Mainly 3 types of anxiety we deal with:
· GENERALIZED ANXIETY DISORDER (GAD)
· PANIC DISORDER
· SOCIAL ANXIETY DISORDER (SAD)- 2 types: a) Generalized subtype
b) Non-generalized subtype/ Performance type
SYMPTOMS OF ANXIETY DISORDERS:
Depressive symptoms commonly co-exist especially in patients with severe anxiety.
A) GAD
§ Multiple unexplained bodily symptoms;
§ Excessive anxiety;
§ Person finds it difficult to control the worry;
§ Insomnia;
§ Restlessness, irritability, muscle spasm;
§ Easily tired, difficulty in concentrating.
B) Panic Disorder
§ Dizziness;
§ Chest pain or discomfort, shortness of breath
§ Palpitations or tachycardia;
§ Nausea, GI upset
§ Trembling, sweating, hot flushes and chills.
C) SAD
§ Blushing and sweating;
§ Palpitations;
§ Persistent & marked fear of being scrutinized & evaluated negatively by the people when in social gatherings and/or performance situations;
§ Fear is so great that it interferes w/ normal functioning, relationships, social activities or there is excessive distress concerning the phobia.
DIAGNOSIS
A) GAD
1) It is mostly a clinical diagnosis;.
2) Important to elicit history of difficult-to-control worry w/ psychic & somatic symptoms;
3) Inappropriate & persistent worrying lasting for >/= 6 months.
B) Panic Disorder
1) Eliciting the presence of unexpected pain attacks & behavioral changes due to anticipated risk of further attacks is important in establishing diagnosis;
2) Unable to tolerate physical symptoms of anxiety;
3) Agoraphobia (fear of being in a large open space) may or may not be present.
C) SAD
1) Diagnosis is made when fear or anxiety of a social situation results to considerable distress or functional impairment;
2) Basis for diagnosis is clinical presentation.
3) Generalized subtype – Fear & phobias in most social situations;
Usually patient is more functionally disabled.
4) Performance type – Limited to a number of social or performance situations (e.g. Public
Speaking.)
Associated w/ increased autonomic nervous system reactivity in feared
situations.
DIFFERENTIAL / ALTERNATIVE DIAGNOSIS:
A) Medical Illness: Thyroid disorders (Hyper or Hypothyroidism), Cushing’s disease, CVS, Respiratory
Diseases, Mitral Valve Prolapse (MVP) etc can cause symptoms of anxiety.
B) Substance Abuse/ Medication Use:
1. Inquire about withdrawal or use of addictive substances e.g. caffeine, Nicotine, Alcohol, Illegal substance use etc.
2. Obtain history of medications use that may cause anxiety e.g. Steroids, SSRIs, Thyroxine, Theophylline, some Herbal products etc.
3. Assess for substance abuse.
C) Other Psychiatric Disorders: like Major depression, mixed anxiety-depressive disorder.
NON-PHARMACOLOGICAL THERAPY OF ANXIETY DISORDERS:
1) Patient Education:
· Should be provided to all patients regardless of anxiety disorder or treatment type;
· Help the patient & family understand that the disorder is a real illness which requires treatment and support;
· Address patient’s concerns;
· Reassurance and instill hope;
· Interact with patient -- Explain that these are NOT life threatening,
--- Teach family that the attacks can be disabling to the patient;
· Discuss treatment options & risks Vs benefits of both pharmacotherapy & psychosocial treatment with the patient and family members.
2) Relaxation Techniques & Biofeedback
· May be used to treat mild GAD;
· Used to decrease arousal & control somatic manifestations;
· Studies have found that these techniques are more effective if combined with Cognitive therapy; may be combined with Cognitive-behavioral Therapy (CBT) in GAD treatment.
3) Lifestyle Changes
· Stress reduction - by Yoga, meditation etc.
· Reduction of caffeine & alcohol consumption;
· Avoidance of Nicotine & Drug/ Medication abuse;
· Regular exercise.
IMPLICATIONS OF COGNITIVE-BEHAVIORAL THERAPY (CBT) IN ANXIETY DISORDER TREATMENT
· Symptom oriented approach;
· Psychoeducation – identify patient’s symptoms, explain basis of symptoms and outline techniques for dealing with symptoms;
· Continuous panic monitoring;
· Relaxation breathing – e.g. abdominal breathing helps to control psychological overactivity;
· Cognitive restructuring – investigate and reverse fears that arise from misinterpretation of body sensations, to teach patient about different outcomes of situations other than only negative ones i.e. Stopping automatic negative thinking (ANTs);
· In vivo Exposure – Last component of CBT care, involves the actual exposure of patients to their fear cues.
· The vast majority of the controlled research is devoted to cognitive behavior therapy (CBT) and shows its efficiency and effectiveness in all the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) anxiety disorders in meta-analyses. Relaxation, psychoanalytic therapies, Rogerian nondirective therapy, hypnotherapy, and supportive therapy were examined in a few controlled studies, which preclude any definite conclusion about their effectiveness in specific phobias, agoraphobia, panic disorder, obsessive-compulsive disorder (OCD), and posttraumatic stress disorder (PTSD). CBT was clearly better than psychoanalytic therapy in generalized anxiety disorder (GAD) and performance anxiety. Psychological debriefing for PTSD appeared detrimental to the patients in one high-quality meta-analysis.
Tuesday, February 3, 2009
Friday, January 30, 2009
“PREDIABETES” – ARE WE IGNORING?(Part-II)
WHY WORRY ABOUT PREDIABETES?
o Predicts high risk for development of diabetes.
o Predicts high risk for development of atherosclerotic vascular disease.
o Both (IGT & IFG) are largely preventable through lifestyle and pharmacological interventions.
o Relative risk (RR) of prediabetics in developing frank Diabetes Mellitus (DM) after 10 years of diagnosis are as follows:
NGT -----> RR = 1
IGT ------> RR = 3.2
IFG ------> RR = 3.1
(IGT + IFG) ------> RR = 4.9
IMPAIRED GLUCOSE TOLERANCE (IGT)
Natural history of IGT ------ AFTER 10 YEARS ------------------> 25% will be normoglycemic
25% remain as IGT
50% will turn to DM Type2
PREDICTION OF CONVERSION OF IGT TO Type 2 DM:
HOORN Study:
Prospective study in subjects with IGT followed for a mean period of 3 years.
