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        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 .


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