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To: net
Subject: Susan give us your opinion
Date: Sun, 2 Nov 2008 05:15:03 -0800

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Date: Fri, 6 Jun 2008 07:40:03 +1000
From: ssamail@seafoodaustralia.com.au
To:
Subject: HIGH-FISH MEDITERRANEAN DIET FIGHTS TYPE-2 DIABETES

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Media release – 5 June 2008

HIGH-FISH MEDITERRANEAN DIET FIGHTS TYPE-2 DIABETES
International research provides great news for millions of at-risk Australians.

THERE’S great news for the millions of Australians at risk of Type-2 diabetes -- a high-fish Mediterranean diet can help prevent the disease.

An expert in the health benefits of seafood, Mr Roy Palmer, said today a major research project suggested adherence to a Mediterranean diet reduced the risk of Type-2 diabetes by more than 80%. “With 700,000 Australians diagnosed with T2 diabetes already, and 100,000 more people joining them every year, greatly increasing their risk of heart attack, stroke, kidney failure, blindness and amputations, it is already one of our most serious health problems,” Mr Palmer said. “However, Diabetes Australia says that, on present trends, 3.3 million Australians are likely to suffer from T2 diabetes by 2031. That is horrific.”
Mr Palmer, the Australian link in a worldwide network researching and communicating the health benefits of seafood, said details of the research project had just been published in the British Medical Journal.
“The traditional Mediterranean diet is high in fish, olive oil, vegetables, fruits, nuts, cereals and legumes (vegetables such as peas and beans) but relatively low in meat and dairy products. The study found the closer people stick to that type of diet, the less likely they are to develop T2 diabetes.
“Researchers from the University of Navarra in Spain followed the diets and health of more than 13,000 people for an average of almost four-and-a-half years. The best adherents reduced their T2 diabetes risk by 83%, despite sometimes higher than average risk factors for the disease.
“These people were often older, fatter, more sedentary, ex-smokers, and with high blood pressure and a family history of T2, and would have been expected to show higher than average incidence of diabetes. The fact this did not happen indicates the diet has what the researchers called a ‘substantial potential for prevention’
“Overall, they concluded that a traditional Mediterranean food pattern is associated with a significant reduction in the risk of developing Type-2 diabetes.
“This is a very important study,” Mr Palmer said. “We already know the Mediterranean diet protects against heart disease, as does eating oily fish in general, but the fact it also protects against Type-2 diabetes means following this type of diet could potentially extend the lives of millions more Australians. This news should be very widely publicised.”


FURTHER INFORMATION: Mr Roy Palmer 0419 528 733

Download the British Medical Journal paper Recent information on the incidence and impact of T2 diabetes can be found at the Diabetes Australia website and the Australian Institute of Health and Welfare website
For more information on the health benefits of seafood, see the Seafood Services Australia website.

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From: Newsletter@reply.leukemia-lymphoma.org
To: susan_oliver1@hotmail.com
Subject: Christine and Leukemia – The Gift of Appreciation
Date: Thu, 1 May 2008 12:46:39 -0500