2h Post Glucose and not FPG was the most important predictor of conversion
to NIDDM. DIABETOLOGIA 1996; 39:113-18
ANALYSIS OF 6 STUDIES REVEAL 2h Post Glucose VALUE IS THE MOST IMPORTANT PREDICTOR OF CONVERSION. DIABETES 1997; 40:701-10
ADA RECOMMENDATION FOR SCREENING
Men & women ≥ 45 years of age with BMI ≥ 25.
Younger than 45, overweight PLUS 1 or more risk factor.
If positive, follow up test next day to confirm diagnosis.
Prediabetics should be monitored every year for type.
Normal screening results should be retested every 3 years.
NOVEL DIAGNOSTIC MARKER
Spy Diabetes Early
Warning in Eyes.
Retinal Emission - Flavoprotein autofluoroscense
Increased level of FA can predict diabetes. [July 15th The Telegraph; University Of Michigan; Kellog Eye Centre ]
TREATMENT RECOMMENDATION FOR PREDIABETES
POPULATION TREATMENT
1. IGT or IFG Life Style Modification (Wt. Loss 5-10%, Exercise >30min/day weekly)
2. IGT + IFG + Any of the following Life Style Modification and/or Metformin 850 mg/day
a) Age <>/= 35 kg/m2
c) F/H of DM IN 1st degree Relative
d) Elevated TG/ Reduced HDLc
e) Hypertension
f) HbA1c > 6.0%
NOVEL TARGETS FOR DIABETES PREVENTION
Aspirin- reduces NF-kB- reduces islet inflammation.
SALsalate for Type 2 DM can prevent progression of prediabetes to diabetes.
Cholestyramine can reduce glycemia.
Weight Control by any means can prevent development of diabetes in a prediabetic.
Newer agent are HSD-1 Inhibitors.
Statins may be helpful to reduce vascular outcomes in a prediabetic.
[Diabetes care Vol 31. Number 7, July2008]
CONCLUSION
Prediabetes & metabolic syndrome extremely prevalent
Prediabetes + Metabolic syndrome = high risk for diabetes & CVD
Early detection of IFG/IGT in high risk individuals & interventions to prevent progression to diabetes through Intensive lifestyle changes (Low Calorie Diet, Stop smoking, Reduced alcohol consumption to 12-14 pegs/week, Increased Physical activity + exercise, Behaviour therapy) are effective & should be encouraged
Effective pharmacological therapies must be identified.
o Predicts high risk for development of diabetes.
o Predicts high risk for development of atherosclerotic vascular disease.
o Both (IGT & IFG) are largely preventable through lifestyle and pharmacological interventions.
o Relative risk (RR) of prediabetics in developing frank Diabetes Mellitus (DM) after 10 years of diagnosis are as follows:
NGT -----> RR = 1
IGT ------> RR = 3.2
IFG ------> RR = 3.1
(IGT + IFG) ------> RR = 4.9
IMPAIRED GLUCOSE TOLERANCE (IGT)
Natural history of IGT ------ AFTER 10 YEARS ------------------> 25% will be normoglycemic
25% remain as IGT
50% will turn to DM Type2
PREDICTION OF CONVERSION OF IGT TO Type 2 DM:
HOORN Study:
Prospective study in subjects with IGT followed for a mean period of 3 years.
2h Post Glucose and not FPG was the most important predictor of conversion
to NIDDM. DIABETOLOGIA 1996; 39:113-18
ANALYSIS OF 6 STUDIES REVEAL 2h Post Glucose VALUE IS THE MOST IMPORTANT PREDICTOR OF CONVERSION. DIABETES 1997; 40:701-10
ADA RECOMMENDATION FOR SCREENING
Men & women ≥ 45 years of age with BMI ≥ 25.
Younger than 45, overweight PLUS 1 or more risk factor.
If positive, follow up test next day to confirm diagnosis.
Prediabetics should be monitored every year for type.
Normal screening results should be retested every 3 years.
NOVEL DIAGNOSTIC MARKER
Spy Diabetes Early
Warning in Eyes.
Retinal Emission - Flavoprotein autofluoroscense
Increased level of FA can predict diabetes. [July 15th The Telegraph; University Of Michigan; Kellog Eye Centre ]
TREATMENT RECOMMENDATION FOR PREDIABETES
POPULATION TREATMENT
1. IGT or IFG Life Style Modification (Wt. Loss 5-10%, Exercise >30min/day weekly)
2. IGT + IFG + Any of the following Life Style Modification and/or Metformin 850 mg/day
a) Age <>/= 35 kg/m2
c) F/H of DM IN 1st degree Relative
d) Elevated TG/ Reduced HDLc
e) Hypertension
f) HbA1c > 6.0%
NOVEL TARGETS FOR DIABETES PREVENTION
Aspirin- reduces NF-kB- reduces islet inflammation.
SALsalate for Type 2 DM can prevent progression of prediabetes to diabetes.
Cholestyramine can reduce glycemia.
Weight Control by any means can prevent development of diabetes in a prediabetic.
Newer agent are HSD-1 Inhibitors.
Statins may be helpful to reduce vascular outcomes in a prediabetic.
[Diabetes care Vol 31. Number 7, July2008]
CONCLUSION
Prediabetes & metabolic syndrome extremely prevalent
Prediabetes + Metabolic syndrome = high risk for diabetes & CVD
Early detection of IFG/IGT in high risk individuals & interventions to prevent progression to diabetes through Intensive lifestyle changes (Low Calorie Diet, Stop smoking, Reduced alcohol consumption to 12-14 pegs/week, Increased Physical activity + exercise, Behaviour therapy) are effective & should be encouraged
Effective pharmacological therapies must be identified.
“PREDIABETES” – ARE WE IGNORING? (Part -I)
PROLOGUE
British Diabetic Association recommended the use of the term prediabetes only in retrospect in the life of a diabetic before diabetes. WHO replaced this term in 1980’s with statistical risk classes- IGT (Impaired Glucose Tolerance), IFG (Impaired Fasting Glucose). US Secretary of Health Mr.TG Thomson reintroduced the term prediabetes in 2002 & subsequently accepted by ADA and Department of Health and Human Services USA.
DEFINITION
Prediabetes includes persons having IGT (Impaired Glucose Tolerance), IFG (Impaired Fasting Glucose) either isolated or in combination.
