Health:News N Tips

Swine flu offers 'extraordinary super immunity'

noreply@blogger.com (Sridevi. V, M.A) — Tue, 11 Jan 2011 04:09:00 +0000

Swine flu offers 'extraordinary super immunity'

Swine flu infection boosted immunity to surprising degrees

People who recover from swine flu may be left with an extraordinary natural ability to fight off flu viruses, findings suggests.

In beating a bout of H1N1 the body makes antibodies that can kill many other flu strains, a study in the Journal of Experimental Medicine shows.

Doctors hope to harness this power to make a universal flu vaccine that would protect against any type of influenza.

Ultimately this could replace the "best guess" flu vaccines currently used.

Such a vaccine is the "holy grail" for flu researchers. Many scientists are already testing different prototypes to put an end to the yearly race to predict coming flu strains and quickly mass produce a new vaccine each flu season.

Dr Patrick Wilson who led the latest research said the H1N1 swine flu virus that reached pandemic levels infecting an estimated 60 million people last year, had provided a unique opportunity for researchers.

This work gives us more confidence that it will be possible to generate a universal flu vaccine”- Dr Sarah Gilbert Flu vaccine expert at Oxford University

"It demonstrates how to make a single vaccine that could potentially provide immunity to all influenza.

"The surprise was that such a very different influenza strain, as opposed to the most common strains, could lead us to something so widely applicable."

Extraordinary immunity

In the nine patients they studied who had caught swine flu during the pandemic, they found the infection had triggered the production of a wide range of antibodies that are only very rarely seen after seasonal flu infections or flu vaccination.

Five antibodies isolated by the team could fight all the seasonal H1N1 flu strains from the last decade, the devastating "Spanish flu" strain from 1918 which killed up to 50m people, plus a potentially deadly bird flu H5N1 strain.

The researchers believe the "extraordinarily" powerful antibodies were created as the body learned how to fight the new infection with swine flu using its old memory of how to fight off other flu viruses.

Next they plan to examine the immune response of people who were vaccinated against last year's swine flu but did not get sick to see if they too have the same super immunity to flu.

Dr Sarah Gilbert is a expert in viruses at Oxford University and has been testing her own prototype universal flu vaccine.

She said: "Many scientists are working to develop a vaccine that would protect against the many strains of flu virus.

"This work gives us more confidence that it will be possible to generate a universal flu vaccine."

But she said it would take many years for a product to go through the necessary tests and trials.

"It will take at least five years before anything like this could be widely available."

The number of deaths this winter from flu verified by the Health Protection Agency currently is 50, with 45 of these due to swine flu.

Baldness treatments / Hair falling / loss prevention - Top / Popular Health News N Tips

noreply@blogger.com (Sridevi. V, M.A) — Thu, 24 Dec 2009 12:15:00 +0000

Baldness treatments

More than half of men are affected by male pattern baldness by age 50, and baldness treatments are estimated to be a US $1 billion per year industry.^[1] Since the 1980s, drug therapy has increasingly become a realistic management option for baldness for men and women. Increased understanding of the role of dihydrotestosterone (DHT) in male and female pattern baldness has led to targeted intervention to prevent this hormone from acting on receptors in the scalp.

However, experts warn that many treatments marketed as hair loss cures are ineffective aside from the placebo effect.

Approved treatments

U.S.

There are only two drug treatments approved by the U.S. Food and Drug Administration (FDA) for male baldness: Minoxidil^[2] and Finasteride . Finasteride is recommended first for male pattern baldness. There is also a medical device that has FDA 510(k) Clearance for Marketing that is indicated to promote hair growth in males with certain clases of androgenetic alopecia.

Minoxidil (Rogaine/Regaine)

Minoxidil is a vasodilator and originally was exclusively used as an oral drug (Loniten) to treat high blood pressure. It was discovered, however, to have the side effect of hair growth and reversing baldness, and in the 1980s, Upjohn Corporation received FDA approval to market a topical solution that contained 2% minoxidil to be used to treat baldness and hair loss as Rogaine, marketed as Regaine outside the USA.

Objective evidence shows that minoxidil is effective in both the frontal areas of the scalp and the vertex area in treating male-pattern hair loss. At the conclusion of a 48 week study, improvements were seen in the frontal scalp regions of 51% of men using 5% minoxidil, 42% using 2% minoxidil, and 13% of placebo users. Among these men, moderate to great increases in hair growth were seen in the frontal scalp regions of 19% of men using 5% minoxidil, 10% using 2% minoxidil, and 3% of placebo users.

The method of action for minoxidil is not known.

Finasteride (Propecia)

Finasteride, initially marketed as the brand-name drugs Propecia and Proscar by Merck, belongs to a class of drugs called aza-steroids. Finasteride is a "DHT inhibitor" and was originally approved by the US FDA for the treatment of benign prostatic hyperplasia (BPH). The drug works by binding to 5-alpha-reductase, the enzyme responsible for the conversion of free testosterone to DHT.

Merck sought to find the smallest effective quantity of finasteride and test its long-term effects on 1,553 men between ages 18 and 41 with mildly to moderately thinning hair. Based on their research, 1 mg daily was selected, and after two years of daily treatment, over 83% of the 1,553 men experiencing male hair loss had actually maintained or increased their hair count from baseline. Visual assessments concluded that over 80% had improved appearances.

In 1997, finasteride was approved by the US FDA for the treatment of male pattern baldness. A 5-year study revealed that 9 of 10 men taking finasteride (1 mg daily) experienced visible results (42% of men taking Propecia experienced no further hair loss while 48% experienced no further hair loss and hair regrowth). In clinical studies, finasteride, like minoxidil, was shown to work on both the crown area and the hairline area, but is most successful in the crown area.

Finasteride is usually only prescribed for men and should not be used by pregnant or potentially pregnant women, as it has been speculated that it could cause severe birth defects in male fetuses. Finasteride's supporters respond that the studies on post-menopausal women whose hairloss were more likely related to the loss of estrogen versus a sensitivity to testosterone.

Antiandrogens

Antiandrogens block DHT already produced and present in the blood stream from binding with hair follicles. Their specificity varies greatly from specific antiandrogens such as finasteride which inhibit the conversion of testosterone to DHT by interfering with 5-alpha-reductase to more broad spectrum antiandrogens (fluconazole, spironolactone, etc.). Although unusual in clinical doses, antiandrogens can have serious side effects including gynecomastia.

Dutasteride

In 2001, GlaxoSmithKline released another aza-steroid called dutasteride, marketed as Avodart. Like finasteride, dutasteride was originally developed for the treatment of benign prostatic hyperplasia (BPH). It is not currently sold for baldness treatment.

While hair count studies showed that 2.5 mg of dutasteride was about 1.5 times as effective as finasteride for hair regrowth (adding on average 108 versus 72 hair per 1" diameter area), Glaxo stopped FDA hair loss studies after phase II. Although the exact reason was never made public, it was speculated that the product was too similar to finasteride, which itself had not lived up to expectations commercially. As such, the 2.5 mg dosage was not released. The FDA trials for BPH continued, and Avodart became the first drug shown to shrink an enlarged prostate in a clinical study. The .5 mg version of the drug (shown in the same study to add on average 92 hairs to the same area) is increasingly available to hair loss sufferers via the grey-market of online prescription medication, and physicians increasingly willing to prescribe drugs "off-label."

In December 2006, GlaxoSmithKline embarked on a new Phase III, six month study in Korea to test the safety, tolerability and effectiveness of a once-daily dose of dutasteride (0.5 mg) for the treatment of male pattern baldness in the vertex region of the scalp (types IIIv, IV and V on the Hamilton-Norwood scale). GlaxoSmithKline has published the results of the study, concluding

This study demonstrated dutasteride 0.5 mg /day administered for 6 months was well tolerated and slowed the progression of hair loss and increased hair growth in Korean men. For hair counts as assessed by macrophotography in the vertex at 6 months (primary endpoint), the dutasteride 0.5 mg group was significantly superior to the placebo group. The hair count difference at 6 months between dutasteride and placebo group was 7.5 ± 20.4 (95% CI = 0.8, 14.3). The overall incidence of adverse events and adverse drug reactions during treatment was similar in the two groups.. The most commonly reported adverse event in both groups was nasopharyngitis. One serious adverse event was reported during the trial (thyroid cancer in the placebo group).

The future impact that this study will have on the US FDA's approval or disapproval of Avodart for the treatment of male pattern baldness in the United States is yet to be determined.

Ketoconazole

Ketoconazole is a synthetic antifungal drug used to prevent and treat skin and fungal infections, especially in immunocompromised patients such as those with AIDS. Because it is both an anti-fungal, a 5-alpha reductase inhibitor and a hair growth stimulant, it can help to slow the balding process. There has been some suggestion that ketoconazole could inhibit testosterone synthesis in utero, which could potentially inhibit genital development of a male fetus. However, this has not been documented in any controlled studies. Ketoconazole has not been FDA-approved for hair loss, though it is used for other scalp conditions.

In 2009 a new study result was released including pictures of before and after treatment. In this study six Japanese males with male pattern baldness (androgenetic alopecia) from 23 to 51 years old were enrolled and The subjects applied topical 2% KCZ lotion (Nizoral® cream) every day during or immediately after hair washing with their own un-medicated shampoos. All subjects reported a stop in hair loss and a regrowth of part of their lost hair after three months of continous use.

Copper peptides

Copper peptides are applied topically to the scalp, and shorten the resting phase of hairs, resulting in more hair follicles on the scalp being in the growing phase (as opposed to the resting or falling out phase) at one time. Copper peptides generally have superoxide dismutation activity.

SOD work by dismuting the superoxide anion into hydrogen peroxide, thereby preventing the converson of the superoxide anion to peroxynitrite (a free-radical) by combining with nitric oxide (a naturally occurring chemical messenger). The double effect of SOD therefore is the reduction in free-radical and increase in nitric oxide. It is thought that a key mechanism of action for minoxidil is the production of Nitric oxide (NO). Superoxide has an "agonist-antagonist" relationship with Nitric oxide or "Endothelium-derived Relaxing Factor".

Various SOD generating products are now available. However, one problem with SOD is the production of Hydrogen Peroxide as a by-product of singlet oxygen (superoxide anion) quenching. In the human body, the enzyme catalase converts the SOD hydrogen peroxide byproduct into water and oxygen. Nanogen, a UK-based skin research company, is undergoing Phase I trials to ascertain the hair regrowth potential on a new "broad-spectrum" molecule which has been shown in extensive independent laboratory in-vitro testing to have both SOD and Catalase mimetic activity. The company has not released details of the molecule as it is pending patent but it is copper II based.

Herbal Treatment

he shou wu (traditional Chinese: 何首烏; simplified Chinese: 何首乌; pinyin: hé shǒu wū) is a chinese herb that can be boiled to form a brown colored tea which is believed by some to cause moderate hair regrowth. The tea has a taste similar to roasted barley tea.

Saw palmetto extract has been suggested as a potential treatment for male pattern baldness. It has been shown to inhibit both isoforms of 5-alpha-reductase without eliminating the cellular capacity to secrete PSA.

Gingko biloba has been suggested as a treatment for baldness because is believed to increase blood circulation to the brain and skin.

Green tea contains compounds called catechins, which inhibits 5 alpha reductase enzymes used by the body to transform testosterone into DHT. Some claim that it relaxes the blood vessels and increases circulation to the scalp.

Spin labels

In animal models, the nitroxide spin labels TEMPO and TEMPOL enhance hair regrowth following radiation. National Cancer Institute-sponsored clinical trials TEMPOL is similarly effective in humans.

Diet and lifestyle

There are a number of genetic factors which determine a person's susceptibility to androgenic alopecia including androgen receptor polymorphisms, 5-alpha-reductase levels in the scalp, androgen receptor density and distribution in the scalp, and other factors some of which may not have been discovered.

Daily, vigorous aerobic exercise (as opposed to short workout periods designed to raise androgen levels and build muscle, or more sporadic exercise) and a diet which is adequate yet more moderate in terms of fat and total calorie intake have been shown to reduce baseline insulin levels as well as baseline total and free testosterone.

Lower insulin levels and reduced stress both result in raised levels of Sex Hormone Binding Globulin (SHBG). SHBG binds to testosterone, and prevents it from circulating free in the blood. Only free testosterone is converted to DHT. It is the level of free androgens and not total androgens which is relevant to the levels of DHT in the scalp and the progression of MPB. In short, aerobic exercise is capable of significantly lowering DHT.

Androgenic alopecia has been shown to correlate with metabolic syndrome. Medically increasing androgen levels does not worsen this condition, demonstrating that androgens do not cause metabolic syndrome. Instead, high insulin levels (and possibly chronic inflammation) seem the likely link in the demonstrated correlation between baldness and metabolic syndrome. This reinforces the notion that behaviors which help to keep insulin levels low and reduce chronic inflammation might also help to preserve hair.

Hair transplantation

Hair transplantation involves relocating (transplanting) bald resistant hair follicles from the back and sides of the head (the donor areas) to a person’s bald or thinning areas. The transplanted hair follicles will typically grow hair for a lifetime because they are genetically resistant to going bald. In recent years hair transplantation techniques have evolved from using large plugs and mini grafts to exclusively using large numbers of small grafts that contain from between 1 to 4 hairs. The grafting may cause localized loss of existing hair, the graft then typically grows in within a year.

Since hair naturally grows in follicles that contain groupings of 1 to 4 hairs, today’s most advanced techniques transplant these naturally occurring 1–4 hair "follicular units" in their natural groupings. Thus modern hair transplantation can achieve a natural appearance by mimicking nature hair for hair.

Another method is scalp reduction, in which skin in the balding area of the scalp is surgically excised. The left over skin is then pulled together and sutured.

Hair multiplication

Stem cells and dermal papilla cells have been discovered in hair follicles and some researchers predict research on these follicular cells may lead to successes in treating baldness through hair multiplication (HM), also called hair cloning.

HM is being developed by two independent companies: ARI (Aderans Research Institute, a Japanese owned company in the USA) and Intercytex, a company in Manchester (UK).

In 2008, Intercytex announced positive results of a Phase II trial for a form of cloning hair follicles from the back of the neck, multiplying them and then reimplanting the cells into the scalp. The initial testing resulted in at least two thirds of male patients regrowing hair. As of 2009, the company estimates this treatment will take "a number of years to complete" Phase III trials before it can go to market.

WNT Protein Introduction

In May 2007, U.S. company Follica Inc, announced they have licensed technology from the University of Pennsylvania which can regenerate hair follicles by reawakening genes which were once active only in the embryo stage of human development. Skin apparently can be brought back to this embryonic state when a wound is healing. Hair growth was discovered in the skin wounds of mice when Wnt proteins were introduced to the site. Development of a human treatment is expected to take several years.

Scalp massage

A randomized clinical trial of patients with bald patches on their scalp or skin showed a daily scalp massage with essential oils to be a safe and effective treatment for hair loss resulting from alopecia areata, a condition affected 0.1%–0.2% of humans (mostly women).

Low-level laser therapy

Low-level laser therapy is a growing field in medical science. A number of devices are sold that use low level laser energy directly on the scalp with the intent to stimulate hair growth through "Photo-Biostimulation" of the hair follicles. The Hairmax Lasercomb is the only laser phototherapy device to receive FDA clearance for marketing, although the FDA did not determine whether the LaserComb is safe or effective. Instead, it determined that the device is similar to devices sold before 1976. This means that the device can be sold without proof of safety or efficacy.

The Leimo laser is registered with the Therapeutic Goods Administration of Australia as a Class IIa Medical Device. It was approved for safety, but the TGA did not rule on its effectiveness. In 2009 the TGA reprimanded Leimo, stating that there is no evidence that the device would regrow hair, and said that the company must "withdraw any representations that the advertised product can provide benefits such as hair regrowth, reversal of hair loss, or reversal of hair thinning."

Unsaturated fatty acids

Particular unsaturated fatty acids such as gamma linolenic acid are 5 alpha reductase inhibitors if taken internally.

Hedgehog agonists

Through 2006, a drug development company spent $1,000,000 on a hair growth program focused on the potential development of a topical hedgehog agonist for hair growth disorders such as male pattern baldness and female hair loss. The hair loss research program was shut down in May 2007 because the process did not meet the proper safety standards.

Plant remedies

Caffeine

Caffeine has been identified as a stimulator of human hair growth in vitro, and reduced testosterone-induced follicle growth suppression. It has been demonstrated that the addition of caffeine to a shampoo-formulation is effective in administering caffeine to the hair follicles in the scalp. Further research must be done to evaluate the efficacy and adequate dosage of caffeine in the treatment of androgenetic alopecia.

A spray made with coffee beans is claimed to prevent age-related hair loss in women.

Black Cohosh

Black Cohosh (the most popular non-synthetic treatment in women for menopause in the world) has also been patented as a baldness treatment. Its mechanism of action is not fully understood but it is known to cause estrogen/progesterone receptors to bias in favour of estrogen, thus increasing the amounts present in the male user. Estrogen has a limited effect as an anti-androgen, but it is also responsible for the production of a soft layer of fat and thus a softening of the scalp.