This is the first in a series of communications that are being sent to our friends and contacts.  We have launched this series to provide insight as to the difference your support is making in the lives of people who you may never meet, but to whom you are nonetheless connected.  We also intend to share with you relevant breaking news or updates on our research progress.  You are free to unsubscribe from this series of emails at any time, but I hope instead you will find the material informative, uplifting and will help keep you connected to LLS. Today, I'd like to share with you Christine Wonica's story, she is a blood cancer patient who became part of the LLS family through our First Connection program, one of the many support programs available to patients across the U.S. and Canada.    Christine and Tom Wonika had what many would call the perfect life - they had a new daughter, they would soon move into a new home, and Tom had just started a new job.  But in March 2002 Christine found out that she had acute myelogenous leukemia (AML).  It was a major challenge  and they tackled it together. Christine, like most AML patients, was encouraged to begin chemotherapy. While Christine was getting this treatment, her husband Tom contacted The Leukemia & Lymphoma Society (LLS) for advice and guidance.  He soon learned about the First Connection program, which matches patients with trained peer volunteers who have been through blood cancer.  Christine was able to talk to someone else who had also had AML.  It was a great relief. "We shared our experiences.  Just hearing the similarities that we had was very comforting.  It was good to know that I wasn't alone or crazy and that other people felt the same way," says Christine. Christine was in remission after her first phase of chemotherapy, but her cancer returned nine months later.  She had more chemotherapy, and then had a successful bone marrow transplant in November 2003.  Throughout the entire ordeal, the family counted their blessings.  Christine and Tom's parents were able to step in when needed, and Tom was able to continue working. Despite the challenges that came with cancer Christine admits that she feels the experience of living with AML was one of the best things that could have happened to her.  She's stronger, and has more compassion and passion for life. "The fight against cancer is really bad. But the light at the end of the tunnel is more amazing than you can ever imagine.  Now I have the chance to really appreciate the things that I fought so hard to keep in my life - like the sun shining and my daughter's smiles." To learn more about LLS, please visit us at www.lls.org. Best of health, John E. Walter President & CEO     The Leukemia & Lymphoma Society is the world's largest voluntary health organization dedicated to funding blood cancer research, education and patient services. The Society's mission: Cure leukemia, lymphoma, Hodgkin's disease and myeloma, and improve the quality of life of patients and their families. See how your donations are invested wisely.   Home Office 1311 Mamaroneck Avenue • White Plains, NY 10605 914.949.5213 • www.LLS.org © 2008 The Leukemia & Lymphoma Society All Rights Reserved

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http://braininjury.com/littleknownsymptoms.html
http://braininjury.com/symptoms.html

LITTLE KNOWN SYMPTOMS/INJURIES
FROM TRAUMATIC BRAIN INJURY

Along with the standard injuries involving cognitive ability, personality change, executive function decline, and others which have been widely reported on, there are additional injuries and symptoms suffered by those who have had traumatic brain injury, which are not widely known but can cause profound problems. These include:

1. VISION DISTURBANCES:
   Vision disturbances following traumatic brain injury are common, seen in 30% to 85% of cases. These symptoms are often one of the last to be treated and often escapes detection. Standard treatment by an eye doctor or ophthalmologist can often fail to find the cause of blurred vision, photo sensitivity, change in field of vision and anomalies of accommodation commonly found after TBI. The most common, difficulties of 'accommodation,' may result in blurred vision. This is the eyes inability to accurately change focus from far to near or from near to far. Difficulties of 'version' are seen in such abnormalities as saccads, pursuit and fixation, and other changes which result in lost of place while reading, skipping lines, or re-reading lines due to abnormal movements of the eye. Thirdly, there are abnormalities of 'vergence' which result in occasional or constant eye strain or sense that the print on a book is 'shimmering' or 'floating' on the page. There can also be abnormalities of the field of vision can result in lack of awareness of the field of vision on one side or the other side of the body. Finally, there can be abnormalities in light sensitivity which can cause pain and headache in patients.
   
   
2. SUDDEN SENSORINEURAL HEARING LOSS:
   Sudden sensorineural hearing loss (SNHL) is a common phenomena which can be caused by trauma, infectious disease, or tumor. It is often found in conjunction with damage to the vestibular system of the body, which deals with balance. A common test done by physicians called Romberg Test provides information on the integrity of the system. Audiologist can do hearing tests which can confirm or point to this diagnosis. Many patients recovery full or partial hearing loss after a year or two.
   
   
3. ALTERATION OF SMELL OR TASTE:
   Cranial nerve damage is a common finding in mild to moderate head injury. One of the results can be a loss or alteration in the sense of smell and because of that the sense of taste. The loss of smell is called anosmia. Many neurologist and other physicians now have the ability to test for loss of smell. This loss can occur on each or both sides, so do not forget to have each nostril tested separately. In a recent study by Varney and others a PET scan was able to detect the specific brain damage associated with anosmia. If there is an alteration in the way food taste or commonly an inability to cook properly because of lack of smell, please have this testing done.
   