• Prediabetes – a condition that raises a person’s risk of developing Type 2 Diabetes, Heart Disease & Stroke. (DHHS US)
• ADA (American Diabetic Association) Practice Guidelines for diagnosis of prediabetes-
1 FBG: 100 – 125 mg/dl
2 OGT: 140 – 199 mg/dl (Oral Glucose Tolerance)
OGTT & PREDIABETES
STATE FPG Level (mg/dl) 2-h plasma glucose in OGTT (mg/dl)
IFG 100-125 <200
Isolated IFG 100-125 <140>IGT <126>
Isolated IGT <100FPG = Fasting Plasma Glucose OGTT = Oral Glucose Tolerance Test]
FALLACY OF THE TERM PREDIABETES
According to Dr. George Alberti at International Congress on Prediabetes 2005, the term “prediabetes” has some serious fallacy as noted below:
Only 50% prediabetics develop diabetes in 10 years.--- so 50% escapes.
The definition does not include some people at risk of developing diabetes– like those with strong family history, other normoglycemic risk group, and some ethnic groups.
Difficulty of communicating to general public about a high-risk situation.
PREVALENCE OF PREDIABETES IN INDIANS
South India: 14% have IGT (A. Ramchandran; BMJ 1988)
Prevalence of IGT & IFG are high in India and expected to increase from 85.6 million (2003) to 132 million (by 2025) (A. Ramchandran; Netaji Oration 2005)
IGT occurs early in Indians. (A. Ramchandran; Netaji Oration 2005)
British Diabetic Association recommended the use of the term prediabetes only in retrospect in the life of a diabetic before diabetes. WHO replaced this term in 1980’s with statistical risk classes- IGT (Impaired Glucose Tolerance), IFG (Impaired Fasting Glucose). US Secretary of Health Mr.TG Thomson reintroduced the term prediabetes in 2002 & subsequently accepted by ADA and Department of Health and Human Services USA.
DEFINITION
Prediabetes includes persons having IGT (Impaired Glucose Tolerance), IFG (Impaired Fasting Glucose) either isolated or in combination.
• Prediabetes – a condition that raises a person’s risk of developing Type 2 Diabetes, Heart Disease & Stroke. (DHHS US)
• ADA (American Diabetic Association) Practice Guidelines for diagnosis of prediabetes-
1 FBG: 100 – 125 mg/dl
2 OGT: 140 – 199 mg/dl (Oral Glucose Tolerance)
OGTT & PREDIABETES
STATE FPG Level (mg/dl) 2-h plasma glucose in OGTT (mg/dl)
IFG 100-125 <200
Isolated IFG 100-125 <140>IGT <126>
Isolated IGT <100FPG = Fasting Plasma Glucose OGTT = Oral Glucose Tolerance Test]
FALLACY OF THE TERM PREDIABETES
According to Dr. George Alberti at International Congress on Prediabetes 2005, the term “prediabetes” has some serious fallacy as noted below:
Only 50% prediabetics develop diabetes in 10 years.--- so 50% escapes.
The definition does not include some people at risk of developing diabetes– like those with strong family history, other normoglycemic risk group, and some ethnic groups.
Difficulty of communicating to general public about a high-risk situation.
PREVALENCE OF PREDIABETES IN INDIANS
South India: 14% have IGT (A. Ramchandran; BMJ 1988)
Prevalence of IGT & IFG are high in India and expected to increase from 85.6 million (2003) to 132 million (by 2025) (A. Ramchandran; Netaji Oration 2005)
IGT occurs early in Indians. (A. Ramchandran; Netaji Oration 2005)
Sunday, January 25, 2009
ADRENAL FATIGUE part-2
ADRENAL GLANDS BASICS
The adrenal glands are two small glands situated on top of the kidneys. Their purpose is to help the body to cope with stress and help it to survival. Each adrenal gland has two compartments.
Ø Inner or Adrenal Medulla modulates the sympathetic nervous system through secretion and regulation of two hormones called Epinephrine and Nor-epinephrine that are responsible for the “fight or flight response”.
Ø Outer Adrenal Cortex comprises 80 % of the adrenal gland and is responsible for producing over 50 different types of hormones in three major classes –
1) Glucocorticoids - most important glucocorticoid is CORTISOL. When this is lowered, the body will be unable to deal with stress as in the case of adrenal fatigue.
2) Mineralcorticoids - most important is ALDOSTERONE which modulates the delicate balance of minerals in the cell, especially sodium and potassium. It therefore regulates blood pressure. Stress increases the release of aldosterone, causing sodium retention (leading to water retention and high blood pressure) and loss of potassium and magnesium. When the body lacks magnesium, it will suffer from a variety of pathological conditions such as cardiac arrhythmias, uterine fibroids and osteoporosis.
3) Androgens - the adrenal cortex is also responsible for producing all sex hormones, although in small amounts. One exception is DHEA, a weak androgenic hormone that is made in large amounts in both sexes. DHEA, together with testosterone and estrogen, are made from Pregnenolone, which in turn comes from cholesterol. Pregnenolone also leads to the production of progesterone and as one of the intermediary steps in the making of cortisol. Pregnenolone is therefore one of the most important intermediate hormones being produced in the hormonal cascade. Prolonged deficiencies in Pregnenolone as that in adrenal fatigue will lead to reduction of both glucocortico-steroids and mineralcorticoids such as cortisol and aldosterone respectively.
Cortisol
The most important anti-stress hormone in the body is cortisol. Cortisol protects the body from excessive stress and adrenal fatigue by:
· Normalizes blood sugar - Cortisol increase blood sugar level in the body, thus providing the energy for the body to physically escape threat of injury in order to survive. Cortisol works in tandem with insulin from the pancreas to provide adequate glucose to the cells for energy. More energy is required when the most important anti-stress hormone in the body is cortisol.
· Anti-inflammation Response - Cortisol is a powerful anti-inflammatory agent. Cortisol is secreted as part of the anti-inflammatory response. It's objective is to remove and prevent swelling and redness of nearly all tissues. The cortisol response may be blunted in adrenal fatigue.
· Immune System Suppression - People with high cortisol levels are very much weaker from the immunological point of view. Cortisol influences most cells that participate in the immune reaction, especially white blood cells. Cortisol suppresses white blood cells, natural killer cells, monocytes, macrophages, and mast cells. It also suppresses the auto-immune system response to foreign insult. The immune response can be blunted in adrenal fatigue.
