Diabetes and Stress?

[Kumar]

Hello,

Can you tell me about relations of persisting stress with persisting hyperglycemia and insulin resistance?

Can environment in big, polluted and crowded cities and modern lifestyles be considered as a cause to prsisting stress resulting into persisting hyperglycemia?

Excessive noise levels, over-illumination, late night sleeps(more light exposure), crowding (more exposure to pathogenic microbes), pollution (shallow breathing and excessive exposure to polluting and strange particles), fast travels, over-use of TV/computes/mobile phones, modern fast foods, work stress etc. can be common in big cities.

Can above factors cause excessive and persisting stress and more influence of "sympathetic nervous system's and lesser of "para-sympathetic system" resulting into persisting hyperglycemia?

Somogyi effect, also called rebound hyperglycemia (suh-MOH-jee)
when the blood glucose level swings high following hypoglycemia. The Somogyi effect may follow an untreated hypoglycemic episode during the night and is caused by the release of stress hormones. From ADA

Does Somogyi effect indicates higher stress during the day(sympathetic nervous system's influence) and relaxation during night(para-sympathetic nervous system's influence)?

Best wishes.

 

[Kumar]

Unfortunately, in our current high-stress culture, the body’s stress response is activated so often that functioning often doesn’t have a chance to return to normal, producing chronic stress.

Higher and more prolonged levels of cortisol in the bloodstream (like those associated with chronic stress) have been shown to have negative effects, such as:


Impaired cognitive performance
Suppressed thyroid function
Blood sugar imbalances such as hyperglycemia
Decreased bone density
Decrease in muscle tissue
Higher blood pressure
Lowered immunity and inflammatory responses in the body, as well as other health consequences
Increased abdominal fat, which is associated with a greater amount of health problems than fat deposited in other areas of the body. Some of the health problems associated with increased stomach fat are heart attacks, strokes, the development of , higher levels of “bad” cholesterol (LDL) and lower levels of “good” cholesterol (HDL), which can lead to other health problems!
http://stress.about.com/od/stresshealth/a/cortisol.htm

In view of above, can persisting stress due to big cities environment be responsible for uncontroled glucose levels?

 

[Kumar]

Ectopic Fat Storage Syndrome

The ectopic fat storage syndrome hypothesis suggests that as adipocytes hypertrophy and reach their capacity for storing more fat, then additional fat from excess dietary lipids or calories is deferred to non-adipose tissues intracellularly, e.g. liver, skeletal muscle, heart, and the beta cells of the pancreas where they can exert toxic effects and dysfunction . This "lipotoxicity" may also be exacerbated by impaired oxidation of fat within tissues . Furthermore, adipose tissue is a major endocrine organ that secretes numerous polypeptide hormones and cytokines that are proinflammatory and proatherogenic. These play a major role in affecting insulin action in skeletal muscle and creating a low-grade state of inflammation and endothelial dysfunction . Compared to SCAT, VAT has been correlated more with endothelial dysfunction .

CVATT—A Working Hypothesis

It must be emphasized that the current proposal is a working hypothesis. Figure 1 describes a critical VAT threshold (CVATT) which is unique for a given individual and represents a range for the accumulation of a critical mass of VAT (CVATT) that when achieved, leads to the development of metabolic syndrome. Note that insulin sensitivity is important for weight gain and accumulation of VAT, and investigators have proposed that insulin resistance may actually, to a certain extent, be beneficial by protecting cells with already impaired fatty acid oxidation. Once the CVATT is reached, insulin resistance (IR) occurs, which may be protective initially . In addition to protecting against further weight and fat gain , insulin resistance prevents glucose and more fat from entering the cell and becoming preferentially oxidized. Hence, insulin resistance also allows intracellular fat already present within the cell to become oxidized rather than cause further damage through "lipotoxicity ."
http://www.diabetesincontrol.com/modules.php?name=News&file=article&sid=2260

As such, can lipotoxity is a stress and stimulate ANS?

 

[Kumar]

Sorry to find no response. Lastly,

Whether studies to evaulate above mentioned effects are done or not? Whether effect on diabetic people, when living in stressful,big/crowded/polluted cities and living in remore green stressfree area is studies or not? Cheking, stress hormones of diabetics look to be not regular practice.

 

[TimeTraveler]

Hello,

Can you tell me about relations of persisting stress with persisting hyperglycemia and insulin resistance?

