
Huge
costs to NHS
Obesity
is measured using the Body Mass Index (BMI), which is a person's weight in
kilogrammes divided by their height in metres squared.
|
Body
Mass Index
|
|
BMI for
a person who is 5ft 9ins:
130 lbs
- BMI = 19.2 (underweight)
160lbs
- BMI = 23.6 (normal weight)
190lbs
- BMI = 28.1 (overweight)
220lbs
- BMI = 32.5 (obese)
|
A BMI
of 20 to 25 is normal, more than 25 is overweight and more than 30 is defined as
obese.
In
1980, 8% of women and 6% of men in England were obese - by 1998, that had almost
trebled to 21% of women and 17% of men.
A
further 32% of women and 46% of men are overweight, meaning that most people in
England (58%) are now either fat or obese.
The
report estimates that 18,000 sick days a year are lost due to obesity.
Changes
to the way obesity is dealt with, both in the NHS and at government level were
identified in the report.
Sir
John added "There are no easy solutions to the problem, but progress is
possible. There is scope to do more to promote healthier lifestyles and improve
NHS services for the increasing number of people whose health is at risk from
excess weight."
Lifestyle changes
The
combination of a less active lifestyle and changes to eating patterns are blamed
by experts for the rise in obesity.
The
report says that part of the solution is to prevent people becoming obese in the
first place.
Stress in
Middle-Age Increases Diabetes Risk
Psychological
stress caused by the death of a spouse, a financial crisis or other
life-altering event may increase the risk of developing diabetes in middle age.
Their study found that these types of major life events were associated with
type 2 diabetes regardless of family history of the disease, exercise or alcohol
use. Type 2 diabetes usually occurs later in life, and in many cases can be
controlled with diet and exercise.
A high number
of rather common major life events that probably indicate chronic psychological
stress during the past 5 years was indeed related to a higher prevalence of
previously unknown type 2 diabetes.
The researchers
asked more than 2,000 white adults between 50 and 74 years about stressful life
events in the past five years, such as the death of a loved one, the end of a
relationship or long-lasting financial problems. Diabetes was diagnosed in 5% of
people participating in the study and those with the highest number of stressful
events (three or more) were 60% more likely to have diabetes as those with fewer
stressful life events. However, there was no association between stressful
work-related events such as a forced job change, retirement or long-lasting
problems at work, the study found. The study could not conclusively determine
that stress causes diabetes. However, the researchers believe that it is
unlikely that the diabetes was the cause of the stress, or that some underlying
factor -- such as poverty -- contributed to both conditions.
The authors
conclude that the findings are at least ''partially consistent'' with a theory
that says that stressful life events increase the diabetes risk by increasing
levels of the hormone cortisol and decreasing levels of sex steroids such as
testosterone, which have been shown to influence the action of insulin. Insulin
is the hormone that regulates blood sugar. Although that theory suggests that
stress results in a higher diabetes risk due to weight gain in the abdomen, the
researchers found no link between stress, abdominal fat and diabetes.
COMMENT: Stress
is a large part of the reason why most chronic illness develops. I believe the
most powerful intervention for stress is prayer.
Stress Linked to
Undetected Diabetes
What the Study
Showed
In this 2000 Dutch study published in Diabetes Care, stressful life
events were associated with the onset of undetected non-insulin-dependent
diabetes (type 2) as well as increased fat around the abdomen.
How It
Was Done
Researchers asked 2,262 individuals, all men and women between the ages of 50
and 74 and with no history of diabetes, about the number of major stressful
events they had experienced during the previous five years. Such events included
the death of a relative or a child, moving from one house to another,
work-related developments including retirement, and serious financial problems.
Participants
were also asked what kind of physical activity they engaged in regularly, how
much alcohol they drink, and whether any present or past family members had
diabetes.
As part of a
physical exam, blood samples were taken to assess blood sugar and insulin
levels, and the amount of fat around the waist and hip was measured.
Why It's
Important
There are several biologically based theories about how psychological stress
could prompt the development of type 2 diabetes. For example, psychological
stress that includes feelings of helplessness or defeat may jump-start and
perpetuate the release of stress hormones such as adrenaline that then boost
blood sugar. This may, in turn, prompt the accumulation of fat around the middle
of the body and an associated resistance to insulin (a key sign of type 2
diabetes).
In this Dutch
study, researchers tested this biological theory in human beings. Blood tests
revealed 112 cases of previously undetected diabetes among the more than 2,260
participants. Significantly, many of these individuals were ones who had
experienced stressful life events. For example, nearly 11% of participants who
reported the death of a partner had developed the disease. And nearly 7% of
those who moved households did, too.
Overall, the
higher the number of stressful events, the higher the risk for the presence of
the disease. There were notable exceptions, however. Work-related events that
could potentially cause stress, such as retirement or serious work problems, did
not pose an increased risk for the development of diabetes.
In addition, the amount of fat
around the waist and hip tended to be slightly larger in people who experienced
a number of stressful life events. However, the amount of fat (in this part of
the body) did not appear to be the main link between stress and diabetes, at
least not in the white, middle-aged population investigated here.