· Vasoconstriction - Cortisol contracts mid-size arteries. People with low cortisol (as in advance stages of adrenal fatigue) have low blood pressure and reduced reactivity to other body agents that constrict blood vessels. Cortisol tends to increase blood pressure that is moderated by calcium and magnesium.
· Physiology of Stress - People with adrenal fatigue cannot tolerate stress and will then succumb to severe stress. As their stress increases, progressively higher levels of cortisol are required. When the cortisol level cannot rise in response to stress, it is impossible to maintain the body in optimum stress response.
In summary, cortisol sustains life via two opposite but related kinds of regulatory actions:
Ø releasing and activating of existing defense mechanisms of the body, and
Ø shutting down and modifying the same mechanisms to prevent them from overshooting and causing damage or cell death.
Cortisol Regulation
The adrenal glands are controlled via the hypothalamus-pituitary-adrenal (HPA) axis. There is an existing negative feedback loop that governs the amount of adrenal hormones secreted under normal circumstances in people with adrenal fatigue.
Cortisol and Adreno-Cortico Trophic Hormone (ACTH) are not secreted uniformly throughout the day. They follow a diurnal pattern, with the highest level secreted at around 8:00 a.m. in the morning after which there is a gradual decline throughout the day. Episodic spikes during the day can also occur when the body is stressed or when certain foods are taken. The cortisol level is at its lowest between midnight and 4:00 a.m.
COMMON CAUSES OF ADRENAL FATIGUE
Chronic stress is very common in the western society. The most common causes of stress are work pressure, death of a love one, moving house, changing jobs, illness and marital disruptions. Adrenal fatigue occurs when the amount of stress overextends the capacity of the body to compensate and recover from stress.
Stressors that can lead to adrenal fatigue include:
· Anger
· Chronic fatigue
· Chronic illness
· Chronic infection
· Chronic pain
· Depression
· Excessive exercise
· Fear and guilt
· Gluten intolerance
· Low blood sugar
· Mal-absorption
· Mal-digestion
· Toxic exposure
· Severe or chronic stress
· Surgery
· Late hours
· Sleep deprivation
· Excessive Exercise
· Excessive sugar in diet
· Excessive caffeine intake from coffee and tea
One of the most commonly overlooked causes of adrenal fatigue is chronic or severe infection that gives rise to an inflammatory response. Such infection can occur sub-clinically with no obvious signs at all. Parasitic and bacterial infections including Giardia lamblia and H. pylori are often the main culprits.
The adrenal glands are two small glands situated on top of the kidneys. Their purpose is to help the body to cope with stress and help it to survival. Each adrenal gland has two compartments.
Ø Inner or Adrenal Medulla modulates the sympathetic nervous system through secretion and regulation of two hormones called Epinephrine and Nor-epinephrine that are responsible for the “fight or flight response”.
Ø Outer Adrenal Cortex comprises 80 % of the adrenal gland and is responsible for producing over 50 different types of hormones in three major classes –
1) Glucocorticoids - most important glucocorticoid is CORTISOL. When this is lowered, the body will be unable to deal with stress as in the case of adrenal fatigue.
2) Mineralcorticoids - most important is ALDOSTERONE which modulates the delicate balance of minerals in the cell, especially sodium and potassium. It therefore regulates blood pressure. Stress increases the release of aldosterone, causing sodium retention (leading to water retention and high blood pressure) and loss of potassium and magnesium. When the body lacks magnesium, it will suffer from a variety of pathological conditions such as cardiac arrhythmias, uterine fibroids and osteoporosis.
3) Androgens - the adrenal cortex is also responsible for producing all sex hormones, although in small amounts. One exception is DHEA, a weak androgenic hormone that is made in large amounts in both sexes. DHEA, together with testosterone and estrogen, are made from Pregnenolone, which in turn comes from cholesterol. Pregnenolone also leads to the production of progesterone and as one of the intermediary steps in the making of cortisol. Pregnenolone is therefore one of the most important intermediate hormones being produced in the hormonal cascade. Prolonged deficiencies in Pregnenolone as that in adrenal fatigue will lead to reduction of both glucocortico-steroids and mineralcorticoids such as cortisol and aldosterone respectively.
Cortisol
The most important anti-stress hormone in the body is cortisol. Cortisol protects the body from excessive stress and adrenal fatigue by:
· Normalizes blood sugar - Cortisol increase blood sugar level in the body, thus providing the energy for the body to physically escape threat of injury in order to survive. Cortisol works in tandem with insulin from the pancreas to provide adequate glucose to the cells for energy. More energy is required when the most important anti-stress hormone in the body is cortisol.
· Anti-inflammation Response - Cortisol is a powerful anti-inflammatory agent. Cortisol is secreted as part of the anti-inflammatory response. It's objective is to remove and prevent swelling and redness of nearly all tissues. The cortisol response may be blunted in adrenal fatigue.
· Immune System Suppression - People with high cortisol levels are very much weaker from the immunological point of view. Cortisol influences most cells that participate in the immune reaction, especially white blood cells. Cortisol suppresses white blood cells, natural killer cells, monocytes, macrophages, and mast cells. It also suppresses the auto-immune system response to foreign insult. The immune response can be blunted in adrenal fatigue.
· Vasoconstriction - Cortisol contracts mid-size arteries. People with low cortisol (as in advance stages of adrenal fatigue) have low blood pressure and reduced reactivity to other body agents that constrict blood vessels. Cortisol tends to increase blood pressure that is moderated by calcium and magnesium.
· Physiology of Stress - People with adrenal fatigue cannot tolerate stress and will then succumb to severe stress. As their stress increases, progressively higher levels of cortisol are required. When the cortisol level cannot rise in response to stress, it is impossible to maintain the body in optimum stress response.
In summary, cortisol sustains life via two opposite but related kinds of regulatory actions:
Ø releasing and activating of existing defense mechanisms of the body, and
Ø shutting down and modifying the same mechanisms to prevent them from overshooting and causing damage or cell death.
Cortisol Regulation
The adrenal glands are controlled via the hypothalamus-pituitary-adrenal (HPA) axis. There is an existing negative feedback loop that governs the amount of adrenal hormones secreted under normal circumstances in people with adrenal fatigue.