   
4. ENDOCRINE/GLANDULAR DYSFUNCTION:
   Especially in cases of moderate and severe brain injury, patients should be routinely given blood tests to see if the human hormonal glands are functioning normally. The pituitary gland is particularly at risk, and blood work should be done to show whether or not the gland is functioning properly. If there is a decrease in the production of growth hormone, rather expensive hormone therapy may need to be implemented because of the long term ill effects of low pituitary output which may affect the heart, the psychiatric status of the patient, and may have other effects not fully know at this time. Many physicians feel that there needs to be observable damage to the small but powerful glands in the brain in order to consider testing for output. There does not have to be observable damage for such an injury to occur, if there otherwise was a moderate to severe brain injury involved in the patient. These glandular disruptions would be the cause of the very common sexual dysfunction seen in TBI survivors.
   
   Another result of glandular dysfunction following TBI is the onset of cranial diabetes insipidus. Therefore, it is important to be on the lookout for signs of diabetes (unusual thirst, change in urination, lightheadedness or fainting) following TBI.

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Brain Stem: deep within the brain

• Decreased vital capacity in breathing, important for speech.
• Swallowing food and water (Dysphagia).
• Difficulty with organization/perception of the environment.
• Problems with balance and movement.
• Dizziness and nausea (Vertigo).
• Sleeping difficulties (Insomnia, sleep apnea).

Cerebellum: base of the skull

• Loss of ability to coordinate fine movements.
• Loss of ability to walk.
• Inability to reach out and grab objects.
• Tremors.
• Dizziness (Vertigo).
• Slurred Speech (Scanning Speech).
• Inability to make rapid movements.

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Occipital Lobes: most posterior, at the back of the head

• Defects in vision (Visual Field Cuts).
• Difficulty with locating objects in environment.
• Difficulty with identifying colors (Color Agnosia).
• Production of hallucinations.
• Visual illusions - inaccurately seeing objects.
• Word blindness - inability to recognize words.
• Difficulty in recognizing drawn objects.
• Inability to recognize the movement of object (Movement Agnosia).
• Difficulties with reading and writing.

Temporal Lobes: side of head above ears

• Difficulty in recognizing faces (Prosopagnosia).
• Difficulty in understanding spoken words (Wernicke's Aphasia).
• Disturbance with selective attention to what we see and hear.
• Difficulty with identification of, and verbalization about objects.
• Short term memory loss.
• Interference with long term memory.
• Increased and decreased interest in sexual behavior.
• Inability to catagorize objects (Categorization).
• Right lobe damage can cause persistent talking.
• Increased aggressive behavior.

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Updated: 06 February 2008

PROOF OF MILD TRAUMATIC BRAIN INJURY IN MICE
Because it is unethical to produce traumatic brain injury in humans, many of the most cutting edge experiments are done on mice. Although this is unfortunate, studies show that mild traumatic brain injury, when induced in mice, shows signs of apoptotic cell death in the brain.“"Apoptotic cell death" is a fancy word for programed cell death. All of the cells in our body have the ability to regulate their population, if needed. In addition to this internal balance in the body, it has been discovered that traumatic brain injury can give rise to disregulation of brain chemicals, and can thus lead to apoptotic cell death in brain cells. This study at the University of Pennsylvania found objective signs of apoptotic cell death following mild traumatic brain injury to rats. Findings of this occur as a result of mild traumatic brain injury helps explain why in some cases mild traumatic brain injury has long standing and profound effects.