FUEL METABOLISM
Catecholamines
stimulate the break down of stored fuels into utilizable substrate for
generation of energy, one of the major metabolic functions of catecholamines is
the rapid mobilization of substrates from liver, adipose tissue, and skeletal
muscle. Substrate mobilization depends on levels of hormones and substrate on
the nerve supply, and on blood flow through storage tissues. The effects of
catecholamines, glucagons, and glucocorticoids are generally opposite to those
of insulin, and the net activity of a given process reflects the interactions
among these regulators.
Liver
Catecholamines promote hepatic glucose output by activating
glycogenolysis, accelerating gluconeogenesis, and inhibiting glycogen synthesis.
Interactions of catecholamines with the -adrenergic receptor stimulates
adenylyl cyclase and leads to generation of cAMP – dependent enzymatic cascades,
and conversion of glycogen phosphorylase from the inactive to the active form.
1- Receptor stimulation also activates phosporylase, thereby increasing
glycogenolysis, and enhance glyconeogenesis in isolated hepatocytes by
mechanisms that are independent of cAMP. Amino acids uptake into liver – and
perhaps lactate entry also – is augmented by -agonists, which increase the
availability the substrates for gluconeogenesis. Suppression of insulin and
stimulation of glucagons secretion by catecholamines augment their direct
effects on hepatic glucose production. The contributions of and -adrenergic
receptor mechanisms to hepatic glucose production vary among species and in
different conditions within the same species. Adrenergic effects predominate
in rats, whereas -adrenegic effects predominate in dogs and humans.
-Adrenergic stimulation also enhances hepatic glucose productions in humans.
Epinephrine and NE decrease and dopamine increases hepatic blood flow. In
addition, glucagons may decrease catecholamine – induced hepatic arterial
vasoconstriction.
Muscle
Catecholamines stimulation of glycogenolysis in
muscle occurs by – receptors activation. Unlike the situation in liver or
adipose tissue, -receptor mechanisms do not affect this process, at least in
skeletal muscle. Because muscle backs glucose – 6 – phosphatase, the glucose – 6
– phosphatase generated by glycogenolysis is metabolized to lactate before
release into the circulation. The effects of catecholamines on muscle glycogen
metabolism are antagonized by insulin and require glucocorticoids.
Catecholamines also enhance free fatty acid entry and mobilize triglyceride from
skeletal muscle by a – receptors mediated process. Energy metabolism in
skeletal muscle is also increased by catecholamines cannot always be separated
from those of muscle activity.
Muscle protein constitutes a large reserve of
stored fuel that is catabolized in prolonged starvation or severe injury, and
the role of catecholamines in regulation of muscle protein metabolism is
complex. In contrast to their enhancement of lipid and glycogen mobilization,
catecholamines inhibit release of amino acids from skeletal muscle in vitro and
in the intact animal by a –adrenergic process. Chronic administrations of –
adrenergic agonist, particularly - agonist, increases skeletal muscle protein
in animals conversely, removal of the adrenal medulla is associated with a
reduction in body protein. –adrenergic agonist act primarily to decrease
protein breakdown rather than to enhance protein synthesis, possibly by
suppression of the ATP-ubiquitin-dependent proteolytic pathway. The effect of
epinephrine on protein breakdown is counter to that of glucococrticoids, which
suggest a role for the adrenal medulla in restraining proteolysis when both
cortex and medulla are stimulated by fasting or by stress.
Kidney
Catecholamines stimulate renal glucose production by an -arenergic mechanism.
When plasma epinephrine levels are in the high-normal range, the kidney accounts
for 30 to 40% of the increase in glucose entry into the systemic circulation.
Renal glucose production largely reflects glucocon genesis in proximal tubular
cells and may be particularly important in prolonged fasting, in poorly
controlled diabetes mellitus, and in stress associated with elevations in
circulating epinephrine.
Comment :
1- The prayers at
stated times
There 5 times
prayer a day befor sun rise untile nearly to sleeping time to control GH
glucocoticoids and Thyroxin befor sun rise as will as stress hormone
Catecholamines during aday .
2- Bathe whole
body after sexual inter course
The bath after
inter course it maybe effects insulin receptors sensitivity and resistance
3- Befor paryer
you should do ablution
Same as the bathe
4- How eats
offensive food like garlice should not go mosque till its odur dies
It has
psychological effect it other people in the same time no smell from other people
to not effect on you
5- The prayer
should not performed when the food is brought or when any feeling the call of
nature
If any one
hungery or has feeling of calling the nature he has difficulty inconcntrate in
calmness to avoidance stress
6- No prayer in
the period of menstruation
During
menstration the femal hormones in the lowest level the factors which
produceinsulin resistance and decrease sexual behavior
7- You have to go
to the mosque walking exercise
Walking will
decrease weight and insulin resistance asa will as improve psychological
status
8- Wher you are
your face during prayer in the direction of sacred mosque
- To stand and
your face in the dirction of sacred mosque I don’t know why but I can say what
is written in islam
[The Holy Quran said in
The Night Journey versa]
[85]
of knowledge it is only a little that
is communicated to you, (O men!)"
9-During prayer
you have to in calmness
Calmness in
prayer is to be far away 5 times aday form stress and the effect of stress
hormones in glucose production .