Cortisol and Adreno-Cortico Trophic Hormone (ACTH) are not secreted uniformly throughout the day. They follow a diurnal pattern, with the highest level secreted at around 8:00 a.m. in the morning after which there is a gradual decline throughout the day. Episodic spikes during the day can also occur when the body is stressed or when certain foods are taken. The cortisol level is at its lowest between midnight and 4:00 a.m.
COMMON CAUSES OF ADRENAL FATIGUE
Chronic stress is very common in the western society. The most common causes of stress are work pressure, death of a love one, moving house, changing jobs, illness and marital disruptions. Adrenal fatigue occurs when the amount of stress overextends the capacity of the body to compensate and recover from stress.
Stressors that can lead to adrenal fatigue include:
· Anger
· Chronic fatigue
· Chronic illness
· Chronic infection
· Chronic pain
· Depression
· Excessive exercise
· Fear and guilt
· Gluten intolerance
· Low blood sugar
· Mal-absorption
· Mal-digestion
· Toxic exposure
· Severe or chronic stress
· Surgery
· Late hours
· Sleep deprivation
· Excessive Exercise
· Excessive sugar in diet
· Excessive caffeine intake from coffee and tea
One of the most commonly overlooked causes of adrenal fatigue is chronic or severe infection that gives rise to an inflammatory response. Such infection can occur sub-clinically with no obvious signs at all. Parasitic and bacterial infections including Giardia lamblia and H. pylori are often the main culprits.
ADRENAL FATIGUE-part1
One of the most common complaints of adult patients in our clinic is – Fatigue and Lethargy. Adrenal fatigue has a broad spectrum of non-specific yet often debilitating symptoms. The onset of this disease is often slow and insidious. The truth is that Stress and Adrenal Fatigue is not a mysterious entity at all. Our body has a built-in mechanism to deal with it. Being able to handle stress is a key to survival, and the control center in our bodies is the adrenal glands. When our adrenal glands become fatigue and unable to handle stress, dysfunctional physiological symptomatology sets in.
Despite effective diagnostic tools and treatment programs, most conventional physicians were simply not informed of adrenal fatigue and not prepared to treat adrenal fatigue as a serious threat to health. This condition was seldom diagnosed as a sickness for the past 50 years. Instead, adrenal fatigue was considered as a condition whereby no treatment was available other than to tell the patient to "relax". This dilemma in diagnosis is mainly due to the fact that laboratory tests were unable to detect any abnormality, until recently. Today, adrenal fatigue could be accurately diagnosed, overcome and treated properly.
Adrenal fatigue should not be confused with another medical condition called Addison's disease where the adrenal glands are not functioning. While Addison's disease is often caused by auto-immune dysfunction, Adrenal Fatigue is largely caused by stress. Adrenal fatigue is the non-Addison's form of adrenal dysfunction.
Signs and Symptoms of Adrenal Fatigue
· Fatigue
· Feeling tired despite sufficient hours of sleep
· Insomnia
· Weight gain
· Depression
· Hair loss
· Acne
· Reliance on stimulants like caffeine
· Cravings for carbohydrates or sugars & meat and cheese
· Cravings for salt
· Poor immune functions
· Increase symptoms of PMS for women; period are heavy and then stop, or almost stopped on the 4th day, only to start flow again on the 5th or 6th day.
· Pain in the upper back or neck with no apparent reasons.
· Feels better when stress is relieved, such as on a vacation.
· Difficulties in getting up in the morning
· Light-headedness.
Other signs and symptoms include:
· Mild depression
· Food and or inhalant allergies
· Lethargy and lack of energy
· Increased effort to perform daily tasks
· Decreased ability to handle stress
· Dry and thin skin
· Hypoglycemia
· Low Body Temperature
· Nervousness
· Palpitation
· Unexplained hair loss
· Alternating constipation and diarrhea
· Dyspepsia
Related conditions
Adrenal fatigue is a likely factor in several medical conditions such as the following:
· Hypotension
· Fibromyalgia
· Hypothyroidism
· Chronic fatigue syndrome
· Arthritis
· Premature menopause
None of the signs or symptoms by itself can definitively diagnose adrenal fatigue. When taken as a group, these signs and symptoms do form a specific adrenal fatigue syndrome or picture - that is of a person under stress. These signs and symptoms are often the end result of acute severe or chronic excessive stress and the inability of the body to reduce such stress. The ability to handle stress, physical or emotional, is a cornerstone to human survival. Our body has a complete set of stress modulation system in place, and the control center is the adrenal glands. When this gland becomes dysfunctional, our body's ability to handle stress reduces, and symptoms will arise, and the result is adrenal fatigue.
Despite effective diagnostic tools and treatment programs, most conventional physicians were simply not informed of adrenal fatigue and not prepared to treat adrenal fatigue as a serious threat to health. This condition was seldom diagnosed as a sickness for the past 50 years. Instead, adrenal fatigue was considered as a condition whereby no treatment was available other than to tell the patient to "relax". This dilemma in diagnosis is mainly due to the fact that laboratory tests were unable to detect any abnormality, until recently. Today, adrenal fatigue could be accurately diagnosed, overcome and treated properly.
Adrenal fatigue should not be confused with another medical condition called Addison's disease where the adrenal glands are not functioning. While Addison's disease is often caused by auto-immune dysfunction, Adrenal Fatigue is largely caused by stress. Adrenal fatigue is the non-Addison's form of adrenal dysfunction.
Signs and Symptoms of Adrenal Fatigue
· Fatigue
· Feeling tired despite sufficient hours of sleep
· Insomnia
· Weight gain
· Depression
· Hair loss
· Acne
· Reliance on stimulants like caffeine
· Cravings for carbohydrates or sugars & meat and cheese
· Cravings for salt
· Poor immune functions
· Increase symptoms of PMS for women; period are heavy and then stop, or almost stopped on the 4th day, only to start flow again on the 5th or 6th day.
· Pain in the upper back or neck with no apparent reasons.
· Feels better when stress is relieved, such as on a vacation.
· Difficulties in getting up in the morning
· Light-headedness.