Genetic research

In February 2008 researchers at the University of Bonn announced they have found the genetic basis of two distinct forms of inherited hair loss, opening a broad path to treatments for baldness. They found that a gene, P2RY5, causes a rare, inherited form of hair loss called Hypotrichosis simplex. It is the first receptor in humans known to play a role in hair growth. The fact that any receptor plays a specific role in hair growth was previously unknown to scientists and with this new knowledge a focus on finding more of these. In May 2009, researchers in Japan identified a gene, Sox21, that appears to be responsible for hair loss in people.

External links

Children's Alopecia Project
"Medical Treatments for Balding in Men," April 1999, American Family Physician (medical journal)
North American Hair Research Society Frequently asked questions
Health Alternatives: zinc, silica, methylsulphonylmethane (MSM) and cod-liver oil, to slow down the process.
The Trichological Society
International Society of Hair Restoration Surgery
How Hair Replacement Works

Other dermatological preparations

Medicated shampoos

Cetrimide - Cadmium compounds - Selenium compounds - Povidone-iodine - Sulfur compounds - Xenysalate

Other dermatologicals

Seborrhoeic dermatitis/dandruff	Lithium succinate · Pyrithione zinc

Skin whitening/depigmenting	Hydroquinone · Mequinol · Monobenzone

Anti-inflammatory/Immunomodulators	Oxaceprol · Gamolenic acid · Pimecrolimus · Tacrolimus · Alitretinoin

Baldness treatments	5-alpha-reductase inhibitor (Finasteride) · potassium channel opener (Minoxidil)

Hair growth inhibitors	Eflornithine

Other	Calcium gluconate · Magnesium sulfate · Tiratricol

List of Homeopathic medicines for various diseases/ disorders - Top / Popular Health News N Tips

noreply@blogger.com (Sridevi. V, M.A) — Thu, 24 Dec 2009 11:50:00 +0000

List of homeopathic preparations

The following substances are commonly used in homeopathy today.

Homeopathic name	Substance	Common name	Claimed homeopathic use	Homeopathic potency
Aconite	Aconitum napellus	Monkshood, Monk's Blood, Fuzi, Wolf's Bane	shock, influenza and fevers	6c, 30c, 200c
Aesculus hippocastanum	Aesculus hippocastanum	Horse-chestnut	haemorrhoids and varicose veins	tincture as ointment, 3c, 6c
Anthracinum, Anthracinum bovum, Anthracinum suum	Anthrax poison extracted from the spleen of affected sheeps		All types of furuncles (like Acne, carbuncles, malignant pustules), septic wounds, grangrenous degenerations, anthrax poisoning,	6X 30X
Allium cepa	Onion		itching eyes, lachrymation, allergies, hayfever	3x to 30c
Antimonium Arsenicate			Skin conditons, Minor lethargy	All potencies 6c to CM
Antimonium tartaricum	Antimony tartrate		Impetigo	6c to 200c
Argentum nitricum	Silver nitrate		Fear, anticipation, apprehension, nervous excitement, exam nerves	6c to 200c
Arnica	Arnica montana	Leopard's bane	shock and bruising	all potencies 6c to CM
Arsenicum album	Arsenic trioxide	White arsenic	colds/flu, diarrhoea, food poisoning	all potencies 6c to CM
Baptisia	Baptisia tinctoria	Wild Indigo; horseflyweed	fevers	all potencies 6c to CM
Belladonna	Atropa belladonna	Deadly nightshade	high fevers with redness & delirium	all potencies 6c to CM
Bellis perennis	Bellis perennis	Common Daisy	healing of cuts and wounds	6c to 200c
Bryonia	Bryonia alba	White bryony	fevers, joint pains, coughs and pleurisy	all potencies 6c to CM
Calcarea carbonica	Oyster shell	Calcium carbonate	Indigestion, Acidity	all potencies 6c to CM
Calendula	Calendula officinalis	Marigold	healing of wounds	tincture, 3c, 6c
Chamomilla	Matricaria chamomilla	German Chamomile	teething in infants	3c, 6c, 30c
Camphor	Cinnamomum camphora		Cholera (used by Hahnemann on a 1831 cholera outbreak on Central Europe, and by Dr. Quin in 1854 London's epidemic )
Colocynthis	Citrullus colocynthis	Squirting cucumber	Diarrhoea	6c to 200c
Cuprum metallicum	Copper		Cholera, diarrhoea, griping in the guts	6c to 200c
Digitalis	Digitalis purpurea	Foxglove	Heart conditions, angina	6c to 30c
Drosera	Drosera rotundifolia	Sundew	a cough remedy	6c, 30c
Dulcamara	Solanum dulcamara	Woody nightshade	wide range of chronic ailments	all potencies 6c to CM
Ferrum phosphoricum	Iron phosphate	Ferr phos	haemorrhages and nosebleeds	3x, 6x, 6c, 30c
Gelsemium	Gelsemium sempervirens	Yellow jasmine	joint pains and fevers	all potencies 6c to CM
Glonoinum	Nitroglycerine		Facial neuralgias	all potencies 6c to CM
Graphites	Graphite		Itching cracked skin, eczema, psoriasis	all potencies 6c to CM
Hamamelis	Hamamelis viginiana	Witch-hazel	haemorrhoids, varicose veins	tincture and low potencies 3x, 3c, 6c
Hepar sulfuris calcareum	Calcium sulfide	Hepar sulf	wide range of chronic ailments, boils, abscesses	all potencies 6c to CM
Ignatia amara	Strychnos ignatii	St. Ignatius Bean	recovery from grief	all potencies 6c to CM
Kalium bichromicum	Potassium dichromate	used in Head-on	thick secretions from the mucous membranes of the sinuses and respiratory tract	all potencies 6c to CM
Lachesis	Lachesis muta	Bushmaster snake	wide range of uses	all potencies 6c to CM
Ledum	Ledum palustre	Marsh Tea	bites, stings, punctured wounds	all potencies 6c to CM
Lycopodium	Lycopodium clavatum	Wolf's foot, clubmoss	wide range of chronic use	all potencies 6c to CM
Mercurius vivus	Mercury (element)		wide range of chronic ailments	all potencies 6c to CM
Natrum muriaticum	Sodium chloride	Natrum mur; table salt	varied chronic uses; irritable, touchy, dislikes consolation	6c to 10M
Natrum sulphuricum	Sodium sulphate	Natrum sulph	asthma, headaches, worse for damp, warts	6c to 10M
Nux vomica	Strychnos nux-vomica	Strychnine tree	nausea, hangovers, substance abuse & chronic ailments	all potencies 6c to CM
Oscillococcinum	Cairina moschata liver	Muscovy duck liver	colds/flu; (rarely used outside France and US; not notable)	generally 30c, 200c
Petroleum	Crude oil		Skin affections, eczema, psoriasis	all potencies 6c to CM
Phosphorus	Phosphorus	Phos	wide range of chronic ailments	all potencies 6c to CM
Picricum acidum	Picric acid	Picric acid	Water retention, Confusion	tincture to 200c
Pulsatilla	Pasque flower	Wind flower	various childhood, menstrual and chronic ailments	all potencies 6c to CM
Rhus toxicodendron	Toxicodendron radicans	Poison ivy	joint pains and fevers	all potencies 6c to CM
Ruta	Ruta graveolens	Rue	trauma or sprain of the ligaments; conditions involving the tendons, fibrous tissue, or periosteum; joint stiffness, eye strain	4x to CM
Sepia	Cuttlefish ink		many female problems	all potencies 6c to CM
Silicea	Flint		Various chronic conditions, sensitivity to cold	all potencies 6c to CM
Sulphur	Sulfur		chronic ailments, skin complaints, general debility	all potencies 6c to CM
Thea Sinensis / Camellia Sinensis	leafs of tea plant		neurologics (insomny, nightmares), digestives (dyspepsia caused by drinking tea often)	5C to 15C
Thuja	Thuja occidentalis		warts & chronic conditions	all potencies 6c to CM
Urtica urens	Stinging Nettle		Bites and stings	mostly 3c, 6c, 30c

____________________________________________________________________

Notes on potencies

This list contains notes of commonly used potencies, either by homeopaths or available in store-bought preparations. In clinical homeopathy, the choice of potency (dilution & succussion levels) to be used is determined by homeopathic practitioners or physicians on an individual basis. Some limit their use to the lower potencies of 4x (4D) through 30x (30D), while others use 3C through CM (100,000C) potencies.

External links

Keynotes of Homeopathy Remedies H.C.Allen
Materia Medica Pura Samuel Hahnemann
Homeopathic Remedies A-Z
iHomeopathy Reference Application for Apple iPhone Michelle Hillis, ND
Homeopathic Remedies for Sleep
Materia Medica of Homeopathy Remedies J.T. Kent
Plants and fungi used in homeopathy London Natural History Museum
Homeopathic Remedies: an illustrated guide presented by Médi-T
Regional Leaders in Homeopathic Therapeutics E. B. Nash
Questions and Answers About Homeopathy U.S. National Center for Complementary and Alternative Medicine

Bird Flu / Avian influenza - Top / Popular Health News And Tips

noreply@blogger.com (Sridevi. V, M.A) — Thu, 24 Dec 2009 10:47:00 +0000

Avian influenza

Influenza (Flu)

Types
Avian (A/H5N1 subtype) · Canine Equine · Swine (A/H1N1 subtype)
Vaccines
2009 pandemic (Pandemrix) ACAM-FLU-A · Fluzone · Influvac Live attenuated (FluMist) · Optaflu
Treatment
Amantadine · Arbidol · Laninamivir Oseltamivir · Peramivir · Rimantadine Vitamin D · Zanamivir
Pandemics
2009 · 1968-1969 Hong Kong · 1918
Outbreaks
2008 West Bengal 2007 Bernard Matthews H5N1 2007 Australian equine 2006 H5N1 India · 1976 swine flu

Avian influenza, sometimes avian flu, and commonly bird flu, refers to "influenza caused by viruses adapted to birds." Of the greatest concern is highly pathogenic avian influenza (HPAI).

"Bird flu" is a phrase similar to "swine flu," "dog flu," "horse flu," or "human flu" in that it refers to an illness caused by any of many different strains of influenza viruses that have adapted to a specific host. All known viruses that cause influenza in birds belong to the species influenza A virus. All subtypes (but not all strains of all subtypes) of influenza A virus are adapted to birds, which is why for many purposes avian flu virus is the influenza A virus (note that the "A" does not stand for "avian").

Adaptation is non-exclusive. Being adapted towards a particular species does not preclude adaptations, or partial adaptations, towards infecting different species. In this way strains of influenza viruses are adapted to multiple species, though may be preferential towards a particular host. For example, viruses responsible for influenza pandemics are adapted to both humans and birds. Recent influenza research into the genes of the Spanish flu virus shows it to have genes adapted to both birds and humans; with more of its genes from birds than less deadly later pandemic strains.

Genetics

Genetic factors in distinguishing between "human flu viruses" and "avian flu viruses" include:

PB2: (RNA polymerase): Amino acid (or residue) position 627 in the PB2 protein encoded by the PB2 RNA gene. Until H5N1, all known avian influenza viruses had a Glu at position 627, while all human influenza viruses had a Lys.

HA: (hemagglutinin): Avian influenza HA bind alpha 2-3 sialic acid receptors while human influenza HA bind alpha 2-6 sialic acid receptors. Swine influenza viruses have the ability to bind both types of sialic acid receptors. Hemagglutinin is the major antigen of the virus against which neutralizing antibodies are produced and influenza virus epidemics are associated with changes in its antigenic structure. This was originally derived from pigs, and should technically be referred to as "Pig Flu" (see ref. 7a)

Subtypes

There are many subtypes of avian influenza viruses, but only some strains of four subtypes have been highly pathogenic in humans. These are types H5N1, H7N3, H7N7 and H9N2.

Examples of avian influenza A virus strains:

HA subtype designation	NA subtype designation	Avian influenza A viruses
H1	N1	A/duck/Alberta/35/76(H1N1)
H1	N8	A/duck/Alberta/97/77(H1N8)
H2	N9	A/duck/Germany/1/72(H2N9)
H3	N8	A/duck/Ukraine/63(H3N8)
H3	N8	A/duck/England/62(H3N8)
H3	N2	A/turkey/England/69(H3N2)
H4	N6	A/duck/Czechoslovakia/56(H4N6)
H4	N3	A/duck/Alberta/300/77(H4N3)
H5	N3	A/tern/South Africa/300/77(H4N3)
H5	N4	A/jyotichinara/Ethiopia/300/77(H6N6)
H5	N9	A/turkey/Ontario/7732/66(H5N9)
H5	N1	A/chick/Scotland/59(H5N1)
H6	N2	A/turkey/Massachusetts/3740/65(H6N2)
H6	N8	A/turkey/Canada/63(H6N8)
H6	N5	A/shearwater/Australia/72(H6N5)
H6	N1	A/duck/Germany/1868/68(H6N1)
H7	N7	A/fowl plague virus/Dutch/27(H7N7)
H7	N1	A/chick/Brescia/1902(H7N1)
H7	N3	A/turkey/England/639H7N3)
H7	N1	A/fowl plague virus/Rostock/34(H7N1)
H8	N4	A/turkey/Ontario/6118/68(H8N4)
H9	N2	A/turkey/Wisconsin/1/66(H9N2)
H9	N6	A/duck/Hong Kong/147/77(H9N6)
H10	N7	A/chick/Germany/N/49(H10N7)
H10	N8	A/quail/Italy/1117/65(H10N8)
H11	N6	A/duck/England/56(H11N6)
H11	N9	A/duck/Memphis/546/74(H11N9)
H12	N5	A/duck/Alberta/60/76/(H12N5)
H13	N6	A/gull/Maryland/704/77(H13N6)
H14	N4	A/duck/Gurjev/263/83(H14N4)
H15	N9	A/shearwater/Australia/2576/83(H15N9)

Influenza pandemic

Pandemic flu viruses have some avian flu virus genes and usually some human flu virus genes. Both the H2N2 and H3N2 pandemic strains contained genes from avian influenza viruses. The new subtypes arose in pigs coinfected with avian and human viruses and were soon transferred to humans. Swine were considered the original "intermediate host" for influenza, because they supported reassortment of divergent subtypes. However, other hosts appear capable of similar coinfection (e.g., many poultry species), and direct transmission of avian viruses to humans is possible. The Spanish flu virus strain may have been transmitted directly from birds to humans.

In spite of their pandemic connection, avian influenza viruses are noninfectious for most species. When they are infectious they are usually asymptomatic, so the carrier does not have any disease from it. Thus while infected with an avian flu virus, the animal doesn't have a "flu". Typically, when illness (called "flu") from an avian flu virus does occur, it is the result of an avian flu virus strain adapted to one species spreading to another species (usually from one bird species to another bird species). So far as is known, the most common result of this is an illness so minor as to be not worth noticing (and thus little studied). But with the domestication of chickens and turkeys, humans have created species subtypes (domesticated poultry) that can catch an avian flu virus adapted to waterfowl and have it rapidly mutate into a form that kills in days over 90% of an entire flock and spread to other flocks and kill 90% of them and can only be stopped by killing every domestic bird in the area. Until H5N1 infected humans in the 1990s, this was the only reason avian flu was considered important. Since then, avian flu viruses have been intensively studied; resulting in changes in what is believed about flu pandemics, changes in poultry farming, changes in flu vaccination research, and changes in flu pandemic planning.

H5N1 has evolved into a flu virus strain that infects more species than any previously known flu virus strain, is deadlier than any previously known flu virus strain, and continues to evolve becoming both more widespread and more deadly causing Robert G. Webster, a leading expert on avian flu, to publish an article titled "The world is teetering on the edge of a pandemic that could kill a large fraction of the human population" in American Scientist. He called for adequate resources to fight what he sees as a major world threat to possibly billions of lives. Since the article was written, the world community has spent billions of dollars fighting this threat with limited success.

Vaccines have been formulated against several of the avian H5N1 influenza varieties. Vaccination of poultry against the ongoing H5N1 epizootic is widespread in certain countries. Some vaccines also exist for use in humans, and others are in testing, but none have been made available to civilian populations, nor produced in quantities sufficient to protect more than a tiny fraction of the Earth's population in the event that an H5N1 pandemic breaks out. The World Health Organization has compiled a list of known clinical trials of pandemic influenza prototype vaccines, including those against H5N1.

H5N1

H5N1

Further information: Influenza A virus subtype H5N1 and Transmission and infection of H5N1

The highly pathogenic influenza A virus subtype H5N1 virus is an emerging avian influenza virus that has been causing global concern as a potential pandemic threat. It is often referred to simply as "bird flu" or "avian influenza" even though it is only one subtype of avian influenza causing virus.

H5N1 has killed millions of poultry in a growing number of countries throughout Asia, Europe and Africa. Health experts are concerned that the co-existence of human flu viruses and avian flu viruses (especially H5N1) will provide an opportunity for genetic material to be exchanged between species-specific viruses, possibly creating a new virulent influenza strain that is easily transmissible and lethal to humans.

Since the first H5N1 outbreak occurred in 1987, there has been an increasing number of HPAI H5N1 bird-to-human transmissions leading to clinically severe and fatal human infections. However, because there is a significant species barrier that exists between birds and humans, the virus does not easily cross over to humans, though some cases of infection are being researched to discern whether human to human transmission is occurring. More research is necessary to understand the pathogenesis and epidemiology of the H5N1 virus in humans. Exposure routes and other disease transmission characteristics such as genetic and immunological factors, that may increase the likelihood of infection, are not clearly understood.