A second study on mice published in the Journal of Neurotrauma showed mice with induced mild traumatic brain injury suffered long lasting cognitive defects, emotional difficulties and behavioral disturbances. Again, the prejudice against those who complain of ongoing symptoms after mild traumatic brain injury is increasingly misplaced. These studies show not only objective signs of brain injury after a mild trauma but show that long term symptomology is shown in mice similar to those reported in humans with post concussive syndrome.

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CENTER FOR DISEASE CONTROL DEFINITION OF MILD TRAUMATIC BRAIN INJURY
The Center for Disease Control (CDC) in 2003 published the following:

Recommended definitions for mild traumatic brain injury.

Incident cases of MTBI

The conceptual definition of MTBI is an injury to the head as a result of blunt trauma or acceleration or deceleration forces that result in one or more of the following conditions:

Any period of observed or self reported:

• transient confusion, disorientation, or impaired consciousness;
• dysfunction of memory around the time of injury;
• loss of consciousness lasting less than 30 minutes.

Observed signs of neurological or neuropsychological dysfunction, such as:

• seizures acutely following injury to the head;
• symptoms among older children and adults such as headache, dizziness, irritability, fatigue or poor concentration, when identified soon after injury, can be used to support he diagnosis of mild TBI, but cannot be used to make the diagnosis in the absence of loss of consciousness or altered consciousness. Research may provide additional guidance in this area.

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MEMORY/PROBLEM SOLVING CONTINUE TO IMPROVE AFTER TBI
In a study (Hammond FM et al., 2004) patients who had suffered TBI were tested between the years one and five post injury. The greatest amount of improvement noted was observed in memory and problem solving (34%) which was higher than previous studies had indicated.

The greatest amount of decline was observed for social interaction, which was consistent with previous studies.

These results are more hopeful for victims of TBI that the previous idea that little, if any, cognitive recovery occurs after one or two years post injury.

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http://braininjury.com/cranial-nerve-injury.html

CRANIAL NERVE INJURY

The cranial nerves are nerves that run from the base of the brain into different parts of the head. They can commonly be involved in traumatic injury which also includes injury to the brain itself. Unlike injuries to nerves and other parts of the body, injuries to the cranial nerves can also involve alteration or destruction of some of our senses themselves. Treating physicians also refer to cranial nerves by there number. There are twelve below which are described and represented by roman numerals.

I. Olfactory
Special Sensory - Sensation of smell

II. Optic
Special Sensory - Sensation of vision

III. Oculomotor
Somatic Motor - Movement of the eyes and eyelids
Visceral Motor - Parasympathetic control of pupil size

IV. Trochlear
Somatic Motor - Movement of eyes

V. Trigeminal
Somatic Sensory - Sensation of touch to the face
Somatic Motor - Movement of muscles of mastication (chewing)

VI. Abducens
Somatic Motor - Movements of the eye

VII. Facial
Somatic Sensory - Movement of muscles of facial expression
Special Sensory - Sensation of taste in anterior two-thirds of the tongue

VIII. Auditory- vestibular
Special Sensory - Sensation of hearing and balance

IX. Glossopharyngeal
Somatic Motor - Movement of muscles in the throat (oropharynx)
Visceral Motor - Parasympathetic control of the salivary glands
Special Sensory - Sensation of taste in posterior one-third of the tongue
Visceral Sensory - Detection of blood pressure changes in the aorta

X. Vagus
Visceral motor - Parasympathetic control of the heart, lungs, and abdominal organs

XI. Spinal accessory
Somatic motor - Movement of muscles in the throat and neck

XII. Hypoglossal
Somatic motor - Movement of the tongue

One of the most commonly injured cranial nerves is cranial nerve I the olfactory nerve, which controls the sense of smell. Because our sense of taste depends primarily on smell, our sense of taste might be altered as well. Terms used to describe problems in this include:

• Dysnosmia- impaired sense of smell
• Ansomia- Complete lost of smell
• Prosmia- Sensation of smell without cause
• Cosmia- Smelling an offensive odor that does not exist

Generally cranial nerves are not injured in cases of mild tbi. However, it is well document that cranial nerve 1 can be disrupted in the context of a mild tbi.