Other signs and symptoms include:
· Mild depression
· Food and or inhalant allergies
· Lethargy and lack of energy
· Increased effort to perform daily tasks
· Decreased ability to handle stress
· Dry and thin skin
· Hypoglycemia
· Low Body Temperature
· Nervousness
· Palpitation
· Unexplained hair loss
· Alternating constipation and diarrhea
· Dyspepsia
Related conditions
Adrenal fatigue is a likely factor in several medical conditions such as the following:
· Hypotension
· Fibromyalgia
· Hypothyroidism
· Chronic fatigue syndrome
· Arthritis
· Premature menopause
None of the signs or symptoms by itself can definitively diagnose adrenal fatigue. When taken as a group, these signs and symptoms do form a specific adrenal fatigue syndrome or picture - that is of a person under stress. These signs and symptoms are often the end result of acute severe or chronic excessive stress and the inability of the body to reduce such stress. The ability to handle stress, physical or emotional, is a cornerstone to human survival. Our body has a complete set of stress modulation system in place, and the control center is the adrenal glands. When this gland becomes dysfunctional, our body's ability to handle stress reduces, and symptoms will arise, and the result is adrenal fatigue.
Monday, January 12, 2009
Lycopene Antioxidant: The Rediscovered Carotene
According to the Linus Pauling Institute of Micronutrient Information Center, lycopene antioxidant activity is extremely important to plants, but the importance to human health is still unclear. Partly because of this, there has been no established lycopene daily requirement.
Beta-carotene from carrots is known for its antioxidant action. But did you know that there are over 600 known carotenoids besides beta? About 40 are found in the human diet, and not all of them turn into vitamin A. Lycopene is one that does not convert to vitamin A. Studies have shown that eating foods with lycopene provides stronger antioxidant protection against certain types of free radicals and does reduce the risk of some types of cancer and possibly heart disease. The carotenoid lycopene is the most common carotenoid found in the human body yet very little research has been done on it.
Carotenoids are organic chemicals that give plants their colors. Plant foods with lycopene are red like tomatoes, watermelons, grapefruits and papaya. A pigment synthesized by some plants and animals to protect them from the sun, lycopene evolved as a weapon against certain types of free radicals. Lycopene is so effective at quenching free radicals; it beat out vitamin E in one study on oxidized fat. This suggests that lycopene might have importance in preventing heart disease, which involves oxidized LDL cholesterol. The first evidence for a protective effect in heart disease was reported in the journal Lipids A group from Canada demonstrated that lycopene significantly lowers LDL oxidation in human blood. Lycopene works better in combination with lutein, another carotenoid which is found mostly in spinach and corn. (Lutein is associated with maintenance of the macula.) People with high cholesterol have been found to have high levels of free radicals and low levels of lycopene and beta-carotene. Humans get most of their lycopene from tomatoes, by far the richest source, yet tomato products offer a more concentrated source of lycopene than the fresh fruit itself. For example, tomato powder contains approximately 120 milligrams per 100 grams of fruit whereas fresh tomatoes have about 2 milligrams per 100. Since lycopene is a nutrient that can stand the heat, cooked tomato products, such as tomato paste, provide more of it than fresh tomatoes. It has been theorized that heating tomatoes makes their lycopene more absorbable.
Researchers are realizing that the cancer-preventive effects of the Mediterranean diet, which have been attributed to olive oil, may in fact be due to lycopene. Lycopene's cancer protection is in part due to its antioxidant protection. But some studies show that it may also modulate immunity, inhibit angiogenesis and affect hormonal effects in human.
There are no known lycopene antioxidant deficiency diseases. The reason that it is included in some dietary supplements, however, is because of scientific studies that indicate it may reduce the risk of some life threatening diseases and improve health. The FDA regulates health claims made by manufacturers of dietary supplements and food stuffs. In 2005, they addressed the issue of a lycopene daily requirement and proposed health claims of foods with lycopene. Their conclusion was that the limited scientific evidence suggests that consuming one-half to one cup of tomatoes or tomato sauce per week may reduce the risk of prostate cancer.
The carotenes are lipid soluble-they must have fat to be absorbed. It has been consistently demonstrated that foods with fat in them deliver more lycopene into the body. Lycopene is carried in the blood by the lipoprotein molecule (LDL) that also carries cholesterol. Drugs that lower cholesterol can drastically interfere with the carotenes. In one study, cholestyramine (Questran) decreased lycopene by 30% in the blood. It also reduced beta-carotene by 40% and vitamin E by 7%.
Other parts of the body besides the prostate that accumulate lycopene are the adrenal glands, liver, colon and testes. Aging reduces levels of lycopene in the blood. Elderly people are consistently deficient in nutrients, including ones that interact with lycopene such as vitamins C and E.
Lycopene: Promote Prostate Health
Epidemiological evidence strongly suggests that lycopene consumption contributes to prostate cancer risk reduction. Preclinical studies show that lycopene acts via different mechanisms, which have the potential to cooperate in reducing the proliferation of normal and cancerous prostate epithelial cells, in reducing DNA damage, and in improving oxidative stress defense. The mechanisms include inhibition of prostatic IGF-I signaling, IL-6 expression, and androgen signaling. Moreover, lycopene improves gap-junctional communication and induces phase II drug metabolizing enzymes as well as oxidative defense genes. These findings provide plausible explanations for the epidemiological findings how lycopene can contribute to reduced prostate cancer risk. The novel finding that lycopene reduces local androgen signaling in the prostate suggests also efficacy in prevention of benign prostate hyperplasia.
Lycopene: Implication in Other Cancers
Lycopene appears to be protective against cancer of the digestive tract. Several studies have found a lower risk for colorectal cancer in people who eat a lot of tomato products and/or have higher levels of lycopene in their blood. More direct evidence has been provided by researchers in Japan who did a study on colon cancer in rats. It's important to note, however, that pure lycopene did not. The authors of the study speculate that lycopene's action depends on other factors present in the juice that is missing in pure lycopene. Recent thinking in carotene research is that the carotenes are both interdependent and dependent on other vitamins and minerals, and this must be taken into account when studying them.
One of the largest and most important cancer/diet studies ever done shows the importance of the carotenes in digestive cancers. The study was begun in 1980 in Linxian, China. Linxian has one of the highest rates of esophageal and gastric cancer in the world. Its population also has subnormal levels of vitamins C, E, A, riboflavin and the carotenes. In an effort to see whether supplementation would cut the cancer rate, over twenty-nine thousand people were given four different nutrient combinations in the Linxian study. Four different combinations were tested: riboflavin, niacin; vitamin C, molybdenum; retinol, zinc; or beta-carotene, vitamin E, selenium. After five years, the results showed that the beta-carotene, Vitamin E, selenium combination cut the cancer rate and overall mortality. The others did not. Reduction in risk began to occur one to two years after supplements were begun. It was also discovered that men who took the combination had a lower risk of stroke, and better immune response.