On January 18, 2009, a 27-year-old woman from eastern China has died of bird flu, Chinese authorities said, making her the second person to die this year from the deadly virus. Two tests on the woman were positive for H5N1 avian influenza, said the ministry, which did not say how she might have contracted the virus.

Although millions of birds have become infected with the virus since its discovery, 262 humans have died from the H5N1 in twelve countries according to WHO data as of August 31, 2009.

The avian flu claimed at least 200 humans in Indonesia, Vietnam, Laos, Romania, China, Taiwan, Turkey and Russia. Epidemiologists are afraid that the next time such a virus mutates, it could pass from human to human; however, the current A/H5N1 virus does not transmit easily from human to human. If this form of transmission occurs, another pandemic could result. Thus disease-control centers around the world are making avian flu a top priority. These organizations encourage poultry-related operations to develop a preemptive plan to prevent the spread of H5N1 and its potentially pandemic strains. The recommended plans center on providing protective clothing for workers and isolating flocks to prevent the spread of the virus.

The Thailand outbreak of avian flu causes massive economic losses especially among poultry workers. Infected birds were culled and sacrificed. The public loss its confidence with the poultry products and thus decreasing the consumption of chicken and its products. This also elicited a ban from importing countries. There were however, factors which aggravated the spread of the virus which includes bird migration, cool temperature (increases virus survival) and several festivals at that time.

In domestic animals

Several domestic species have been infected with and shown symptoms of H5N1 viral infection including cats, dogs, ferrets, pigs,and birds.

Birds

Attempts are made in the United States to minimize the presence of highly pathogenic avian influenza (HPAI) in poultry in through routine surveillance of poultry flocks in commercial poultry operations. Detection of a HPAI virus may result in immediate elimination of the flock. Less pathogenic viruses are controlled by vaccination, which is done primarily in turkey flocks (ATCvet codes: QI01AA23 for the inactivated fowl vaccine, QI01CL01 for the inactivated turkey combination vaccine).

External links

International

United Nations System Coordinator for Avian and Human Influenza (UNSIC).

Avian Influenza and the Pandemic Threat

World Health Organisation (WHO)

Food and Agriculture Organization of the UN (FAO)

FAO Avian Influenza portal Information resources, animations, videos, photos
FAO Bird Flu disease card

World Organisation for Animal Health (OIE)

Avian influenza resource By Dr. Nati Elkin - Atlases, vaccines and information.

United States

PandemicFlu.Gov U.S. Government avian and pandemic flu information
US Avian Influenza Response U.S. Agency for International Development (USAID)
Avian influenza research and recommendations National Institute for Occupational Safety and Health
Influenza Research Database Database of influenza sequences and related information.
Wildlife Disease Information Node A part of the National Biological Information Infrastructure and partner of the NWHC, this agency collects and distributes news and information about wildlife diseases such as avian influenza and coordinates collaborative information sharing efforts.
Avian Influenza information AVMA - The American Veterinary Medical Association.

Europe

Health-EU Portal EU response to Avian Influenza.
Avian Influenza: Prevention and Control Proceedings of the Frontis workshop on Avian Influenza: Prevention and Control, Wageningen, The Netherlands
Avian Influenza: Questions & Answers European Centre for Disease Prevention and Control - Official website
FluTrop: Avian Influenza Research in Tropical Countries French Agricultural Research Center for Developing Countries (CIRAD), Avian Influenza website

Swine Flu / Swine influenza - Top / Popular Health News And Tips

noreply@blogger.com (Sridevi. V, M.A) — Thu, 24 Dec 2009 09:53:00 +0000

Swine influenza

Electron microscope image of the reassorted H1N1 influenza virus photographed at the CDC Influenza Laboratory. The viruses are 80–120 nanometres in diameter.

Influenza (Flu)

Types

Avian (A/H5N1 subtype) · Canine
Equine · Swine (A/H1N1 subtype)

Vaccines

2009 pandemic (Pandemrix)
ACAM-FLU-A · Fluzone · Influvac
Live attenuated (FluMist) · Optaflu

Treatment

Amantadine · Arbidol · Laninamivir
Oseltamivir · Peramivir · Rimantadine
Vitamin D · Zanamivir

Pandemics

2009 · 1968-1969 Hong Kong · 1918

Outbreaks

2008 West Bengal
2007 Bernard Matthews H5N1
2007 Australian equine
2006 H5N1 India · 1976 swine flu

Swine influenza (also called Pig influenza, swine flu, hog flu and pig flu) is an infection by any one of several types of swine influenza virus. Swine influenza virus (SIV) or S-OIV (swine-origin influenza virus) is any strain of the influenza family of viruses that is endemic in pigs.[2] As of 2009, the known SIV strains include influenza C and the subtypes of influenza A known as H1N1, H1N2, H3N1, H3N2, and H2N3.

Swine influenza virus is common throughout pig populations worldwide. Transmission of the virus from pigs to humans is not common and does not always lead to human influenza, often resulting only in the production of antibodies in the blood. If transmission does cause human influenza, it is called zoonotic swine flu. People with regular exposure to pigs are at increased risk of swine flu infection. The meat of an infected animal poses no risk of infection when properly cooked.

During the mid-20th century, identification of influenza subtypes became possible, allowing accurate diagnosis of transmission to humans. Since then, only 50 such transmissions have been confirmed. These strains of swine flu rarely pass from human to human. Symptoms of zoonotic swine flu in humans are similar to those of influenza and of influenza-like illness in general, namely chills, fever, sore throat, muscle pains, severe headache, coughing, weakness and general discomfort.

Classification

Of the three genera of influenza viruses that cause human flu, two also cause influenza in pigs, with influenza A being common in pigs and influenza C being rare. Influenza B has not been reported in pigs. Within influenza A and influenza C, the strains found in pigs and humans are largely distinct, although because of reassortment there have been transfers of genes among strains crossing swine, avian, and human species boundaries.

Influenza C

Influenza C viruses infect both humans and pigs, but do not infect birds. Transmission between pigs and humans have occurred in the past. For example, influenza C caused small outbreaks of a mild form of influenza amongst children in Japan and California. Because of its limited host range and the lack of genetic diversity in influenza C, this form of influenza does not cause pandemics in humans.

Influenza A

Swine influenza is known to be caused by influenza A subtypes H1N1, H1N2, H2N3, H3N1, and H3N2. In pigs, three influenza A virus subtypes (H1N1, H1N2, and H3N2) are the most common strains worldwide. In the United States, the H1N1 subtype was exclusively prevalent among swine populations before 1998; however, since late August 1998, H3N2 subtypes have been isolated from pigs. As of 2004, H3N2 virus isolates in US swine and turkey stocks were triple reassortants, containing genes from human (HA, NA, and PB1), swine (NS, NP, and M), and avian (PB2 and PA) lineages.

Surveillance

Although there is no formal national surveillance system in the United States to determine what viruses are circulating in pigs, there is an informal surveillance network in the United States that is part of a world surveillance network.

Veterinary medical pathologist, Tracey McNamara, set up a national disease surveillance system in zoos because the zoos do active disease surveillance and many of the exotic animals housed there have broad susceptibilities. Many species fall below the radar of any federal agencies (including dogs, cats, pet prairie dogs, zoo animals, and urban wildlife), even though they may be important in the early detection of human disease outbreaks.

History

Swine influenza was first proposed to be a disease related to human influenza during the 1918 flu pandemic, when pigs became sick at the same time as humans. The first identification of an influenza virus as a cause of disease in pigs occurred about ten years later, in 1930. For the following 60 years, swine influenza strains were almost exclusively H1N1. Then, between 1997 and 2002, new strains of three different subtypes and five different genotypes emerged as causes of influenza among pigs in North America. In 1997–1998, H3N2 strains emerged. These strains, which include genes derived by reassortment from human, swine and avian viruses, have become a major cause of swine influenza in North America. Reassortment between H1N1 and H3N2 produced H1N2. In 1999 in Canada, a strain of H4N6 crossed the species barrier from birds to pigs, but was contained on a single farm.

The H1N1 form of swine flu is one of the descendants of the strain that caused the 1918 flu pandemic. As well as persisting in pigs, the descendants of the 1918 virus have also circulated in humans through the 20th century, contributing to the normal seasonal epidemics of influenza. However, direct transmission from pigs to humans is rare, with only 12 cases in the U.S. since 2005. Nevertheless, the retention of influenza strains in pigs after these strains have disappeared from the human population might make pigs a reservoir where influenza viruses could persist, later emerging to reinfect humans once human immunity to these strains has waned.

Swine flu has been reported numerous times as a zoonosis in humans, usually with limited distribution, rarely with a widespread distribution. Outbreaks in swine are common and cause significant economic losses in industry, primarily by causing stunting and extended time to market. For example, this disease costs the British meat industry about £65 million every year.^[

1918 pandemic in humans

The 1918 flu pandemic in humans was associated with H1N1 and influenza appearing in pigs; this may reflect a zoonosis either from swine to humans, or from humans to swine. Although it is not certain in which direction the virus was transferred, some evidence suggests that, in this case, pigs caught the disease from humans. For instance, swine influenza was only noted as a new disease of pigs in 1918, after the first large outbreaks of influenza amongst people. Although a recent phylogenetic analysis of more recent strains of influenza in humans, birds, and swine suggests that the 1918 outbreak in humans followed a reassortment event within a mammal,^[23] the exact origin of the 1918 strain remains elusive. It is estimated that anywhere from 50 to 100 million people were killed worldwide.

1976 U.S. outbreak

On February 5, 1976, in the United States an army recruit at Fort Dix said he felt tired and weak. He died the next day and four of his fellow soldiers were later hospitalized. Two weeks after his death, health officials announced that the cause of death was a new strain of swine flu. The strain, a variant of H1N1, is known as A/New Jersey/1976 (H1N1). It was detected only from January 19 to February 9 and did not spread beyond Fort Dix.

President Ford receives swine flu vaccination

This new strain appeared to be closely related to the strain involved in the 1918 flu pandemic. Moreover, the ensuing increased surveillance uncovered another strain in circulation in the U.S.: A/Victoria/75 (H3N2) spread simultaneously, also caused illness, and persisted until March. Alarmed public-health officials decided action must be taken to head off another major pandemic, and urged President Gerald Ford that every person in the U.S. be vaccinated for the disease.

The vaccination program was plagued by delays and public relations problems. On October 1, 1976, immunizations began and three senior citizens died soon after receiving their injections. This resulted in a media outcry that linked these deaths to the immunizations, despite the lack of any proof that the vaccine was the cause. According to science writer Patrick Di Justo, however, by the time the truth was known—that the deaths were not proven to be related to the vaccine—it was too late. "The government had long feared mass panic about swine flu—now they feared mass panic about the swine flu vaccinations." This became a strong setback to the program.

There were reports of Guillain-Barré syndrome, a paralyzing neuromuscular disorder, affecting some people who had received swine flu immunizations. Although if a link exists is still not clear, this syndrome may be a rare side-effect of influenza vaccines. As a result, Di Justo writes that "the public refused to trust a government-operated health program that killed old people and crippled young people." In total, 48,161,019 Americans, or just over 22% of the population, had been immunized by the time the National Influenza Immunization Program (NIIP) was effectively halted on December 16, 1976.

Overall, there were 1098 cases of Guillain-Barré Syndrome (GBS) recorded nationwide by CDC surveillance, 532 of which occurred after vaccination and 543 before vaccination. There are about one to two cases of GBS per 100,000 people every year, whether or not people have been vaccinated. The vaccination program seems to have increased this normal risk of developing GBS by about to one extra case per 100,000 vaccinations. The CDC states that most studies on modern influenza vaccines have seen no link with GBS, Although one review gives an incidence of about one case per million vaccinations.

1988 zoonosis

In September 1988, a swine flu virus killed one woman and infected others. 32-year old Barbara Ann Wieners was eight months pregnant when she and her husband, Ed, became ill after visiting the hog barn at a county fair in Walworth County, Wisconsin. Barbara died eight days later, after developing pneumonia. The only pathogen identified was an H1N1 strain of swine influenza virus. Doctors were able to induce labor and deliver a healthy daughter before she died. Her husband recovered from his symptoms.

Influenza-like illness (ILI) was reportedly widespread among the pigs exhibited at the fair. Of the 25 swine exhibitors aged 9 to 19 at the fair, 19 tested positive for antibodies to SIV, but no serious illnesses were seen. The virus was able to spread between people, since 1-3 health care personnel who had cared for the pregnant woman developed mild influenza-like illnesses, and antibody tests suggested that they had been infected with swine flu. However, there was no community outbreak.

1998 US outbreak in swine

In 1998, swine flu was found in pigs in four U.S. states. Within a year, it had spread through pig populations across the United States. Scientists found that this virus had originated in pigs as a recombinant form of flu strains from birds and humans. This outbreak confirmed that pigs can serve as a crucible where novel influenza viruses emerge as a result of the reassortment of genes from different strains. Genetic components of these 1998 triple-hybrid stains would later form six out of the eight viral gene segments in the 2009 flu outbreak.

2007 Philippine outbreak in swine

On August 20, 2007 Department of Agriculture officers investigated the outbreak (epizootic) of swine flu in Nueva Ecija and Central Luzon, Philippines. The mortality rate is less than 10% for swine flu, unless there are complications like hog cholera. On July 27, 2007, the Philippine National Meat Inspection Service (NMIS) raised a hog cholera "red alert" warning over Metro Manila and 5 regions of Luzon after the disease spread to backyard pig farms in Bulacan and Pampanga, even if these tested negative for the swine flu virus.

2009 outbreak in humans

The H1N1 viral strain implicated in the 2009 flu pandemic among humans often is called "swine flu" because initial testing showed many of the genes in the virus were similar to influenza viruses normally occurring in North American swine. Further research has shown that three-quarters or six out of the eight gene segments of the 2009 virus arose from the 1998 North American swine flu strains which emerged from the first-ever reported triple-hybrid virus of 1998.

In late April, Margaret Chan, the World Health Organization's director-general, declared a "public health emergency of international concern" under the rules of the WHO's new International Health Regulations when the first two cases of the H1N1 virus were reported in the United States, followed by hundreds of cases in Mexico. Following the initial cases in the USA and Mexico, on May 2, 2009, it was reported in pigs at a farm in Alberta, Canada, with a link to the outbreak in Mexico. The pigs are suspected to have caught this new strain of virus from a farm worker who recently returned from Mexico, then showed symptoms of an influenza-like illness. These are probable cases, pending confirmation by laboratory testing.

The new strain was initially described as an apparent reassortment of at least four strains of influenza A virus subtype H1N1, including one strain endemic in humans, one endemic in birds, and two endemic in swine. Subsequent analysis suggested it was a reassortment of just two strains, both found in swine. Although initial reports identified the new strain as swine influenza (i.e., a zoonosis originating in swine), its genetic origin was only later revealed to have been mostly a descendant of the triple-reassortment virus which emerged in factory farms in the United States in 1998.Several countries took precautionary measures to reduce the chances for a global pandemic of the disease. The 2009 swine flu has been compared to other similar types of influenza virus in terms of mortality: "in the US it appears that for every 1000 people who get infected, about 40 people need admission to hospital and about one person dies."There are fears that swine flu will become a major global pandemic at the end of the year (coinciding with the Northern Hemisphere winter months), with many countries planning major vaccination campaigns.

Transmission

Transmission between pigs

Influenza is quite common in pigs, with about half of breeding pigs having been exposed to the virus in the US. Antibodies to the virus are also common in pigs in other countries.

The main route of transmission is through direct contact between infected and uninfected animals.These close contacts are particularly common during animal transport. Intensive farming may also increase the risk of transmission, as the pigs are raised in very close proximity to each other. The direct transfer of the virus probably occurs either by pigs touching noses, or through dried mucus. Airborne transmission through the aerosols produced by pigs coughing or sneezing are also an important means of infection. The virus usually spreads quickly through a herd, infecting all the pigs within just a few days. Transmission may also occur through wild animals, such as wild boar, which can spread the disease between farms.

Transmission to humans

People who work with poultry and swine, especially people with intense exposures, are at increased risk of zoonotic infection with influenza virus endemic in these animals, and constitute a population of human hosts in which zoonosis and reassortment can co-occur. Vaccination of these workers against influenza and surveillance for new influenza strains among this population may therefore be an important public health measure. Transmission of influenza from swine to humans who work with swine was documented in a small surveillance study performed in 2004 at the University of Iowa. This study among others forms the basis of a recommendation that people whose jobs involve handling poultry and swine be the focus of increased public health surveillance. Other professions at particular risk of infection are veterinarians and meat processing workers, although the risk of infection for both of these groups is lower than that of farm workers.

Interaction with avian H5N1 in pigs

Pigs are unusual as they can be infected with influenza strains that usually infect three different species: pigs, birds and humans. This makes pigs a host where influenza viruses might exchange genes, producing new and dangerous strains. Avian influenza virus H3N2 is endemic in pigs in China and has been detected in pigs in Vietnam, increasing fears of the emergence of new variant strains. H3N2 evolved from H2N2 by antigenic shift. In August 2004, researchers in China found H5N1 in pigs.