Can environment in big, polluted and crowded cities and modern lifestyles be considered as a cause to prsisting stress resulting into persisting hyperglycemia?

Excessive noise levels, over-illumination, late night sleeps(more light exposure), crowding (more exposure to pathogenic microbes), pollution (shallow breathing and excessive exposure to polluting and strange particles), fast travels, over-use of TV/computes/mobile phones, modern fast foods, work stress etc. can be common in big cities.

Can above factors cause excessive and persisting stress and more influence of "sympathetic nervous system's and lesser of "para-sympathetic system" resulting into persisting hyperglycemia?



Does Somogyi effect indicates higher stress during the day(sympathetic nervous system's influence) and relaxation during night(para-sympathetic nervous system's influence)?

Best wishes.

Eating habits, don't eat so much high fructose corn syrup and inorganic foods and you might lower your risk.

 

[S.A.M.]

Kumar

There is currently a working hypothesis which relates high consumption of sugars to increase in insulin resistance. The exact mechanism is unknown but is postulated to be through changes in visceral fat deposition. (Fat deposition in abdominal areas and around organs). It is believed that these changes lead to insulin resistance through several possible mechanisms:

1. the adipose tissue on reaching a certain cell size undergoes changes which cause inflammation, monocyte infiltration and release of cytokines into blood stream. Cytokines are associated with changes in glucose uptake and increased insulin resistance.

2. the high intake of sugar may lead to changes in insulin secretion or production due to other factors like lack of certain micronutrients in a diet high in sugars. The lack of these micronutrients may affect the procesing of glucose by unknown mechanisms and/or lead to changes in peripheral insulin resistance by other unknown mechanisms.

3. there may be oxidative damage following the intake of certain high energy but low nutrient foods (again due to lack of micronutrients) leading to increase in reactive oxygen species which can cause adverse effects leading to insulin resistance . The effect of lipotoxity is also assumed to be due to the effects of the ROS.


Insulin resistance is the preliminary step towards diabetes (Type II).

 

[Kumar]

samcdkey

Thanks. Visceral adiposity is commonly though factor to insulin resistace. But I think it may be related to getting IR in fat cells instead of muscle's cells. Stimulation of sympathetic system also impair insulin's some actions to increase needed energy. It is also indicated to mediate vaisceral adiposity by cortisol secretions which in one stress hormone. We may therefore have to evaluate effect of chronic stress in this respect.

 

[S.A.M.]

samcdkey

Thanks. Visceral adiposity is commonly though factor to insulin resistace. But I think it may be related to getting IR in fat cells instead of muscle's cells. Stimulation of sympathetic system also impair insulin's some actions to increase needed energy. It is also indicated to mediate vaisceral adiposity by cortisol secretions which in one stress hormone. We may therefore have to evaluate effect of chronic stress in this respect.

I'm not certain what you are saying here.

Insulin resistance is usually defined as peripheral insulin resistance in skeletal muscles. The glucose is converted in the liver not in the adipose. The adipose just takes up the free fatty acids there is very little actual synthesis of fatty acids in the adipose.

The SNS actually works opposite to insulin so it suppresses insulin secretion, not insulin receptor activity. All hormones (cortisol, epinephrine, glucagon) increase blood glucose only insulin increases glucose uptake by muscle.

Visceral adiposity is a separate issue and may be caused by several factors but when it is endocrine in nature there are other changes not just insulin resistance. e.g. increase in cortisol secretion leads to increase in appetite, suppression of immune and inflammatory responses and obesity. Since cortisol suppresses cytokine production it actually reduces stress from inflammation. It also has effects on mood memory and behaviour so it is hard to evaluate all its effects in isolation.

 

[Kumar]

samcdkey,

Stress hormones are related to decrease in appetite. Somewhere hese are also elated to increase in appetite. Probably, some stress hormones are related to increase in appetite whereas some with decrease--still elevating glucose levels. Hyperthroidism is also linked to increase in appetite. Laterral hypothalamus is also linked to increase in appetite. So all this looks to be bi complicated. Pls tell me;

Can different chronic stimulation of different stress hormones mediate different type of diabetes2 i.e. expressing increased and decreased appetite, metabolic rate and central obesity?

Can there be insulin resistance to glucose intake be cells without visceral adiposity?