Another cancer that may relate to lycopene is pancreatic cancer. Researchers at Johns Hopkins tested the stored blood of twenty-two people with pancreatic cancer for levels of certain vitamins and selenium before treatment began. The levels of these were lower in patients than controls. In hamsters, palm carotene (which contains lycopene) inhibits pancreatic cancer.
Beta-carotene from carrots is known for its antioxidant action. But did you know that there are over 600 known carotenoids besides beta? About 40 are found in the human diet, and not all of them turn into vitamin A. Lycopene is one that does not convert to vitamin A. Studies have shown that eating foods with lycopene provides stronger antioxidant protection against certain types of free radicals and does reduce the risk of some types of cancer and possibly heart disease. The carotenoid lycopene is the most common carotenoid found in the human body yet very little research has been done on it.
Carotenoids are organic chemicals that give plants their colors. Plant foods with lycopene are red like tomatoes, watermelons, grapefruits and papaya. A pigment synthesized by some plants and animals to protect them from the sun, lycopene evolved as a weapon against certain types of free radicals. Lycopene is so effective at quenching free radicals; it beat out vitamin E in one study on oxidized fat. This suggests that lycopene might have importance in preventing heart disease, which involves oxidized LDL cholesterol. The first evidence for a protective effect in heart disease was reported in the journal Lipids A group from Canada demonstrated that lycopene significantly lowers LDL oxidation in human blood. Lycopene works better in combination with lutein, another carotenoid which is found mostly in spinach and corn. (Lutein is associated with maintenance of the macula.) People with high cholesterol have been found to have high levels of free radicals and low levels of lycopene and beta-carotene. Humans get most of their lycopene from tomatoes, by far the richest source, yet tomato products offer a more concentrated source of lycopene than the fresh fruit itself. For example, tomato powder contains approximately 120 milligrams per 100 grams of fruit whereas fresh tomatoes have about 2 milligrams per 100. Since lycopene is a nutrient that can stand the heat, cooked tomato products, such as tomato paste, provide more of it than fresh tomatoes. It has been theorized that heating tomatoes makes their lycopene more absorbable.
Researchers are realizing that the cancer-preventive effects of the Mediterranean diet, which have been attributed to olive oil, may in fact be due to lycopene. Lycopene's cancer protection is in part due to its antioxidant protection. But some studies show that it may also modulate immunity, inhibit angiogenesis and affect hormonal effects in human.
There are no known lycopene antioxidant deficiency diseases. The reason that it is included in some dietary supplements, however, is because of scientific studies that indicate it may reduce the risk of some life threatening diseases and improve health. The FDA regulates health claims made by manufacturers of dietary supplements and food stuffs. In 2005, they addressed the issue of a lycopene daily requirement and proposed health claims of foods with lycopene. Their conclusion was that the limited scientific evidence suggests that consuming one-half to one cup of tomatoes or tomato sauce per week may reduce the risk of prostate cancer.
The carotenes are lipid soluble-they must have fat to be absorbed. It has been consistently demonstrated that foods with fat in them deliver more lycopene into the body. Lycopene is carried in the blood by the lipoprotein molecule (LDL) that also carries cholesterol. Drugs that lower cholesterol can drastically interfere with the carotenes. In one study, cholestyramine (Questran) decreased lycopene by 30% in the blood. It also reduced beta-carotene by 40% and vitamin E by 7%.
Other parts of the body besides the prostate that accumulate lycopene are the adrenal glands, liver, colon and testes. Aging reduces levels of lycopene in the blood. Elderly people are consistently deficient in nutrients, including ones that interact with lycopene such as vitamins C and E.
Lycopene: Promote Prostate Health
Epidemiological evidence strongly suggests that lycopene consumption contributes to prostate cancer risk reduction. Preclinical studies show that lycopene acts via different mechanisms, which have the potential to cooperate in reducing the proliferation of normal and cancerous prostate epithelial cells, in reducing DNA damage, and in improving oxidative stress defense. The mechanisms include inhibition of prostatic IGF-I signaling, IL-6 expression, and androgen signaling. Moreover, lycopene improves gap-junctional communication and induces phase II drug metabolizing enzymes as well as oxidative defense genes. These findings provide plausible explanations for the epidemiological findings how lycopene can contribute to reduced prostate cancer risk. The novel finding that lycopene reduces local androgen signaling in the prostate suggests also efficacy in prevention of benign prostate hyperplasia.
Lycopene: Implication in Other Cancers
Lycopene appears to be protective against cancer of the digestive tract. Several studies have found a lower risk for colorectal cancer in people who eat a lot of tomato products and/or have higher levels of lycopene in their blood. More direct evidence has been provided by researchers in Japan who did a study on colon cancer in rats. It's important to note, however, that pure lycopene did not. The authors of the study speculate that lycopene's action depends on other factors present in the juice that is missing in pure lycopene. Recent thinking in carotene research is that the carotenes are both interdependent and dependent on other vitamins and minerals, and this must be taken into account when studying them.
One of the largest and most important cancer/diet studies ever done shows the importance of the carotenes in digestive cancers. The study was begun in 1980 in Linxian, China. Linxian has one of the highest rates of esophageal and gastric cancer in the world. Its population also has subnormal levels of vitamins C, E, A, riboflavin and the carotenes. In an effort to see whether supplementation would cut the cancer rate, over twenty-nine thousand people were given four different nutrient combinations in the Linxian study. Four different combinations were tested: riboflavin, niacin; vitamin C, molybdenum; retinol, zinc; or beta-carotene, vitamin E, selenium. After five years, the results showed that the beta-carotene, Vitamin E, selenium combination cut the cancer rate and overall mortality. The others did not. Reduction in risk began to occur one to two years after supplements were begun. It was also discovered that men who took the combination had a lower risk of stroke, and better immune response.
Another cancer that may relate to lycopene is pancreatic cancer. Researchers at Johns Hopkins tested the stored blood of twenty-two people with pancreatic cancer for levels of certain vitamins and selenium before treatment began. The levels of these were lower in patients than controls. In hamsters, palm carotene (which contains lycopene) inhibits pancreatic cancer.