Main symptoms of swine flu in swine.

These H5N1 infections may be quite common: in a survey of 10 apparently healthy pigs housed near poultry farms in West Java, where avian flu had broken out, five of the pig samples contained the H5N1 virus. The Indonesian government has since found similar results in the same region. Additional tests of 150 pigs outside the area were negative.

Signs and symptoms

In swine

In pigs influenza infection produces fever, lethargy, sneezing, coughing, difficulty breathing and decreased appetite. In some cases the infection can cause abortion. Although mortality is usually low (around 1–4%), the virus can produce weight loss and poor growth, causing economic loss to farmers. Infected pigs can lose up to 12 pounds of body weight over a 3 to 4 week period.

In humans

Main symptoms of swine flu in humans

Direct transmission of a swine flu virus from pigs to humans is occasionally possible (called zoonotic swine flu). In all, 50 cases are known to have occurred since the first report in medical literature in 1958, which have resulted in a total of six deaths. Of these six people, one was pregnant, one had leukemia, one had Hodgkin disease and two were known to be previously healthy. Despite these apparently low numbers of infections, the true rate of infection may be higher, since most cases only cause a very mild disease, and will probably never be reported or diagnosed.

In this video, Dr. Joe Bresee, with CDC's Influenza Division, describes the symptoms of swine flu and warning signs to look for that indicate the need for urgent medical attention.
See also: See this video with subtitles on YouTube

According to the Centers for Disease Control and Prevention (CDC), in humans the symptoms of the 2009 "swine flu" H1N1 virus are similar to those of influenza and of influenza-like illness in general. Symptoms include fever, cough, sore throat, body aches, headache, chills and fatigue. The 2009 outbreak has shown an increased percentage of patients reporting diarrhea and vomiting. The 2009 H1N1 virus is not zoonotic swine flu, as it is not transmitted from pigs to humans, but from person to person.

Because these symptoms are not specific to swine flu, a differential diagnosis of probable swine flu requires not only symptoms but also a high likelihood of swine flu due to the person's recent history. For example, during the 2009 swine flu outbreak in the United States, CDC advised physicians to "consider swine influenza infection in the differential diagnosis of patients with acute febrile respiratory illness who have either been in contact with persons with confirmed swine flu, or who were in one of the five U.S. states that have reported swine flu cases or in Mexico during the 7 days preceding their illness onset." A diagnosis of confirmed swine flu requires laboratory testing of a respiratory sample (a simple nose and throat swab).

The most common cause of death is respiratory failure. Other causes of death are pneumonia (leading to sepsis), high fever (leading to neurological problems), dehydration (from excessive vomiting and diarrhea) and electrolyte imbalance. Fatalities are more likely in young children and the elderly.

Diagnosis

Thermal scanning of passengers arriving at Singapore Changi airport.

The CDC recommends real time RT-PCR as the method of choice for diagnosing H1N1.^[78] This method allows a specific diagnosis of novel influenza (H1N1) as opposed to seasonal influenza. Near-patient point of care tests are in development.

Prevention

Prevention of swine influenza has three components: prevention in swine, prevention of transmission to humans, and prevention of its spread among humans.

In swine

Methods of preventing the spread of influenza among swine include facility management, herd management, and vaccination (ATCvet code: QI09AA03). Because much of the illness and death associated with swine flu involves secondary infection by other pathogens, control strategies that rely on vaccination may be insufficient.

Control of swine influenza by vaccination has become more difficult in recent decades, as the evolution of the virus has resulted in inconsistent responses to traditional vaccines. Standard commercial swine flu vaccines are effective in controlling the infection when the virus strains match enough to have significant cross-protection, and custom (autogenous) vaccines made from the specific viruses isolated are created and used in the more difficult cases. Present vaccination strategies for SIV control and prevention in swine farms typically include the use of one of several bivalent SIV vaccines commercially available in the United States. Of the 97 recent H3N2 isolates examined, only 41 isolates had strong serologic cross-reactions with antiserum to three commercial SIV vaccines. Since the protective ability of influenza vaccines depends primarily on the closeness of the match between the vaccine virus and the epidemic virus, the presence of nonreactive H3N2 SIV variants suggests that current commercial vaccines might not effectively protect pigs from infection with a majority of H3N2 viruses. The United States Department of Agriculture researchers say that while pig vaccination keeps pigs from getting sick, it does not block infection or shedding of the virus.

Facility management includes using disinfectants and ambient temperature to control virus in the environment. The virus is unlikely to survive outside living cells for more than two weeks, except in cold (but above freezing) conditions, and it is readily inactivated by disinfectants. Herd management includes not adding pigs carrying influenza to herds that have not been exposed to the virus. The virus survives in healthy carrier pigs for up to 3 months and can be recovered from them between outbreaks. Carrier pigs are usually responsible for the introduction of SIV into previously uninfected herds and countries, so new animals should be quarantined. After an outbreak, as immunity in exposed pigs wanes, new outbreaks of the same strain can occur.

In humans

Prevention of pig to human transmission

Swine can be infected by both avian and human influenza strains of influenza, and therefore are hosts where the antigenic shifts can occur that create new influenza strains.

The transmission from swine to human is believed to occur mainly in swine farms where farmers are in close contact with live pigs. Although strains of swine influenza are usually not able to infect humans this may occasionally happen, so farmers and veterinarians are encouraged to use a face mask when dealing with infected animals. The use of vaccines on swine to prevent their infection is a major method of limiting swine to human transmission. Risk factors that may contribute to swine-to-human transmission include smoking and not wearing gloves when working with sick animals.

Prevention of human to human transmission

Influenza spreads between humans through coughing or sneezing and people touching something with the virus on it and then touching their own nose or mouth. Swine flu cannot be spread by pork products, since the virus is not transmitted through food. The swine flu in humans is most contagious during the first five days of the illness although some people, most commonly children, can remain contagious for up to ten days. Diagnosis can be made by sending a specimen, collected during the first five days for analysis.

Thermal imaging camera & screen, photographed in an airport terminal in Greece. Thermal imaging can detect elevated body temperature, one of the signs of the virus N1H1 (Swine influenza).

Recommendations to prevent spread of the virus among humans include using standard infection control against influenza. This includes frequent washing of hands with soap and water or with alcohol-based hand sanitizers, especially after being out in public. Chance of transmission is also reduced by disinfecting household surfaces, which can be done effectively with a diluted chlorine bleach solution.

Experts agree that hand-washing can help prevent viral infections, including ordinary influenza and the swine flu virus. Also avoiding touching eyes, nose and mouth with hands prevents flu. Influenza can spread in coughs or sneezes, but an increasing body of evidence shows small droplets containing the virus can linger on tabletops, telephones and other surfaces and be transferred via the fingers to the mouth, nose or eyes. Alcohol-based gel or foam hand sanitizers work well to destroy viruses and bacteria. Anyone with flu-like symptoms such as a sudden fever, cough or muscle aches should stay away from work or public transportation and should contact a doctor for advice.

Social distancing is another tactic. It means staying away from other people who might be infected and can include avoiding large gatherings, spreading out a little at work, or perhaps staying home and lying low if an infection is spreading in a community. Public health and other responsible authorities have action plans which may request or require social distancing actions depending on the severity of the outbreak.

Vaccination

Vaccines are available for different kinds of swine flu. The U.S. Food and Drug Administration (FDA) approved the new swine flu vaccine for use in the United States on September 15, 2009. Studies by the National Institutes of Health (NIH), show that a single dose creates enough antibodies to protect against the virus within about 10 days.

Treatment

In swine

As swine influenza is rarely fatal to pigs, little treatment beyond rest and supportive care is required. Instead veterinary efforts are focused on preventing the spread of the virus throughout the farm, or to other farms. Vaccination and animal management techniques are most important in these efforts. Antibiotics are also used to treat this disease, which although they have no effect against the influenza virus, do help prevent bacterial pneumonia and other secondary infections in influenza-weakened herds.

In humans

If a person becomes sick with swine flu, antiviral drugs can make the illness milder and make the patient feel better faster. They may also prevent serious flu complications. For treatment, antiviral drugs work best if started soon after getting sick (within 2 days of symptoms). Beside antivirals, supportive care at home or in hospital, focuses on controlling fevers, relieving pain and maintaining fluid balance, as well as identifying and treating any secondary infections or other medical problems. The U.S. Centers for Disease Control and Prevention recommends the use of Tamiflu (oseltamivir) or Relenza (zanamivir) for the treatment and/or prevention of infection with swine influenza viruses; however, the majority of people infected with the virus make a full recovery without requiring medical attention or antiviral drugs. The virus isolates in the 2009 outbreak have been found resistant to amantadine and rimantadine.

In the U.S., on April 27, 2009, the FDA issued Emergency Use Authorizations to make available Relenza and Tamiflu antiviral drugs to treat the swine influenza virus in cases for which they are currently unapproved. The agency issued these EUAs to allow treatment of patients younger than the current approval allows and to allow the widespread distribution of the drugs, including by non-licensed volunteers.

Seasonal Flu / Flu season - Top / Popular Health News / Tips

noreply@blogger.com (Sridevi. V, M.A) — Thu, 24 Dec 2009 09:28:00 +0000

Seasonal Flu / Flu season

Influenza (Flu)

Types
Avian (A/H5N1 subtype) · Canine Equine · Swine (A/H1N1 subtype)
Vaccines
2009 pandemic (Pandemrix) ACAM-FLU-A · Fluzone · Influvac Live attenuated (FluMist) · Optaflu
Treatment
Amantadine · Arbidol · Laninamivir Oseltamivir · Peramivir · Rimantadine Vitamin D · Zanamivir
Pandemics
2009 · 1968-1969 Hong Kong · 1918
Outbreaks
2008 West Bengal 2007 Bernard Matthews H5N1 2007 Australian equine 2006 H5N1 India · 1976 swine flu
See also
Flu season · Influenza evolution Influenza research Influenza-like illness

Flu season is a regularly recurring time period characterized by the prevalence of outbreaks of influenza (flu). The season occurs during the cold half of the year in each hemisphere. Influenza activity can sometimes be predicted and even tracked geographically. While the beginning of major flu activity in each season varies by location, in any specific location these minor epidemics usually take about 3 weeks to peak and another 3 weeks to significantly diminish. Individual cases of the flu however, usually only last a few days. In some countries such as Japan, Korea, and China, infected persons sometimes wear a surgical mask out of consideration for others.

Cause

Main article: Influenza

Three virus families, Influenzavirus A, B, and C are the main infective agents that cause influenza. During periods of cooler temperature, influenza cases increase roughly tenfold or more. Despite higher incidence of manifestations of the flu during the season, the viruses are actually transmitted throughout populations all year round.

Each annual flu season is normally associated with a major influenzavirus subtype. The associated subtype changes each year, due to development of immunological resistance to a previous year's strain (through exposure and vaccinations), and mutational changes in previously dormant viruses strains.

Mechanism for seasonal nature of influenza

The exact mechanism behind the seasonal nature of influenza outbreaks is unclear. Some proposed explanations are:

People are indoors more often during the winter, they are in close contact more often, and this promotes transmission from person to person.
Cold temperatures lead to drier air, which may dehydrate mucus, preventing the body from effectively expelling virus particles.
The virus may linger longer on exposed surfaces (doorknobs, countertops, etc.) in colder temperatures.
Vitamin D production from Ultraviolet-B in the skin changes with the seasons and affects the immune system.^[2]^[3]^[4]

Research in guinea pigs has shown that the aerosol transmission of the virus is enhanced when the air is cold and dry. The dependence on aridity appears to be due to degradation of the virus particles in moist air, while the dependence on cold appears to be due to infected hosts shedding the virus for a longer period of time. The researchers did not find that the cold impaired the immune response of the guinea pigs to the virus.

A recent research done by National Institute of Child Health and Human Development (NICHD) found that the influenza virus has a "butter-like coating". The coating melts when it enters the respiratory tract. In the winter, the coating becomes a hardened shell; therefore, it can survive in the cold weather similar to a spore. In the summer, the coating melts before the virus reaches the respiratory tract.

Flu vaccinations

Main article: Influenza vaccine

Flu vaccinations have been used to diminish the effects of the flu season. Since the Northern and Southern Hemisphere have winter at different times of the year, there are actually two flu seasons each year. Therefore, the World Health Organization (assisted by the National Influenza Centers) makes two vaccine formulations every year; one for the Northern, and one for the Southern Hemisphere.

According to the U.S. Department of Health, a growing number of large companies provide their employees with seasonal flu shots, either at a small cost to the employee or as a free service.

The annually updated trivalent influenza vaccine consists of hemagglutinin (HA) surface glycoprotein components from influenza H3N2, H1N1, and B influenza viruses. The dominant strain in January 2006 was H3N2. Measured resistance to the standard antiviral drugs amantadine and rimantadine in H3N2 has increased from 1% in 1994 to 12% in 2003 to 91% in 2005.

Cost

The cost of a flu season in lives lost, medical expenses and economic impact can be severe. A recent study estimated that in the United States, annual inﬂuenza epidemics result in approximately 600,000 life-years lost, 3 million hospitalized days, and 30 million outpatient visits, resulting in medical costs of $10 billion annually. According to this study, lost earnings due to illness and loss of life amounted to over $15 billion annually and the total economic burden of annual inﬂuenza epidemics amounts to over $80 billion.

External links

Health-EU portal EU response to influenza
European Commission - Public Health EU coordination on Pandemic (H1N1) 2009

Social anxiety disorder - Top/popular Health News/Tips

noreply@blogger.com (Sridevi. V, M.A) — Thu, 24 Dec 2009 08:56:00 +0000

Social anxiety disorder

Social anxiety disorder (DSM-IV 300.23), also called social anxiety and social phobia, is excessive social anxiety (anxiety in social situations) causing considerable distress and impaired ability to function in at least some parts of daily life. The diagnosis can be of a specific disorder (when only some particular situations are feared) or a generalized disorder. Generalized social anxiety disorder typically involves a persistent, intense, chronic fear of being judged by others and of being embarrassed or humiliated by one's own actions. These fears can be triggered by perceived or actual scrutiny from others. While the fear of social interaction may be recognized by the person as excessive or unreasonable, overcoming it can be quite difficult. About 13.3 percent of the general population may meet criteria for social anxiety disorder at some point in their lives, according to the highest survey estimate, with the male:female ratio being 2:3.

Physical symptoms often accompanying social anxiety disorder include excessive blushing, sweating (hyperhidrosis), trembling, palpitations, nausea, and stammering and, in some extreme cases, sialorrhea. Panic attacks may also occur under intense fear and discomfort. An early diagnosis may help minimize the symptoms and the development of additional problems, such as depression.

Some sufferers may use alcohol or other drugs to reduce fears and inhibitions at social events. It is very common for sufferers of social phobia to self-medicate in this fashion, especially if they are undiagnosed, untreated, or both. This can lead to alcoholism or other kinds of substance abuse.

A person with the disorder may be treated with psychotherapy, medication, or both. Research has shown cognitive behavior therapy, whether individually or in a group, to be effective in treating social phobia. The cognitive and behavioral components seek to change thought patterns and physical reactions to anxiety-inducing situations. Prescribed medications include several classes of antidepressants: selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs) and monoamine oxidase inhibitors (MAOIs). Other commonly used medications include beta-blockers and benzodiazepines, as well as newer antidepressants, such as mirtazapine. A herb called kava has also attracted attention as a possible treatment, although safety concerns exist,^[5]^[6] especially given the unregulated nature of herbs in the United States.

Attention given to social anxiety disorder has significantly increased in the United States since 1999 with the approval and marketing of drugs for its treatment.

History

Literary descriptions of shyness can be traced back to the days of Hippocrates around 400 B.C. Hippocrates described someone who 'through bashfulness, suspicion, and timorousness, will not be seen abroad; loves darkness as life and cannot endure the light or to sit in lightsome places; his hat still in his eyes, he will neither see, nor be seen by his good will. He dare not come in company for fear he should be misused, disgraced, overshoot himself in gesture or speeches, or be sick; he thinks every man observes him'.

Charles Darwin wrote about the physiology and social context of blushing and shyness. The first mention of a psychiatric term, social phobia ("phobie des situations sociales"), was made in the early 1900s. Psychologists used the term "social neurosis" to describe extremely shy patients in the 1930s. After extensive work by Joseph Wolpe on systematic desensitization, research in phobias and their treatment grew. The idea that social phobia was a separate entity from other phobias came from the British psychiatrist Isaac Marks, in the 1960s. This was accepted by the American Psychiatric Association and was first officially included in the third edition of the Diagnostic and Statistical Manual of Mental Disorders. The definition of the phobia was revised in 1989 to allow comorbidity with avoidant personality disorder, and introduced generalized social phobia. Social phobia had been largely ignored prior to 1985.

After a call to action by psychiatrist Michael Liebowitz and clinical psychologist Richard Heimberg, there was an increase in attention to and research on the disorder. The DSM-IV gave social phobia the alternative name Social Anxiety Disorder. Research on the psychology and sociology of everyday social anxiety continued. Cognitive Behavioural models and therapies were developed for social anxiety disorder. In the 1990s, paroxetine became the first prescription drug in the U.S. approved to treat social anxiety disorder, with others following.