The optic (cranial nerve II) plays a critical role in human sight. Approximately 5 % of patients with tbi receive optic nerve injury. Injury to the optic nerve can cause the pupil to loose its reactivity to light, visual acuity, or visual fields can be affected. Examination must be done to differentiate between effects of optic nerve damage versus damage to non-nerve related areas to the visual system.

It should be remembered that, like the brain, cranial nerve can recover from a traumatic injury. The cranial nerve is stretched or bruised. Function can recover for up to a year. Post trauma. During that time there may be tingling or sporadic enervation, both of which are uncomfortable, but also show signs of recovery of that nerve.

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http://braininjury.com/coma.html
 
VEGETATIVE STATE:

"Coma" describes a patient whose eyes are continuously closed and who cannot be aroused to a wakeful state. However, another version of diminished consciousness exists, similar to coma, called "vegetative state." Vegetative state is similar to coma but the eyes are open and can briefly track objects or sounds. Many patients limbs are spastic.

The possibility of recovery from vegetative state (VS) depends on how long the state lasts. Bricolo (1980) followed 34 patients with post traumatic VS who opened their eyes spontaneously within two weeks of injury and 74% of those eventually achieved a satisfactory outcome. Of those whose eyes opened between the second and fourth week, 32% improved while only 18% of patients who opened their eyes during the second month eventually recovered.

The chart below gives some indication of probably outcome:

Author	No. of Patients VS	Duration of Period	Follow-up Period	No. of Recovered Patients	Percent Recovery
Bricolo et. al Bricolo et. al Bricolo et. al Sazbon & Groswasser Levine et al. (a) Braakman et al. (b) Levy et al. Sato et al. Nakazawa et al Okui Higashi et al	34 69 22 134 93 140 25 216 1,556 1,183 110	2 weeks 1 month 2 months 1 month 1 month 1 month 1 month >3 months >3 months >3 months >3 months	1 year 1 year 1 year 3-52 mos. 1 year 1 year 1 year 1 year 1 year 1 year 5 years	16 11 6 72 48 59 2 14 18 14 8	47.0 31.8 18.1 53.7 51.6 42.1 8.0 6.5 1.2 1.2 7.2
(a) Report from U.S. Traumatic Coma Data Bank. (b) Report from International Traumatic Coma Data Bank

Follow-up Results in 140 Patients Vegetative
at 1 Month After Injury

Age at Injury	Total Number of cases	% Independent at 1 year
< 20 years 20-40 years > 40 years	53 46 41	19 9 0
Sources: Data from Braakman et al. (1988) and Jennett and Braakman (1990), used with permission.

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FATIGUE AND MILD TRAUMATIC BRAIN INJURY
Although fatigue is one of the most reported symptoms after TBI, there have not been many studies on its effects. A group in the Netherlands (Stuleneijer, M et al. 2006), studies approximately 300 patients with MTBI found that one-third of the patients experienced severe fatigue six months after injury and that the type of fatigue is associated with limitations in daily functioning. Severe fatigue was highly associated with the experience of other symptoms and limitation and did not stand alone.
RELIEF FROM CHRONIC PAIN?
Persons suffering from intractable chronic pain have found relief in monitoring their own brain waves on a functional MRI scanner. After some training, the volunteers were able to make changes in the way their brains processed the pain signals and reported feeling less pain. The Stanford University study physicians caution that much is yet to be done but a company called Omneuron is trying to develop the equipment for commercial use.

CURE FOR COCAINE HABIT?
Because many who suffer traumatic brain injury can develop addiction problems, a recent finding could provide some help. Cocaine addicts, who were hospitalized, were given a supplement known as NAC (N-acetylcysteine), which appear to lessen the desire for the drug. MRI’s taken of the patient’s brain saw a difference associated with the supplement.