Nine Digestive Disease Myths
Only recently many often-complex diseases affecting the digestive system have been explored by the researchers. Accordingly, people are gradually replacing folklore, old wives' tales, and rumors about the causes and treatments of digestive diseases with accurate, up-to-date information. But misunderstandings still exist, and, while some folklore is harmless, some can be dangerous. Listed below are some common misconceptions (fallacies), about digestive diseases, followed by the facts as professionals understand them today.
Myth # 1 Spicy food and stress cause stomach ulcers.
The truth is, the majority of stomach ulcers are caused either by infection with a bacterium called Helicobacter pylori (H. pylori) or by use of NSAIDS (non-steroidal anti-inflammatory drugs) or pain killers. Most H. pylori-related ulcers can be cured with antibiotics. NSAID-induced ulcers can be cured with time, stomach-protective medications like Suralfate, Proton Pump Inhibitors (PPi-s like Omeprazole, pantoprazole, rabeprazole, esomeprazole etc), antacids and avoidance of NSAIDs. Recently ulcers not related to H. pylori or NSAIDS are drawing medical attention, but spicy foods and stress (except when associated with extreme medical conditions) may aggravate ulcer symptoms in some people, but they do not cause ulcers. Certain cancers can be caused by ulcers also.
Myth # 2 Smoking a cigarette helps relieve heartburn.
In fact it is the reverse that actually occurs, cigarette smoking increases heartburn or gastro-esophageal reflux disease (GERD). Heartburn occurs due to chronic inflammation of lower esophagus (esophagitis) occurring due to reflux of acid from the stomach into the esophagus. This is due to relaxation of Lower Esophageal Sphincter (LES) which gets more relaxed due to smoking.
Myth # 3 Celiac disease is a rare childhood disease.
Celiac disease affects both children and adults. Sometimes celiac disease first causes symptoms during childhood, usually diarrhea, growth failure, and failure to thrive. But the disease can also first cause symptoms in adults of any age. These symptoms may be vague and therefore attributed to other conditions. Symptoms can include bloating and abdominal distention, flatulence, diarrhea, and abdominal pain due to the involvement of the small intestine as well as skin rash, anemia and thinning of the bones (osteoporosis) due to malabsorption of nutrients by the diseased intestine. People with celiac disease should not eat any foods containing gluten, a protein in wheat, rye, and barley, whether they have symptoms or not.
Myth # 4 Bowel regularity means a bowel movement every day.
This is a misconception. The frequency of bowel movements among normal, healthy people varies from three a day to thrice a week and some perfectly healthy people fall outside both ends of this range. But sometimes three bowel movements with/without true normal consistency a day in people having one bowel movement usually a day may be abnormal. Patients with Irritable Bowel Syndrome (IBS) may have fluctuating numbers of stools each day as well as fluctuating consistency of their stools along with pain abdomen.
Myth # 5 Habitual use of enemas to treat constipation is harmless.
It is not clear whether or not habitual use of enemas is harmless since there has been very little study of the effects of enemas or laxatives over the long term. Early studies showed that laxatives might injure the colon if taken chronically by impairing contraction of the colonic muscles, and this finding was extrapolated to include enemas. The data from the studies is not strong, however. In fact, some physicians feel that enemas are preferred over laxatives since they are a more "natural" means of stimulating a bowel movement. (Enemas mimic a large amount of stool in the rectum, the usual stimulus for a bowel movement.) An ongoing need for enemas is not normal; you should see a doctor if you find yourself relying on them or any other medication to have a bowel movement.
Myth # 6 Diverticulosis is a serious but uncommon problem.
Actually, the majority of Americans over age 60 have diverticulosis, but only a small percentage has symptoms or complications. Diverticulosis is a condition in which little out-pouching called diverticula develop in the wall of the colon. These sacs tend to appear and increase in number as individuals age. Most people have no symptoms and learn that they have diverticula after an X-ray or intestinal examination (for example, colonoscopy, and small bowel barium enema) that is being done for a purpose unrelated to the diverticulosis. Less than 10 percent of people with diverticulosis ever develop complications such as infection (diverticulitis), bleeding, or perforation of the intestine.
Myth # 7 Inflammatory bowel disease (Ulcerative Colitis and Crohn's Disease) is caused by psychological problems.
Inflammatory bowel disease is the general name for two diseases of opposite spectrum that cause inflammation in the intestines, Crohn's disease and ulcerative colitis. The cause of the disease is unknown, but researchers speculate that it may be a virus or bacteria interacting with the body's immune system. No evidence has been found to support the theory that inflammatory bowel disease is caused by tension, anxiety, or any other psychological factor or disorder, although these can aggravate the discomfort caused by the disease.
Myth # 8 Cirrhosis is caused only by alcoholism.
Alcoholism is just one of many causes of cirrhosis. Cirrhosis is scarring and decreased function of the liver. In the United States, alcohol causes less than one-half of cirrhosis cases. The remaining cases are from diseases that cause liver damage. For example, in children, cirrhosis may result from cystic fibrosis, alpha-1 antitrypsin deficiency, biliary atresia, glycogen storage disease, and other rare diseases. In adults, cirrhosis may be caused by hepatitis B or C, primary biliary cirrhosis, diseases of abnormal storage of metals like iron or copper in the body, severe reactions to prescription drugs, or injury to the ducts that drain bile from the liver. In adults, cirrhosis can also be caused by Nonalcoholic Steatohepatitis (NASH), which is becoming the most common liver disease in the United States, affecting 2 to 5 percent of Americans.
Myth # 9 Ostomy Surgery: After ostomy surgery, men have erectile dysfunction and women have impaired sexual function and are unable to become pregnant.
Ostomy surgery does not, in general, interfere with a person's sexual or reproductive capabilities. Ostomy surgery is a procedure in which the diseased part of the small or large intestine is removed and the remaining intestine is attached to an opening in the abdomen. Stool is collected in a bag taped to the skin over the opening. Alternatively, an internal pouch that collects the stool may be formed from a portion of the intestine. The pouch then can be emptied by insertion of a catheter at regular intervals.
Although some men who have had radical ostomy surgery for cancer lose the ability to achieve and sustain an erection, most men do not, or, if they do, it is temporary. This is caused by damage to the nerves innervating the penis. In women, ostomy surgery does not damage sexual or reproductive organs, so it is not a direct cause of sexual problems or sterility. Factors such as pain and the adjustment to a new body image may create temporary sexual problems, but they can usually be resolved with time and counseling. Unless a woman has had a hysterectomy to remove her uterus, she can still bear children.
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