Social phobia in many cases can be an extremely debilitating disorder, especially because one who struggles with it often suffers alone.

Diagnostic Criteria

According to the DSM-IV-TR, to be diagnosed with Social Phobia all these criteria (A-H) must be met:

A. A marked and persistent fear of one or more social performance situations in which the person is exposed to unfamiliar people or to possible scrutiny by others. The individual fears that he or she will act in a way (or show anxiety symptoms) that will be humiliating or embarrassing. Note: In children, there must be evidence of the capacity for age-appropriate social relationships with familiar people and the anxiety must occur in peer settings, not just in interactions with adults.

B. Exposure to the social or performance situation almost invariably provokes an immediate anxiety response. This response may take the form of a situationally bound or situationally people predisposed Panic Attack. Note: In children, the anxiety may be expressed by crying, tantrums, freezing, or shrinking from social situations with unfamiliar people.

C. The person recognizes that their fear is excessive or unreasonable. Note: In children, this feature may be absent.

D. The social or performance situation is avoided, although it is sometimes endured with dread (intense anxiety or distress).

E. The avoidance, anxious anticipation of, or distress in, the feared social or performance situation interferes significantly with the person's normal routine, occupational (academic) functioning, social life, or if the person is markedly distressed about having the phobia.

F. In individuals under age 18 years, the duration is at least 6 months.

G. The fear or avoidance is not due to the direct physiological effects of a substance or a general medical condition and is not better accounted for by another mental disorder (e.g., Panic Disorder, Separation Anxiety Disorder, Body Dysmorphic Disorder, a Pervasive Developmental Disorder, or Schizoid Personality Disorder).

H. If a general medical condition or another mental disorder is present, the fear in Criterion A or the avoidance in Criterion D, is unrelated to it (e.g., the fear is not of Stuttering, trembling in Parkinson's disease, or exhibiting abnormal eating behavior in Anorexia Nervosa).

Specify if:
Generalized: if the fears include most social situations (also consider the additional diagnosis of Avoidant Personality Disorder).

Symptoms

Cognitive aspects

In cognitive models of Social Anxiety Disorder, social phobics experience dread over how they will be presented to others. They may be overly self-conscious, pay high self-attention after the activity, or have high performance standards for themselves. According to the social psychology theory of self-presentation, a sufferer attempts to create a well-mannered impression on others but believes he or she is unable to do so. Many times, prior to the potentially anxiety-provoking social situation, sufferers may deliberately go over what could go wrong and how to deal with each unexpected case. After the event, they may have the perception they performed unsatisfactorily. Consequently, they will review anything that may have possibly been abnormal or embarrassing. These thoughts do not just terminate soon after the encounter, but may extend for weeks or longer. Those with social phobia tend to interpret neutral or ambiguous conversations with a negative outlook and many studies suggest that socially anxious individuals remember more negative memories than those less distressed.

An example of an instance may be that of an employee presenting to his co-workers. During the presentation, the person may stutter a word, upon which he or she may worry that other people significantly noticed and think that their perceptions of him or her as a presenter have been tarnished. This cognitive thought propels further anxiety which compounds with further stuttering, sweating, and, potentially, a panic attack.

Behavioral aspects

Social anxiety disorder is a persistent fear of one or more situations in which the person is exposed to possible scrutiny by others and fears that he or she may do something or act in a way that will be humiliating or embarrassing. It exceeds normal "shyness" as it leads to excessive social avoidance and substantial social or occupational impairment. Feared activities may include almost any type of social interaction, especially small groups, dating, parties, talking to strangers, restaurants, etc. Possible physical symptoms include "mind going blank", fast heartbeat, blushing, stomach ache, nausea and gagging. Cognitive distortions are a hallmark, and learned about in CBT (cognitive-behavioral therapy). Thoughts are often self-defeating and inaccurate.

The groundless fear of making telephone calls is typical, both answering and picking up, due to conversing's social nature. It may appear early in childhood.

According to psychologist B.F. Skinner, phobias are controlled by escape and avoidance behaviors. For instance, a student may leave the room when talking in front of the class (escape) and refrain from doing verbal presentations because of the previously encountered anxiety attack (avoid). Minor avoidance behaviors are exposed when a person avoids eye contact and crosses arms to avoid recognizable shaking. A fight-or-flight response is then triggered in such events. Preventing these automatic responses is at the core of treatment for social anxiety.

Physiological aspects

Physiological effects, similar to those in other anxiety disorders, are present in social phobics. Faced with an uncomfortable situation, children with social anxiety may display tantrums, weeping, clinging to parents, and shutting themselves out. In adults, it may be tears as well as experiencing excessive sweating, nausea, shaking, and palpitations as a result of the fight-or-flight response. The walk disturbance (where you are so worried about how you walk that you lose balance) may appear, especially when passing a group of people. Blushing is commonly exhibited by individuals suffering from social phobia. These visible symptoms further reinforce the anxiety in the presence of others. A 2006 study found that the area of the brain called the amygdala, part of the limbic system, is hyperactive when patients are shown threatening faces or confronted with frightening situations. They found that patients with more severe social phobia showed a correlation with the increased response in the amygdala.

Prevalence

Country	Prevalence
United States	2-7%
England	0.4% (children)
Scotland	1.8% (children)
Wales	0.6% (children)
Australia	1-2.7%
Brazil	4.7-7.9%

When prevalence estimates were based on the examination of psychiatric clinic samples, social anxiety disorder was thought to be a relatively rare disorder. The opposite was instead true; social anxiety was common but many were afraid to seek psychiatric help, leading to an understatement of the problem. Prevalence rates vary widely because of its vague diagnostic criteria and its overlapping symptoms with other disorders. There has been some debate on how the studies are conducted and whether the illness truly impairs the respondents as laid out in the official criteria. Psychologist Dr. Ray Crozier argues, "it is difficult to ascertain whether the person being interviewed adheres to the DSM-III-R criteria or whether they are merely exhibiting poor social skills or shyness."

The National Comorbidity Survey of over 8,000 American correspondents in 1994 revealed a 12-month and lifetime prevalence rates of 7.9 percent and 13.3 percent making it the third most prevalent psychiatric disorder after depression and alcohol dependence and the most apparent of the anxiety disorders. According to U.S. epidemiological data from the National Institute of Mental Health, social phobia affects 5.3 million adult Americans in any given year. Cross-cultural studies have reached prevalence rates with the conservative rates at 5 percent of the population. However, other estimates vary within 2 percent and 7 percent of the U.S. adult population.

Onset of social phobia typically occurs between 11 and 19 years of age. Onset after age 25 is rare. Social anxiety disorder occurs in females nearly twice as often as males, although men are more likely to seek help. The prevalence of social phobia appears to be increasing among white, married, and well-educated individuals. As a group, those with generalized social phobia are less likely to graduate from high school and are more likely to rely on government financial assistance or have poverty-level salaries. Surveys carried out in 2002 show the youth of England, Scotland, and Wales have a prevalence rate of 0.4 percent, 1.8 percent, and 0.6 percent, respectively. The prevalence of self-reported social anxiety for Nova Scotians older than 14 years was 4.2 percent in June 2004 with women (4.6 percent) reporting more than men (3.8 percent). In Australia, social phobia is the 8th and 5th leading disease or illness for males and females between 15–24 years of age as of 2003. Because of the difficulty in separating social phobia from poor social skills or shyness, some studies have a large range of prevalence. The table also shows higher prevalence in Brazil.

Comorbidity

There is a high degree of comorbidity with other psychiatric disorders. Social phobia often occurs alongside low self-esteem and clinical depression, due to lack of personal relationships and long periods of isolation from avoiding social situations. To try to reduce their anxiety and alleviate depression, people with social phobia may use alcohol or other drugs, which can lead to substance abuse. It is estimated that one-fifth of patients with social anxiety disorder also suffer from alcohol dependence. The most common complementary psychiatric condition is unipolar depression. In a sample of 14,263 people, of the 2.4 percent of persons diagnosed with social phobia, 16.6 percent also met the criteria for clinical depression. Besides depression, the most common disorders diagnosed in patients with social phobia are panic disorder (33 percent), generalized anxiety disorder (19 percent), post-traumatic stress disorder (36 percent), substance abuse disorder (18 percent), and attempted suicide (23 percent). In one study of social anxiety disorder among patients who developed comorbid alcoholism, panic disorder, or depression, social anxiety disorder preceded the onset of alcoholism, panic disorder and depression in 75 percent, 61 percent, and 90 percent of patients, respectively. Avoidant personality disorder is also highly correlated with social phobia. Because of its close relationship and overlapping symptoms with other illnesses, treating social phobics may help understand underlying connection in other psychiatric disorders.

There is research indicating that social anxiety disorder is often correlated with bipolar disorder. Some researchers believe they share an underlying cyclothymic-anxious-sensitive disposition. In addition, studies show that more socially phobic patients treated with anti-depressant medication develop hypomania than non-phobic controls. This can be seen as the medication creating a new problem, and also has this adverse effect in a proportion of those without social phobia.

Causes and perspectives

Research into the causes of social anxiety and social phobia is wide-ranging, encompassing multiple perspectives from neuroscience to sociology. Scientists have yet to pinpoint the exact causes. Studies suggest that genetics can play a part in combination with environmental factors.

Genetic and family factors

It has been shown that there is a two to threefold greater risk of having social phobia if a first-degree relative also has the disorder. This could be due to genetics and/or due to children acquiring social fears and avoidance through processes of observational learning or parental psychosocial education. Studies of identical twins brought up (via adoption) in different families have indicated that, if one twin developed social anxiety disorder, then the other was between 30 percent and 50 percent more likely than average to also develop the disorder. To some extent this 'heritability' may not be specific - for example, studies have found that if a parent has any kind of anxiety disorder or clinical depression, then a child is somewhat more likely to develop an anxiety disorder or social phobia. Studies suggest that parents of those with social anxiety disorder tend to be more socially isolated themselves (Bruch and Heimberg, 1994; Caster et al., 1999), and shyness in adoptive parents is significantly correlated with shyness in adopted children (Daniels and Plomin, 1985);

Adolescents who were rated as having an insecure (anxious-ambivalent) attachment with their mother as infants were twice as likely to develop anxiety disorders by late adolescence,including social phobia.

A related line of research has investigated 'behavioural inhibition' in infants – early signs of an inhibited and introspective or fearful nature. Studies have shown that around 10-15 percent of individuals show this early temperament, which appears to be partly due to genetics. Some continue to show this trait in to adolescence and adulthood, and appear to be more likely to develop social anxiety disorder.

Social experiences

A previous negative social experience can be a trigger to social phobia, perhaps particularly for individuals high in 'interpersonal sensitivity'. For around half of those diagnosed with social anxiety disorder, a specific traumatic or humiliating social event appears to be associated with the onset or worsening of the disorder; this kind of event appears to be particularly related to specific (performance) social phobia, for example regarding public speaking (Stemberg et al., 1995). As well as direct experiences, observing or hearing about the socially negative experiences of others (e.g. a faux pas committed by someone), or verbal warnings of social problems and dangers, may also make the development of a social anxiety disorder more likely. Social anxiety disorder may be caused by the longer-term effects of not fitting in, or being bullied, rejected or ignored (Beidel and Turner, 1998). Shy adolescents or avoidant adults have emphasised unpleasant experiences with peers or childhood bullying or harassment (Gilmartin, 1987). In one study, popularity was found to be negatively correlated with social anxiety, and children who were neglected by their peers reported higher social anxiety and fear of negative evaluation than other categories of children. Socially phobic children appear less likely to receive positive reactions from peers and anxious or inhibited children may isolate themselves.

Social/cultural influences

Cultural factors that have been related to social anxiety disorder include a society's attitude towards shyness and avoidance, affecting ability to form relationships or access employment or education. One study found that the effects of parenting are different depending on the culture - American children appear more likely to develop social anxiety disorder if their parents emphasize the importance of other's opinions and use shame as a disciplinary strategy (Leung et al., 1994), but this association was not found for Chinese/Chinese-American children. In China, research has indicated that shy-inhibited children are more accepted than their peers and more likely to be considered for leadership and considered competent, in contrast to the findings in Western countries. Purely demographic variables may also play a role - for example there are possibly lower rates of social anxiety disorder in Mediterranean countries and higher rates in Scandinavian countries, and it has been hypothesized that hot weather and high density may reduce avoidance and increase interpersonal contact.

Problems in developing social skills, or 'social effectiveness', may be a cause of some social anxiety disorder, through either inability or lack of confidence to interact socially and gain positive reactions and acceptance from others. The studies have been mixed, however, with some studies not finding significant problems in social skills while others have. What does seem clear is that the socially anxious perceive their own social skills to be low. It may be that the increasing need for sophisticated social skills in forming relationships or careers, and an emphasis on assertiveness and competitiveness, is making social anxiety problems more common, at least among the 'middle classes'. An interpersonal or media emphasis on 'normal' or 'attractive' personal characteristics has also been argued to fuel perfectionism and feelings of inferiority or insecurity regarding negative evaluation from others. The need for social acceptance or social standing has been elaborated in other lines of research relating to social anxiety

Evolutionary context

A long-accepted evolutionary explanation of anxiety is that it reflects an in-built 'fight or flight' system, which errs on the side of safety. One line of research suggests that specific dispositions to monitor and react to social threats may have evolved, reflecting the vital and complex importance of social living and social rank in human ancestral environments. Charles Darwin originally wrote about the evolutionary basis of shyness and blushing, and modern evolutionary psychology and psychiatry also addresses social phobia in this context. It has been hypothesized that in modern day society these evolved tendencies can become more inappropriately activated and result in some of the cognitive 'distortions' or 'irrationalities' identified in cognitive-behavioral models and therapies

Neurochemical and neurocognitive influences

Some scientists hypothesize that social phobia is related to an imbalance of the brain chemical serotonin. A recent study report increased Serotonin and Dopamine transporter binding in psychotropic medication-naive patients with Generalized Social Anxiety Disorder. Sociability is also closely tied to dopamine neurotransmission. Low D2 receptor binding is found in people with social anxiety. The efficacy of medications which affect serotonin and dopamine levels also indicates the role of these pathways. There is also increasing focus on other candidate transmitters, e.g. Norepinephrine, which may be over-active in social anxiety disorder, and the inhibitory transmitter GABA.

Individuals with social anxiety disorder have been found to have a hypersensitive amygdala, for example in relation to social threat cues (e.g. someone might be evaluating you negatively), angry or hostile faces, and while just waiting to give a speech. Recent research has also indicated that another area of the brain, the 'Anterior cingulate cortex', which was already known to be involved in the experience of physical pain, also appears to be involved in the experience of 'social pain', for example perceiving group exclusion.

Substance induced

While alcohol initially helps social phobia, excessive alcohol misuse can worsen social phobia symptoms and can cause panic disorder to develop or worsen during alcohol intoxication and especially during alcohol withdrawal syndrome. This effect is not unique to alcohol but can also occur with long term use of drugs which have a similar mechanism of action to alcohol such as the benzodiazepines which are sometimes prescribed as tranquillisers. Benzodiazepines possess anti-anxiety properties and can be useful for the short-term treatment of severe anxiety. Like the anticonvulsants, they tend to be mild, well tolerated, and extremely safe. Benzodiazepines are usually administered orally for the treatment of anxiety; however, occasionally lorazepam or diazepam may be given intravenously for the treatment of panic attacks.

The World Council of Anxiety does not recommend benzodiazepines for the long term treatment of anxiety due to a range of problems associated with long term use of benzodiazepines including tolerance, psychomotor impairment, cognitive and memory impairments, physical dependence and a benzodiazepine withdrawal syndrome upon discontinuation of benzodiazepines. Despite increasing focus on the use of antidepressants and other agents for the treatment of anxiety, benzodiazepines have remained a mainstay of anxiolytic pharmacotherapy due to their robust efficacy, rapid onset of therapeutic effect, and generally favorable side effect profile. (Read about benzodiazepine withdrawal syndrome). Treatment patterns for psychotropic drugs appear to have remained stable over the past decade, with benzodiazepines being the most commonly used medication for panic disorder.

Approximately half of patients attending mental health services for conditions including anxiety disorders such as panic disorder or social phobia are the result of alcohol or benzodiazepine dependence.^{[citation needed]} Sometimes anxiety pre-existed alcohol or benzodiazepine dependence but the alcohol or benzodiazepine dependence act to keep the anxiety disorders going and often progressively making them worse. Many people who are addicted to alcohol or prescribed benzodiazepines when it is explained to them they have a choice between ongoing ill mental health or quitting and recovering from their symptoms decide on quitting alcohol and/or their benzodiazepines. It was noted that every individual has an individual sensitivity level to alcohol or sedative hypnotic drugs and what one person can tolerate without ill health another will suffer very ill health and that even moderate drinking can cause rebound anxiety syndromes and sleep disorders. A person who is suffering the toxic effects of alcohol or benzodiazepines will not benefit from other therapies or medications as they do not address the root cause of the symptoms. Symptoms may temporarily worsen however, during alcohol withdrawal or benzodiazepine withdrawal.