MOLECULAR DAMAGE FROM TBI ONGOING FOR YEARS
In a recent paper further evidence of secondary or delayed cell death following TBI was shown. The diffuse and wide spread damage is progressive and prolonged for months or years after the initial insult. Areas continued to be vulnerable to such ongoing destruction are the cortex, hippocampus, thalamus, striatum and subcortical nuclei.

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OUTCOME 3 TO 5 YEARS AFTER MODERATE TO SEVERE TBI
Investigators (Dikmen, SS 2003) followed persons with moderate to severe TBI for three to five years noting the degree of recovery. Unfortunately, significant functional limitations were observed in all areas. In 65% of cases, there was recovery to pre-injury levels in personal care, 40% recovered in regard to cognitive competency, major activity, leisure and recreation. How long the patient was unconscious appeared to contribute to the outcome more than damage seen on MRI.

EFFECTS OF AGING ON TBI RECOVERY
Researches at the Mayo Clinic (Testa JA et al. 2005) confirmed again what was previously known - that age adversely affects recovery from TBI. Findings show that older patients with TBI have a greater likelihood of becoming physically and financially dependent on others. Older TBI patients were more likely to have changes in employment status compared with younger patients. An earlier study had compared TBI patients over 60 ,and limited to patients with only mild TBI, they showed the same improvement and functional status as the patients under 60. Therefore, the age difference appears to be more significant as the injury goes from mild into the moderate and severe categories.

LONG TERM OUTCOME FOLLOWING MILD TBI
Patients, on an average of 8 years post TBI, most in the mild range, were given follow-up neuropsychological testing and compared with normals than those who were in motor vehicle accident without TBI. Those who suffered the mild TBI continued, an average of 8 years later, to have problems with aspects of attention and working memory. The study’s conclusion was that it showed “that MTBI can have adverse long-term neuropsychological outcomes on subtle aspects of complex attention and working memory.

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PEDIATRIC TBI EQUALS WORSE OUTCOME
An experiment, with one-week old rats who sustained TBI, has clearly shown that the trauma triggered cell death (apoptosis) in the brains of the very young rats was far greater than those in older rats. These results help explain the unfavorable outcomes of very young pediatric head trauma patients and outlines again the importance of trying to prevent secondary cell death following head trauma.

WATCH YOUR PITUITARY
Pituitary gland function and levels of growth hormone can be adversely affected by TBI. A recent study (Aimaretti, G. 2004) suggest that careful screening of the pituitary function should occur following TBI. Keeping these systems in chemical balance will speed TBI recovery.
 
SAY NO TO HERBAL REMEDIES
The use of herbal supplements is common in the U.S. However, following a brain injury, remedies such as St. Johns Wort and Ginko Giloba, SHOULD BE AVOIDED. Studies show that they may induce mania in TBI patients. If you feel that you must take supplements, make sure you clear them with your doctor, especially if taken in conjunction with prescription medication. (Spinella M., 2002)


 

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SLEEP DISORDERS
This study, among others, has confirmed that there is a direct relationship between traumatic brain injury and the emergents of sleep disorders. The severity and impact of chronic sleep disorder is just now beginning to be understood, and is far more of a problem than previously thought. (Beetar 1999)

INVISIBLE INJURIES
In this older study, reconfirmed by more recent studies, 686 victims of mild traumatic brain injury were examined and found to have completely normal neurological exams. The patients then underwent imaging studies and 18% of the patients were found to have lesions in the brain. (Stein 1993)

HYPERTENSION
Contrary to what was previously thought, cognitive decline in patients suffering from diabetes and hypertension starts at middle age rather than old age. (Knopman 2001)

MAGNETIC RESONANCE SPECTROCOPY (MRS)
Yet another study confirms the exciting possibilities of this new diagnostic tool, which measures the relationship of brain chemicals utilizing MRI. The finding of certain relationships is consistent with the diagnosis of brain injury. (Brooks W.M. 2001)

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