Psychological factors

Research has indicated the role of 'core' or 'unconditional' negative beliefs (e.g. I am inept) and 'conditional' beliefs nearer to the surface (e.g. If I show myself, I will be rejected). They are thought to develop based on personality and adverse experiences and to be activated when the person feels under threat. One line of work has focused more specifically on the key role of self-presentational concerns. The resulting anxiety states are seen as interfering with social performance and the ability to concentrate on interaction, which in turn creates more social problems, which strengthens the negative schema. Also highlighted has been a high focus on and worry about anxiety symptoms themselves and how they might appear to others. A similar model emphasizes the development of a distorted mental representation of their self and over-estimates of the likelihood and consequences of negative evaluation, and of the performance standards that others have. Such cognitive-behavioral models consider the role of negatively-biased memories of the past and the processes of rumination after an event, and fearful anticipation before it. Studies have also highlighted the role of subtle avoidance and defensive factors, and shown how attempts to avoid feared negative evaluations or use 'safety behaviors' (Clark & Wells, 1995) can make social interaction more difficult and the anxiety worse in the long run. This work has been influential in the development of Cognitive Behavioral Therapy for social anxiety disorder, which has been shown to have efficacy.

Treatment

The most important clinical point to emerge from studies of social anxiety disorder is the benefit of early diagnosis and treatment. Social anxiety disorder remains under-recognized in primary care practice, with patients often presenting for treatment only after the onset of complications such as clinical depression or substance abuse disorders.

Research has provided evidence for the efficacy of two forms of treatment available for social phobia: certain medications and a specific form of short-term psychotherapy called Cognitive-behavioral therapy (CBT), the central component being gradual exposure therapy.

Psychotherapy

Research has shown that cognitive-behavioral therapy (CBT) can be highly effective for several anxiety disorders, particularly panic disorder and social phobia. CBT, as its name suggests, has two main components, cognitive and behavioral. In cases of social anxiety, the cognitive component can help the patient question how they can be so sure that others are continually watching and harshly judging him or her. The behavioral component seeks to change people's reactions to anxiety-provoking situations. As such it serves as a logical extension of cognitive therapy, whereby people are shown proof in the real world that their dysfunctional thought processes are unrealistic. A key element of this component is gradual exposure, in which the patient is confronted by the things they fear in a structured, sensitive manner. Gradual exposure is an inherently unpleasant technique; ideally it involves exposure to a feared social situation that is anxiety provoking but bearable, for as long as possible, two to three times a week. Often, a hierarchy of feared steps is constructed and the patient is exposed each step sequentially. The aim is to learn from acting differently and observing reactions. This is intended to be done with support and guidance, and when the therapist and patient feel they are ready. Cognitive-behavioral therapy for social phobia also includes anxiety management training, which may include techniques such as deep breathing and muscle relaxation exercises, which may be practiced 'in-situ'. CBT can also be conducted partly in group sessions, facilitating the sharing of experiences, a sense of acceptance by others and undertaking behavioral challenges in a trusted environment (Heimberg).

Some studies have suggested social skills training can help with social anxiety. However, it is not clear whether specific social skills techniques and training are required, rather than just support with general social functioning and exposure to social situations.

Additionally, a recent study has suggested that interpersonal therapy, a form of psychotherapy primarily used to treat depression, may also be effective in the treatment of social phobia.

Pharmacological treatments

SSRIs

Selective serotonin reuptake inhibitors (SSRIs), a class of antidepressants, are considered by many to be the first choice medication for generalised social phobia. These drugs elevate the level of the neurotransmitter serotonin, among other effects. The first drug formally approved by the Food and Drug Administration was paroxetine, sold as Paxil in the U.S. or Seroxat in the UK. Compared to older forms of medication, there is less risk of tolerability and drug dependency.^[70] However, their efficacy and increased suicide risk has been subject to controversy.

In a 1995 double-blind, placebo-controlled trial, the SSRI paroxetine was shown to result in clinically meaningful improvement in 55 percent of patients with generalized social anxiety disorder, compared with 23.9 percent of those taking placebo. An October 2004 study yielded similar results. Patients were treated with either fluoxetine, psychotherapy, fluoxetine and psychotherapy, placebo and psychotherapy, or a placebo. The first four sets saw improvement in 50.8 to 54.2 percent of the patients. Of those assigned to receive only a placebo, 31.7 percent achieved a rating of 1 or 2 on the Clinical Global Impression-Improvement scale. Those who sought both therapy and medication did not see a boost in improvement.

General side-effects are common during the first weeks while the body adjusts to the drug. Symptoms may include headaches, nausea, insomnia and changes in sexual behavior. Treatment safety during pregnancy has not been established. In late 2004 much media attention was given to a proposed link between SSRI use and juvenile suicide. For this reason, the use of SSRIs in pediatric cases of depression is now recognized by the Food and Drug Administration as warranting a cautionary statement to the parents of children who may be prescribed SSRIs by a family doctor. Recent studies have shown no increase in rates of suicide. These tests, however, represent those diagnosed with depression, not necessarily with social anxiety disorder. However, it should be noted that due to the nature of the conditions, those taking SSRIs for social phobias are far less likely to have suicidal ideation than those with depression.

Other drugs

Although SSRIs are often the first choice for treatment, other prescription drugs are also used, sometimes only if SSRIs fail to produce any clinically significant improvement.

In 1985, before the introduction of SSRIs, anti-depressants such as monoamine oxidase inhibitors (MAOIs) were frequently used in the treatment of social anxiety. Their efficacy appears to be comparable or sometimes superior to SSRIs or benzodiazepines. However, because of the dietary restrictions required, high toxicity in overdose, and incompatibilities with other drugs, its usefulness as a treatment for social phobics is now limited. Some argue for their continued use, however, or that a special diet does not need to be strictly adhered to. A newer type of this medication, Reversible inhibitors of monoamine oxidase subtype A (RIMAs) inhibit the MAO enzyme only temporarily, improving the adverse-effect profile but possibly reducing their efficacy.

Benzodiazepines such as alprazolam and clonazepam are an alternative to SSRIs. These drugs are often used for short-term relief of severe, disabling anxiety. Although benzodiazepines are still sometimes prescribed for long-term everyday use in some countries, there is much concern over the development of drug tolerance, dependency and recreational abuse. It has been recommended that benzodiazepines are only considered for individuals who fail to respond to safer medications. Benzodiazepines augment the action of GABA, the major inhibitory neurotransmitter in the brain; effects usually begin to appear within minutes or hours.

The novel antidepressant mirtazapine has been proven effective in treatment of social anxiety disorder. This is especially significant due to mirtazapine's fast onset and lack of many unpleasant side-effects associated with SSRIs (particularly, sexual dysfunction).

In Japan, the serotonin-norepinephrine reuptake inhibitor (SNRI), Milnacipran is used in the treatment of Taijin kyofusho a Japanese variant of social anxiety disorder.

Some people with a form of social phobia called performance phobia have been helped by beta-blockers, which are more commonly used to control high blood pressure. Taken in low doses, they control the physical manifestation of anxiety and can be taken before a public performance.

A novel treatment approach has recently been developed as a result of translational research. It has been shown that a combination of acute dosing of d-cycloserine (DCS) with exposure therapy facilitates the effects of exposure therapy of social phobia (Hofmann, Meuret, Smits, et al., 2006). DCS is an old antibiotic medication used for treating tuberculosis and does not have any anxiolytic properties per se. However, it acts as an agonist at the glutamatergic N-methyl-D-aspartate (NMDA) receptor site, which is important for learning and memory (Hofmann, Pollack, & Otto, 2006). It has been shown that administering a small dose acutely 1 hour before exposure therapy can facilitate extinction learning that occurs during therapy.

Criticisms

Brendan I. Koerner writing in Mother Jones argues that inherent problems with society such as a competitive culture, power imbalances, lack of care and poor social education in families cause social anxiety; he feels the diagnostic boundaries have been stretched too far and that clinical and media work is promoting the idea that any problems with shyness or social worries are a pathological medical condition requiring medical treatment. He sees this as being driven by pharmaceutical companies, either by direct advertising to the public or their financial influence on psychiatry. Proponents of this view argue that drug companies try to increase profits by inventing new diseases or labels (Disease mongering).

Seasonal affective disorder - Top/popular /Health News/Tips

noreply@blogger.com (Sridevi. V, M.A) — Thu, 24 Dec 2009 08:31:00 +0000

Seasonal affective disorder

Seasonal Affective Disorder (SAD), also known as winter depression or winter blues, is a mood disorder in which people who have normal mental health throughout most of the year experience depressive symptoms in the winter or, less frequently, in the summer, spring or autumn, repeatedly, year after year. In the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), SAD is not a unique mood disorder, but is "a specifier of major depression".

The US National Library of Medicine notes that "some people experience a serious mood change when the seasons change. They may sleep too much, have little energy, and crave sweets and starchy foods. They may also feel depressed. Though symptoms can be severe, they usually clear up." The condition in the summer is often referred to as Reverse Seasonal Affective Disorder, and can also include heightened anxiety. It has been estimated that 1.5-9% of adults in the US experience SAD.

There are many different treatments for classic (winter-based) seasonal affective disorder, including light therapy with sunlight or bright lights, antidepressant medication, cognitive-behavioral therapy, ionized-air administration, and carefully timed supplementation of the hormone melatonin.

Symptoms
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Symptoms of SAD may consist of: difficulty waking up in the morning, tendency to oversleep as well as to overeat, and especially a craving for carbohydrates, which leads to weight gain. Other symptoms include a lack of energy, difficulty concentrating on completing tasks, and withdrawal from friends, family, and social activities. All of this leads to the depression, pessimism, and lack of pleasure which characterize a person suffering from this disorder.

People that experience Reverse SAD (spring and summer depression) show symptoms of insomnia, anxiety, irritability, decreased appetite, weight loss, and an increased sex drive. RSAD can also manifest depression, which makes it difficult to diagnose this rare affliction.
Diagnostic criteria

According to the American Psychiatric Association DSM-IV, criteria, Seasonal Affective disorder is not regarded as a separate disorder, but is called a 'course specifier' and may be applied as an added description to the pattern of Major Depressive Episodes in patients with Major Depressive Disorder or patients with Bipolar Disorder. The Seasonal Pattern Specifier must meet four criteria: depressive episodes at a particular time of the year; remissions or mania/hypomania also at a characteristic time of year; these patterns must have lasted two years with no nonseasonal major depressive episodes during that same period; and these seasonal depressive episodes outnumber other depressive episodes throughout the patient's lifetime. The Mayo Clinic describes three types of Seasonal Affective Disorder, each with its own set of symptoms.

Physiology
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Seasonal mood variations are believed to be related to light. An argument for this view is the effectiveness of bright-light therapy. SAD is measurably present at latitudes in the Arctic region, such as Finland (64º 00´N) where the rate of SAD is 9.5% Cloud cover may contribute to the negative effects of SAD.

The symptoms of SAD mimic those of dysthymia or clinical depression. There is also potential risk of suicide in some patients experiencing SAD. One study reports 6-35% of sufferers required hospitalization during one period of illness. At times, patients may not feel depressed, but rather lack energy to perform everyday activities.

Various proximate causes have been proposed. One possibility is that SAD is related to a lack of serotonin, and serotonin polymorphisms could play a role in SAD, although this has been disputed. Mice incapable of turning serotonin into N-acetylserotonin (by Serotonin N-acetyltransferase) appear to express "depression-like" behavior, and antidepressants such as fluoxetine increase the amount of the enzyme Serotonin N-acetyltransferase, resulting in an antidepressant-like effect. Another theory is that the cause may be related to melatonin which is produced in dim light and darkness by the pineal gland, since there are direct connections, via the retinohypothalamic tract and the suprachiasmatic nucleus, between the retina and the pineal gland.

Subsyndromal Seasonal Affective Disorder is a milder form of SAD experienced by an estimated 14.3% vs. 6.1% of the U.S. population.[14] The blue feeling experienced by both SAD and SSAD sufferers can usually be dampened or extinguished by exercise and increased outdoor activity, particularly on sunny days, resulting in increased solar exposure. Connections between human mood, as well as energy levels, and the seasons are well documented, even in healthy individuals.

Mutation of a gene expressing melanopsin has been implicated in the risk of having Seasonal Affective Disorder.

Origin
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In many species, activity is diminished during the winter months in response to the reduction in available food and the difficulties of surviving in cold weather. Hibernation is an extreme example, but even species that do not hibernate often exhibit changes in behavior during the winter. It has been argued that SAD is an evolved adaptation in humans that is a variant or remnant of a hibernation response in some remote ancestor. Presumably, food was scarce during most of human prehistory, and a tendency toward low mood during the winter months would have been adaptive by reducing the need for calorie intake. The preponderance of women with SAD suggests that the response may also somehow regulate reproduction.

If these interpretations are correct, SAD would not be a dysfunction or disorder as most psychiatrists assume, but rather a normal and expected response to seasonal changes.

Treatment
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One type of light therapy lamp

There are many different treatments for classic (winter-based) seasonal affective disorder, including bright light therapy, medication, ionized-air administration, cognitive-behavioral therapy and carefully timed supplementation of the hormone melatonin.

Photoperiod-related alterations of the duration of melatonin secretion may affect the seasonal mood cycles of SAD. This suggests that light therapy may be an effective treatment for SAD. Bright light therapy often includes the use of a lightbox which emits far more lumens than a customary incandescent lamp. White light, or "full spectrum" light is usually preferred, although blue light is also used.

Lightbox therapy is effective at doses of 2500–10,000 lux, with the patient sitting a prescribed distance, commonly 30–60 cm, in front of the box with her/his eyes open but not staring at the light source. Most treatments use 30–60 minute treatments, however this may vary depending on the situation. Many patients use the light box in the morning, and there is evidence that morning light is superior to evening light, although people can respond to evening light as well. Discovering the best schedule is essential. One study has shown that up to 69% of patients find the treatment inconvenient and as many as 19% stop use because of this.

Dawn simulation has also proven to be effective; in some studies, there is an 83% better response when compared to other bright light therapy. When compared in a study to negative air ionization, bright light was proven to be 57.1% effective vs. dawn simulation, 49.5%. Patients using light therapy can experience improvement during the first week, but increased results are evident when continued throughout several weeks. Most studies have found it effective without use year round, but rather as a seasonal treatment lasting for several weeks until frequent light exposure is naturally obtained.

Light therapy can also consist of exposure to sunlight, either in the form of spending more time outside , or using a computer-controlled mirror device called a heliostat to reflect sunlight into the windows of a home or office.

SSRI (selective serotonin reuptake inhibitor) antidepressants have proven effective in treating SAD. Bupropion is also effective as a prophylactic. Effective antidepressants are fluoxetine, sertraline, or paroxetine. Both fluoxetine and light therapy are 67% effective in treating SAD according to direct head-to-head trials conducted during the 2006 CAN-SAD study. Subjects using the light therapy protocol showed earlier clinical improvement, generally within one week of beginning the clinical treatment.

Negative air ionization, which involves releasing charged particles into the sleep environment, has also been found effective with a 47.9% improvement if the negative ions are in sufficient density (quantity). Depending upon the patient, one treatment (ie. lightbox) may be used in conjunction with another therapy (ie. medication).

Modafinil may be also an effective and well-tolerated treatment in patients with seasonal affective disorder/winter depression.

Alfred J. Lewy of Oregon Health and Science University in Portland, OHSU, and others see the cause of SAD as a misalignment of the sleep-wake phase contra the period of the body clock, circadian rhythms out of synch, and treat it with melatonin in the afternoon. Correctly timed melatonin administration shifts the rhythms of several hormones en bloc.

Another explanation is that vitamin D levels are too low when people do not get enough Ultraviolet-B on their skin. An alternative to using bright lights is to take vitamin D supplements. However, one study did not show a link between vitamin D levels and depressive symptoms in elderly Chinese.

Incidence
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Nordic countries

Winter depression is a common slump in the mood of some inhabitants of most of the Nordic countries. It was first described by the 6th century Goth scholar Jordanes in his Getica wherein he described the inhabitants of Scandza (Scandinavia). Iceland, however, seems to be an exception. A study of more than 2000 people there found the prevalence of seasonal affective disorder and seasonal changes in anxiety and depression to be unexpectedly low in both sexes. The study's authors suggested that propensity for SAD may differ due to some genetic factor within the Icelandic population. A study of Canadians of wholly Icelandic descent also showed low levels of SAD. It has more recently been suggested that this may be attributed to the large amount of fish traditionally eaten by Icelandic people, 225 lb per person per year as opposed to about 50 lb in the US and Canada, rather than to genetics. Fish is high in vitamin D. Fish also contains docosahexaenoic acid (DHA), which has been shown to help with a variety of neurological dysfunction.

Other countries

In the United States, a diagnosis of seasonal affective disorder was first proposed by Norman E. Rosenthal, MD in 1984. Rosenthal wondered why he became sluggish during the winter after moving from sunny South Africa to New York. He started experimenting increasing exposure to artificial light, and found this made a difference. In Alaska it has been established that there is a SAD rate of 8.9%, and an even greater rate of 24.9% for subsyndromal SAD.

Around 20% of Irish people are affected by SAD, according to a survey conducted in 2007. The survey also shows women are more likely to be affected by SAD than men. An estimated 10% of the population in the Netherlands suffers from SAD.

SAD and bipolar
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Most people with SAD experience major depressive disorder, but as many as 20% may have or may go on to develop a bipolar disorder, a manic-depressive disorder. It is important to discriminate the improved mood associated with recovery from the winter depression and a manic episode because there are important treatment differences. In these cases, persons with SAD may experience depression during the winter and hypomania in the summer.
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Dengue fever - Top/Popular Health News & Tips

noreply@blogger.com (Sridevi. V, M.A) — Thu, 10 Sep 2009 01:01:00 +0000

Signs and symptoms

The disease manifests as a sudden onset of severe headache, muscle and joint pains (myalgias and arthralgias—severe pain that gives it the nick-name break-bone fever or bonecrusher disease), fever, and rash. The dengue rash is characteristically bright red petechiae and usually appears first on the lower limbs and the chest; in some patients, it spreads to cover most of the body. There may also be gastritis with some combination of associated abdominal pain, nausea, vomiting, or diarrhea. Some cases develop much milder symptoms which can be misdiagnosed as influenza or other viral infection when no rash is present. Thus travelers from tropical areas may pass on dengue in their home countries inadvertently, having not been properly diagnosed at the height of their illness. Patients with dengue can pass on the infection only through mosquitoes or blood products and only while they are still febrile. The classic dengue fever lasts about six to seven days, with a smaller peak of fever at the trailing end of the disease (the so-called biphasic pattern). Clinically, the platelet count will drop until the patient's temperature is normal. Cases of DHF also show higher fever, variable haemorrhagic phenomena, thrombocytopenia, and haemoconcentration. A small proportion of cases lead to dengue shock syndrome (DSS) which has a high mortality rate. DHF combined with a cirrhotic liver has been suspected in rapid development of hepatocellular carcinoma (HCC). Given that the Dengue virus (DEN) is related to the Hepatitis C virus, this is an avenue for further research as HCC is among the top five cancerous causes of death outside Europe and North America. Normally HCC does not occur in a cirrhotic liver for ten or more years after the cessation of the poisoning agent. DHF patients can develop HCC within one year of cessation of poisoning agent.

Diagnosis

The diagnosis of dengue is usually made clinically. The classic picture is high fever with no localising source of infection, a petechial rash with thrombocytopenia and relative leukopenia - low platelet and white blood cell count. Care has to be taken as diagnosis of DHF can mask end stage liver disease and vice versa.

Fever, bladder problem, constant headaches, eye pain, severe dizziness and loss of appetite.
Hemorrhagic tendency (positive tourniquet test, spontaneous bruising, bleeding from mucosa, gingiva, injection sites, etc.; vomiting blood, or bloody diarrhea)
Thrombocytopenia (<100,000>
Evidence of plasma leakage (hematocrit more than 20% higher than expected, or drop in haematocrit of 20% or more from baseline following IV fluid, pleural effusion, ascites, hypoproteinemia)
Encephalitic occurrences.

Dengue shock syndrome is defined as dengue hemorrhagic fever plus:

Weak rapid pulse,
Narrow pulse pressure (less than 20 mm Hg)
Cold, clammy skin and restlessness.

A dependable immediate information of the Dengue diagnostics in the rural areas can be performed by the introduction of Rapid Diagnostic Test kits which also differentiates between primary and secondary dengue infections. Serology and polymerase chain reaction (PCR) studies are available to confirm the diagnosis of dengue if clinically indicated. Dengue can be a life threatening fever.

Etiology

Dengue fever is caused by Dengue virus (DENV), a mosquito-borne flavivirus. DENV is a ssRNA positive-strand virus of the family Flaviviridae; genus Flavivirus. There are four serotypes of DENV. The virus has a genome of about 11000 bases that codes for three structural proteins, C, prM, E; seven nonstructural proteins, NS1, NS2a, NS2b, NS3, NS4a, NS4b, NS5; and short non-coding regions on both the 5' and 3' ends.

Treatment

The mainstay of treatment is timely supportive therapy to tackle shock due to hemoconcentration and bleeding. Close monitoring of vital signs in critical period (between day 2 to day 7 of fever) is critical. Increased oral fluid intake is recommended to prevent dehydration. Supplementation with intravenous fluids may be necessary to prevent dehydration and significant concentration of the blood if the patient is unable to maintain oral intake. A platelet transfusion is indicated in rare cases if the platelet level drops significantly (below 20,000) or if there is significant bleeding. The presence of melena may indicate internal gastrointestinal bleeding requiring platelet and/or red blood cell transfusion.

Aspirin and non-steroidal anti-inflammatory drugs should be avoided as these drugs may worsen the bleeding tendency associated with some of these infections. Patients may receive paracetamol preparations to deal with these symptoms if dengue is suspected.

[edit] Traditional and emerging treatments

Emerging evidence suggests that mycophenolic acid and ribavirin inhibit dengue replication. Initial experiments showed a fivefold increase in defective viral RNA production by cells treated with each drug. In vivo studies, however, have not yet been done. Unlike HIV therapy, lack of adequate global interest and funding greatly hampers the development of a treatment regime.

In Brazilian traditional medicine, dengue is treated with cat's claw herb, which is for inflammation and does not prevent dengue.

In Malaysia, dengue is treated by some using natural medicine. Mas Amirtha and Semalu developed by the Alternative Medicine Research Institute, Center for Asia.^{[citation needed]} The treatment is speculated to be able to arrest and reverse the viral infection and prevent the disease from advancing into a critical stage, though no evidence has yet shown effectiveness. In Philippines dengue patients use tawa-tawa herbs and sweet potato tops juice to increase the platelets counts and revived the patients.^{[citation needed]}

Epidemiology

Worldwide dengue distribution, 2006. Red: Epidemic dengue. Blue: Aedes aegypti.

Dengue is transmitted by Aedes mosquitoes, particularly A. aegypti and A. albopictus. Dengue may also be transmitted via infected blood products (blood transfusions, plasma, and platelets), but the scale of this problem is unknown.

Worldwide dengue distribution, 2000.

The first recognized Dengue epidemics occurred almost simultaneously in Asia, Africa, and North America in the 1780s, shortly after the identification and naming of the disease in 1779. A pandemic began in Southeast Asia in the 1950s, and by 1975 DHF had become a leading cause of death among children in the region. Epidemic dengue has become more common since the 1980s. By the late 1990s, dengue was the most important mosquito-borne disease affecting humans after malaria, with around 40 million cases of dengue fever and several hundred thousand cases of dengue hemorrhagic fever each year. Significant outbreaks of dengue fever tend to occur every five or six months. The cyclical rise and fall in numbers of dengue cases is thought to be the result of seasonal cycles interacting with a short-lived cross-immunity^{[clarification needed]} for all four strains in people who have had dengue. When the cross-immunity wears off the population is more susceptible to transmission whenever the next seasonal peak occurs. Thus over time there remain large numbers of susceptible people in affected populations despite previous outbreaks due to the four different serotypes of dengue virus and the presence of unexposed individuals from childbirth or immigration.

There is significant evidence, originally suggested by S.B. Halstead in the 1970s, that dengue hemorrhagic fever is more likely to occur in patients who have secondary infections by another one of dengue fever's four serotypes. One model to explain this process is known as antibody-dependent enhancement (ADE), which allows for increased uptake and virion replication during a secondary infection with a different strain. Through an immunological phenomenon, known as original antigenic sin, the immune system is not able to adequately respond to the stronger infection, and the secondary infection becomes far more serious.^[14] This process is also known as superinfection.

Reported cases of dengue are an under-representation of all cases when accounting for subclinical cases and cases where the patient did not present for medical treatment.

There was a serious outbreak in Rio de Janeiro in February 2002 affecting around one million people and killing sixteen. On March 20, 2008, the secretary of health of the state of Rio de Janeiro, Sérgio Côrtes, announced that 23,555 cases of dengue, including 30 deaths, had been recorded in the state in less than three months. Côrtes said, "I am treating this as an epidemic because the number of cases is extremely high." Federal Minister of Health, José Gomes Temporão also announced that he was forming a panel to respond to the situation. Cesar Maia, mayor of the city of Rio de Janeiro, denied that there was serious cause for concern, saying that the incidence of cases was in fact declining from a peak at the beginning of February. By April 3, 2008, the number of cases reported rose to 55,000

In Singapore, there are 4,000–5,000 reported cases of dengue fever or dengue haemorrhagic fever every year. In the year 2004, there were seven deaths from dengue shock syndrome.

An epidemic broke out in Bolivia in early 2009, in which 18 people have died and 31,000 infected.

An outbreak of dengue fever was declared in Cairns, located in the tropical north of Queensland, Australia on 1 December 2008. As at 3 March 2009 there were 503 confirmed cases of dengue fever, in a residential population of 152,137. Outbreaks were subsequently declared the neighbouring cities and towns of Townsville (outbreak declared 5 January 2009), Port Douglas (6 February 2009), Yarrabah (19 February 2009), Injinoo (24 February 2009), Innisfail (27 February 2009) and Rockhampton (10 March 2009). There have been occurrences of dengue types one, two, three and four in the region. March 4 2009, Queensland Health had confirmed an elderly woman had died from dengue fever in Cairns, in the first fatality since the epidemic began last year. The statement said that although the woman had other health problems, she tested positive for dengue and the disease probably contributed to her death.

In 2009, in Argentina, a dengue outbreak was declared the northern provinces of Chaco, Catamarca, Salta, Jujuy, and Corrientes, with over 9673 cases reported as of April 11, 2009 by the Health Ministry . Some travelers from the affected zones have spread the fever as far south as Buenos Aires . Major efforts to control the epidemic in Argentina are focused on preventing its vector (the Aedes mosquitoes) from reproducing. This is addressed by asking people to dry out all possible water reservoirs from where mosquitoes could proliferate (which is, in other countries, known as "descacharrado"). There have also been information campaigns concerning prevention of the dengue fever; and the government is fumigating with insecticide in order to control the mosquito population.

The first cases of dengue are currently being reported on the island of Mauritius, in the indian ocean. One of the South Asian country still highly suffering from this problem is Sri Lanka.

Prevention

Vaccine development

There is no commercially available vaccine for the dengue flavivirus. However, one of the many ongoing vaccine development programs is the Pediatric Dengue Vaccine Initiative which was set up in 2003 with the aim of accelerating the development and introduction of dengue vaccine(s) that are affordable and accessible to poor children in endemic countries. Thai researchers are testing a dengue fever vaccine on 3,000–5,000 human volunteers after having successfully conducted tests on animals and a small group of human volunteers. A number of other vaccine candidates are entering phase I or II testing.

Mosquito control

A field technician looking for larvae in standing water containers during the 1965 Aedes aegypti eradication program in Miami, Florida. In the 1960s, a major effort was made to eradicate the principal urban vector mosquito of dengue and yellow fever viruses, Aedes aegypti, from southeast United States.

Primary prevention of dengue mainly resides in mosquito control. There are two primary methods: larval control and adult mosquito control.^{[citation needed]} In urban areas, Aedes mosquitos breed on water collections in artificial containers such as plastic cups, used tires, broken bottles, flower pots, etc. Periodic draining or removal of artificial containers is the most effective way of reducing the breeding grounds for mosquitos.^{[citation needed]} Larvicide treatment is another effective way to control the vector larvae but the larvicide chosen should be long-lasting and preferably have World Health Organization clearance for use in drinking water. There are some very effective insect growth regulators (IGRs) available which are both safe and long-lasting (e.g. pyriproxyfen). For reducing the adult mosquito load, fogging with insecticide is somewhat effective.^{[citation needed]}

Prevention of mosquito bites is another way of preventing disease. This can be achieved by using insect repellent, mosquito traps or mosquito nets.

In 1998, scientists from the Queensland Institute of Medical Research (QIMR) in Australia and Vietnam's Ministry of Health introduced a scheme that encouraged children to place a water bug, the crustacean Mesocyclops, in water tanks and discarded containers where the Aedes aegypti mosquito was known to thrive. This method is viewed as being more cost-effective and more environmentally friendly than pesticides, though not as effective, and requires the continuing participation of the community.

Even though this method of mosquito control was successful in rural provinces, not much is known about how effective it could be if applied to cities and urban areas. The Mesocyclops can survive and breed in large water containers, but would not be able to do so in small containers of which most urban area have within their homes. Also, Mesocyclops are hosts for the guinea worm, a pathogen that causes a parasite infection, and so this method of mosquito control cannot be used in countries that are still susceptible to the guinea worm. The biggest dilemma with Mesocyclops is that its success depends on the participation of the community. This idea of a possible parasite bearing creature in household water containers dissuades people from continuing the process of inoculation, and without the support and work of everyone living in the city, this method would not be successful.

In 2004, scientists from the Federal University of Minas Gerais, Brazil, discovered a fast way to find and count mosquito population inside urban areas. The technology, named Intelligent Monitoring of Dengue (in Portuguese), uses traps with kairomones that capture Aedes gravid females, and upload insect counts with a combination of cell phone, GPS and internet technology. The result is a complete map of the mosquitoes in urban areas, updated in real time and accessible remotely, that can inform control methodologies.^[28] The technology was recognized with a Tech Museum Award in 2006.

In 2009, scientists from the School of Integrative Biology at The University of Queensland revealed that by infecting Aedes mosquitos with the bacterium Wolbachia, the adult lifespan was reduced by half. ^[30] In the study, super-fine needles were used to inject 10,000 mosquito embryos with the bacterium. Once an insect was infected, the bacterium would spread via its eggs to the next generation. A pilot release of infected mosquitoes could begin in Vietnam within three years. If no problems are discovered, a full-scale biological attack against the insects could be launched within five years.

Potential antiviral approaches

Dengue virus belongs to the family Flaviviridae, which includes the hepatitis C virus, West Nile and Yellow fever viruses among others. Possible laboratory-based modification of the yellow fever vaccine YF-17D to target the dengue virus via chimeric replacement has been discussed extensively in scientific literature. To date, however, no full scale studies have been conducted.

In 2006, a group of Argentine scientists discovered the molecular replication mechanism of the virus, which could be specifically attacked by disrupting the viral RNA polymerase.In cell culture and murine experiments, morpholino antisense oligos have shown specific activity against Dengue virus.

In 2007 scientists' attenuated virus replication by interfering with activity of the dengue viral protease; subsequently, a project to identify novel protease disruption mechanisms has been launched.

Etymology

The origins of the word dengue are not clear, but one theory is that it is derived from the Swahili phrase "Ka-dinga pepo", which describes the disease as being caused by an evil spirit. The Swahili word "dinga" may possibly have its origin in the Spanish word "dengue" meaning fastidious or careful, which would describe the gait of a person suffering the bone pain of dengue fever. Alternatively, the use of the Spanish word may derive from the similar-sounding Swahili.

Also known as "Dandy Fever", slaves in the West Indies who contracted dengue were said to have the posture and gait of a dandy.

History

The first recorded potential case of dengue fever comes from a Chinese medical encyclopedia from the Jin Dynasty (265–420 AD). The Chinese referred to a “water poison” associated with flying insects. ^[41] The first definitive case report dates from 1789 and is attributed to Benjamin Rush, who coined the term "breakbone fever" because of the symptoms of myalgia and arthralgia. The viral etiology and the transmission by mosquitoes were deciphered only in the 20th century. Population movements during World War II spread the disease globally. A pandemic of dengue began in Southeast Asia after World War II and has spread around the globe since then.

Use as a biological weapon

Dengue fever was one of more than a dozen agents that the United States researched as potential biological weapons before the nation suspended its biological weapons program.

noreply@blogger.com (Sridevi. V, M.A) — Thu, 25 Dec 2008 06:26:00 +0000

Colds and flu remain mysterious

Scientists hope to learn more about how flu is transmitted

It is the time of year when coughs, colds and flu seem to spread like wildfire.

One person in the office gets sick and it is not long before half the workforce has taken to their bed.

And all those Christmas parties probably aggravate the situation as we mix with more people than we usually would.

But how much do we actually know about how colds and flu spread - for example how many others does one cold sufferer infect?

Researchers are hoping a big-brother style experiment will provide some answers, at least where influenza is concerned.

Next year, Professor John Oxford, an expert in virology from Queen Mary's School of Medicine and Dentistry, in London, will lock volunteers in a hotel for a week, deliberately infect some with the flu virus, and wait to see what happens.

"To start with, we'll take 15 volunteers, with no immunity to the particular flu virus and infect five of them," he said.

"Using CCTV, we'll keep an eye on them and look for patterns of transmission."

It will be the first study looking at the spread of flu by directly infecting volunteers and sitting back to see what happens.

Pandemic planning

Knowing how easily flu can spread will help officials planning for pandemics, said Professor Oxford who is applying for government funding for the research.

"The second phase will be seeing if we can break the chain of transmission with things like hand-washing or wearing a hygiene mask."

The problem is the common cold is not thought to be serious enough to investigate properly

Dr Douglas Fleming
Royal College of General Practitioners

He hopes the experiment, being done with Professor Jonathan Van Tam from Nottingham University, will get underway next year.

It is certainly true that "coughs and sneezes spread diseases".

And it would also seem to make sense to stay away from work or school to avoid sharing the bugs around.

Knowledge gaps

But there are a fair few gaps in our knowledge when it comes to the common cold, says Dr Douglas Fleming, director of the Royal College of GPs Research Unit in Birmingham.

COLDS AND FLU

Colds and flu are both common respiratory illnesses caused by viruses

Whereas there are hundreds of different types of cold viruses, flu is caused by the influenza virus of which there are three major types, A, B and C

The influenza virus constantly changes its structure which is why a new vaccine has to be developed every year

A cold lasts only two to four days and causes a stuffy or runny nose, sneezing, sore throat, cough, mild fever and tiredness

Flu is more severe, can last a week or more and is associated with a high fever, chills, headache, intense muscle pains, exhaustion, loss of appetite, cough and sometimes a blocked nose and sore throat

"The problem is the common cold is not thought to be serious enough to investigate properly," he said.

"Nearly everyone gets better so there isn't the attention given to it, but I think we should be trying to get to know much more about common respiratory infections."

For example, he said people might complain that colds seem to last longer than they used to but is that a sign of age or a sign of the changing nature of the cold virus.

"We don't have the facts - I can say I've never had a cough like that before but is it because you shake things off better in your youth.

"Whether people are having colds that last longer than they did years ago we simply don't know."

Surveillance

He said much of the lack of understanding around colds could be solved by more investment in surveillance.

It's not even entirely clear why we get more colds in winter.

If you have got really horrible flu, the only thing to do is stay away from people -

Professor Steve Field
Royal College of General Practitioners

Over, the past decade there has been much research into the structure of the cold virus with rhinovirus - one of the most common cold viruses - being the most understood.

This includes how it attaches to the lining of the nose to cause infection.

However, even with this information it is unlikely there will ever be a "cure" for the common cold for several reasons.

A cold is caused by many different viruses, by the time you know you have a cold it is probably too late to treat it, and as colds are fairly minor and self-limiting any side effects from medication, however minor, would probably not be worth the hassle.

Also there would be dangers of viruses becoming resistant to effective medications, rendering them useless, just as we are seeing with antibiotics.

So what do we know about colds?

Well according to the Common Cold Centre at Cardiff University, it has been estimated that adults suffer two to five colds per year, and school children may suffer seven to 10 colds per year.

Children to blame

Young children are mainly responsible for spreading common cold viruses and infection usually occurs at home or in the nursery or school.

The incubation period for a common cold is usually around two days before the symptoms begin and a person is most infectious when they are in the early stages of sneezing, runny nose and cough.

Professor Steve Field, chair of the Royal College of GPs said there is certainly a lot of cold and flu circulating this Christmas and it's hard to avoid catching one.

"We really need to try and encourage children and adults to use handkerchiefs and afterwards wash their hands, so if you're shaking people's hands and if you're in close contact you prevent passing it on.

"But if you have got really horrible flu, the only thing to do is stay away from people," he said.

noreply@blogger.com (Sridevi. V, M.A) — Mon, 15 Dec 2008 01:32:00 +0000

Life with a 12-year-old alcoholic

Doctors are seeing younger people with alcohol-related conditions

Jane (not her real name) was faced with the shock discovery that her young son was drinking heavily when somebody knocked on her door to tell her he had collapsed in the street.

At the age of 12, Alan, (not his real name) had drunk himself unconscious and was being revived by paramedics after attending a friend's birthday party.

He had drunk a bottle of vodka, along with half a bottle of Martini.

But he had already been consuming huge amounts of alcohol for a year before that watershed incident brought his problem to the attention of his shocked parents.

"I work full-time and I would send him to a child minders," said the distraught mother from Bournemouth.

"Unbeknown to me, Alan had stopped going after school and had started hanging around with much older children - the wrong crowd basically."

Further signs that all was not well with him began surfacing in primary school and continued into his secondary schooling, where he was constantly "getting into trouble".

I think a lot of it was probably my fault, I did not keep a closer eye on him

Jane

However, his parents bore the full brunt of the side effects symptomatic of excessive drinking.

"He has quite violent rages when he is drunk," added Jane.

"He would head-butt the wall or punch the door - every single door in our house had to be replaced."

Over the years, Alan has also destroyed most of the family furniture.

Neither he nor Jane have been able cope with his drinking, which spiralled out of control - both have been prescribed anti-depressants.

Alan was eventually diagnosed as an alcoholic at 15, by which time he was consuming about 10 to 15 cans of lager a day.

It was then doctors warned him if he continued along this destructive path he would be dead at 25.

However, Alan, now 20, did try two years ago to start afresh by completing an apprenticeship to become a painter and decorator.

But he crashed his car while drunk and lost his job as a result.

He is now on police bail awaiting trial for alcohol-related violence, according to Jane.

"I think a lot of it was probably my fault, I did not keep a closer eye on him," she said.

Anti-social behaviour

Research shows Alan's story is not only far from unique but one that is familiar to a growing number of families across Britain.

Portsmouth is one city which has obtained government funding to combat under-age drinking.

The Paulsgrove area has the highest percentage of 11-16 year olds in the city, and is currently the area with the highest rate of under-age drinkers according to Hampshire police.

A new "Weekend Project", funded with £24,000 from the Home Office, is aimed at educating young people and their parents about the dangers of under-age drinking and offering support.

Figures showed children aged 11 to 13 are drinking more alcohol

Police figures showed 659 alcohol-related anti-social behaviour offences were recorded in Paulsgrove from 1 March to 31 August this year.

In particular, Cheltenham Road and Allaway Avenue featured on the force's top 10 worst streets for anti-social behaviour offences and collectively accounted for more than 20% of this type of offence in the city, a police spokeswoman said.

Insp Eddie Charlton, of Hampshire police, said: "The alcohol tends to give them a bit more bravado and makes them do more stupid things - criminal damage, being abusive to residents and generally making their neighbours and their community's lives much more miserable."

Last year, Alcohol Concern called for parents who give alcohol to children aged under 15 to be prosecuted in its report on the government's Alcohol Harm Reduction Strategy.

The study's figures showed on average boys aged 11 to 13 were drinking 50% more alcohol in 2006 than in 2000.

The alcohol consumption figure for girls almost doubled in the same period.

Dr Nick Sheron, a liver specialist at Southampton University Hospitals Trust, believes the "easy accessibility of cheap alcohol" is one of the major factors fuelling under-age drinking.

"The government should increase tax on alcohol in line with income gradually in order to redress the balance," he said.

"There has been a tenfold increase in liver deaths since the 1970s.

"I think we have got the balance wrong and it's the young people who are paying the price for that."

noreply@blogger.com (Sridevi. V, M.A) — Mon, 15 Dec 2008 01:28:00 +0000

Amish gene 'limits heart disease'

The Amish population is best known for avoiding modern technology

A gene mutation which protects the heart against a high-fat diet has been found in the Amish population.

Researchers found 5% of the US Amish population in Lancaster, Pennsylvania have a mutation in a protein which breaks down fatty particles.

Those with the mutation had higher levels of "good" HDL-cholesterol and lower levels of "bad" LDL-cholesterol, the journal Science reported.

It is hoped the finding will lead to new therapies to reduce cholesterol.

The researchers used blood samples from 800 volunteers in the Old Order Amish community to look for DNA markers that might be associated with levels of fat particles called triglycerides in the blood stream.

The discovery of this mutation may eventually help us to develop new therapies to lower triglycerides and prevent cardiovascular disease

Dr Toni Pollin

High blood levels of triglycerides, one of the most common types of fat in food, have been linked to heart disease.

They found a mutation in the APOC3 gene, which encodes a protein - apoC-III - that inhibits the breakdown of triglycerides.

As part of the study, participants drank a high-fat milkshake and were monitored for the next six hours.

Individuals with the mutation produced half the normal amount of apoC-III and had the lowest blood triglyceride levels - seemingly because they could break down more fat.

They also had relatively low levels of artery-hardening - a sign of cardiovascular disease.

Protection

Study leader Dr Toni Pollin, assistant professor of medicine at the University of Maryland School of Medicine, said: "Our findings suggest that having a lifelong deficiency of apoC-III helps to protect people from developing cardiovascular disease.

"The discovery of this mutation may eventually help us to develop new therapies to lower triglycerides and prevent cardiovascular disease," she added.

The researchers believe the mutation was first introduced into the Amish community in Lancaster County by a person who was born in the mid-1700s.

It appears to be rare or absent in the general population.

Cathy Ross, cardiac nurse at the British Heart Foundation said the benefits of high HDL cholesterol and low LDL cholesterol are already being achieved by drugs such as statins.

"If new drugs can be developed that mimic the effect of this mutation, it may afford more ways in which individuals could be protected from developing cardiovascular disease.

"There are also lots of other simple ways people can reduce your risk of cardiovascular disease such as eating a diet low in saturated fat, having five portions of fruit and vegetables a day and taking regular physical activity."

noreply@blogger.com (Sridevi. V, M.A) — Mon, 15 Dec 2008 01:26:00 +0000

Test 'predicts preterm baby risk'

Around 2% of pregnant women have premature rupture of membranes

Researchers have identified a test which can predict whether a woman is likely to give birth if her waters break early in pregnancy.

High levels of lactate in vaginal fluid is strongly associated with onset of labour within 48 hours, according to Swedish researchers.

UK experts said the test would help to plan care and reassure women whose membranes rupture prematurely.

The study appears in Obstetrics and Gynaecology journal, BJOG.

Known as the "Lac-test", the tool was assessed in 86 women with singleton pregnancies of 20 to 36 weeks gestation.

When membranes rupture unexpectedly there's a big dilemma - do you deliver the baby or not, will this woman go into labour or not?

Professor Andrew Shennan

Among 23 women with high lactate concentrations, 87% had spontaneous onset of labour within 48 hours.

In 58 women with low lactate concentrations - in effect a negative Lac-test - only 5% went into labour within 48 hours.

The median time between examination and onset of labour was 13.6 hours for those with a high lactate concentration and 48 days for those with a low lactate value.

Prediction

The researchers said previous studies had found an association between high lactate concentration in vaginal fluids and rupture of membranes in pregnancies of more than 34 weeks gestation, but this is the first time the link has been seen under 34 weeks.

Being able to predict labour is even more valuable in these premature babies, as steroids can be given to promote lung development and women can be referred to specialist hospitals.

Preterm prelabour rupture of membranes (PPROM) - waters breaking in pregnant women before 37 weeks - occurs in 2% of pregnancies and accounts for one-third of all preterm births.

Study leader, Dr Eva Wiberg-Itzel, from the Department of Clinical Science and Education at the Karolinska Institute, said: "The diagnosis of ruptured membranes is easy when there is an obvious leakage of amniotic fluid, but more difficult when the leak is scanty or intermittent.

"We believe that the Lac-test adds important information in clinical practice."

Professor Philip Steer, editor-in-chief of BJOG, said it seemed a promising tool to predict the onset of labour.

"A more reliable diagnosis of PPROM could help doctors determine when to keep women in hospital, and improve the timing of antenatal steroid therapy."

Professor Andrew Shennan, an obstetrician at St Thomas' Hospital in London, said the test could solve a potentially important problem.

"When membranes rupture unexpectedly there's a big dilemma - do you deliver the baby or not, will this woman go into labour or not?

"We would probably give steroids anyway as it's a high risk situation, but the main thing is being able to tell the women what's likely to happen.

"We can also get them to a specialist unit if needed."

noreply@blogger.com (Sridevi. V, M.A) — Mon, 15 Dec 2008 01:24:00 +0000

Preterm baby 'lung growth hope'

Lung development can be a problem for premature babies

British researchers have identified a potential target for encouraging lung growth in babies in the womb.

A study in mice showed that a well-known molecule called the calcium receptor has a key role in the development of lungs in the foetus.

Drugs targeting the receptor are already available, the Cardiff University researchers said.

The results, which could lead to better outcomes for premature babies, are published in the Journal of Physiology.

If we can show that one of these drugs can modulate the action of the calcium receptor in the lung, it could be used to mature the lungs of a very premature baby as it grows

Professor Paul Kemp, University of Cardiff

The final stages of lung development happen late in pregnancy so babies born prematurely can struggle to get enough oxygen and can develop chronic lung disease.

The latest research found that the calcium receptor "switches on" the growth of the lungs in the foetus.

In the study, the researchers were able to manipulate lung development by interrupting receptor function.

The next step is to carry out studies in individuals who have mutations in the calcium receptor which causes it to be permanently switched on or switched off, the researchers said.

"If that showed correlation between the mutation and post-natal lung health then we could move into clinical trials," said study author Professor Paul Kemp.

"The really exciting thing about the calcium receptor is that there are already drugs available that can alter its function.

"If we can show that one of these drugs can modulate the action of the calcium receptor in the lung, it could be used to mature the lungs of a very premature baby as it grows.

"An existing drug could potentially be approved much more quickly than a new one" he added.

He said the therapy could be something that is done in parallel with steroid treatment which is already given in babies at risk of being born early.

Annette Briley, research midwife for Tommy's, the baby charity said chronic lung disease is one of the major health problems facing premature babies, often presenting problems well into adulthood.

"Whilst this could be a promising breakthrough, it must be stressed that further rigorous randomised control tests must be carried out to assess the effectiveness of these drugs in premature babies."

noreply@blogger.com (Sridevi. V, M.A) — Fri, 05 Dec 2008 01:17:00 +0000

Warning over internet painkillers

Celecoxib was one of the drugs found to be available online

UK experts have warned of the dangers of purchasing drugs online in response to a study showing wide availability of strong painkillers over the internet.

A team at Edinburgh University found 35 websites selling prescription-only pain drugs to UK customers without requiring a prescription.

Government regulators warned that buying medicines online may have "deadly" consequences.

The results appear in the British Journal of Clinical Pharmacology.

By trawling for online pharmacy sites through Google and Yahoo search engines, the researchers found almost 100 selling medicines to UK consumers.

Almost half of those sold prescription-only painkillers but 76% did not require the customer to provide a valid prescription.

Six asked for a prescription but accepted a fax or email copy which the researchers said could be forged or modified.

Side-effects

The drugs available included opioids such as tramadol and non-steroidal anti-inflammatories, such as naproxen and celecoxib, commonly prescribed for conditions such as arthritis.

They can have severe side-effects and some should not be taken in conjunction with other medicines or in people with certain conditions, the researchers said.

At best you will be wasting your money and at worst they could be deadly

Spokeswoman, MHRA

Co-proxamol - a drug which has been removed from the market in the UK due to concerns over the risk of overdose - was available from three websites.

The researchers did not take the final step of actually buying the medicines as they felt it would not be ethical.

Study author Professor David Webb, an expert in clinical pharmacology at the University of Edinburgh, said these were drugs that people should not be taking without advice from a doctor, but they were available with a couple of clicks of the mouse.

"We were surprised at how many sites you could go to and find, in some cases, quite potent painkillers that have addictive potential and that you could get them without prescription."

He added: "The regulators are very aware of this problem and it is not one they can easily manage.

"But there certainly needs to be some sort of international agreement."

Illegal sales

A spokeswoman for the Medicines and Healthcare Products Regulatory Agency, said although the sale of prescription only medicines without a proper patient consultation was illegal it was not illegal to buy medicines online.

"But we strongly advise people that buying drugs or slimming products from the internet is not a good idea, unless buying from a website that has a Royal Pharmaceutical Society of Great Britain (RPSGB) internet pharmacy logo.

"At best you will be wasting your money and at worst they could be deadly.

"You don't know what these products contain and you don't know in what conditions they have been made."

The RPSGB launched their logo scheme for bone fide pharmacy websites at the beginning of 2008.

Priya Sejpal, RPSGB head of professional ethics, said: "Internet pharmacy undoubtedly offers patients easy access and choice, but it also brings increased risk.

"There are a growing number of unregulated suppliers operating online with no professional qualifications or healthcare expertise.

"In many cases, medicines purchased from such suppliers are counterfeit, substandard or unapproved new drugs."

noreply@blogger.com (Sridevi. V, M.A) — Wed, 03 Dec 2008 01:17:00 +0000

NHS pays to rectify cosmetic ops

Thousands of patients head abroad for cosmetic operations

The NHS is having to pick up the tab for cosmetic surgery performed abroad that has gone wrong, doctors say.

The British Association of Plastic, Reconstructive and Aesthetic Surgeons said many patients were turning to the health service for follow-up care.

A poll of 203 NHS surgeons found that more than a third knew of cases where complications followed surgery abroad.

The government warned people that the NHS was only there to deal with emergency complications in such cases.

And it urged those thinking about going abroad for operations to be careful.

It is estimated that up to 100,000 people a year are heading abroad for cheap cosmetic surgery such as breast enlargements, tummy tucks and face-lifts.

What may seem like a bargain could cost them their health

Vivienne Nathanson, of the British Medical Association

BAPRAS said the growing demand was being fuelled by the availability of cheap flights, but warned that the trend was leading to problems.

It said its members had seen a range of complications including blood poisoning, wound infections and blood clots, as well as patients who were not happy with the results of the surgery.

And the association warned that the extra work being caused by having to see these patients could end up delaying other NHS work.

It said patients should be made to pay for rectifying treatment except where there was a life life-threatening situation or if the patient was suffering from acute pain.

Complications following UK-based cosmetic surgery is the responsibility of the private clinic.

Anthony Armstrong, a leading member of BAPRAS, said: "Cosmetic operations involve major surgery.

"Anyone considering cosmetic surgery abroad must make sure they are fully aware of the potential complications that can occur and consider how these will be dealt with.

"They should not assume that the NHS will pick up the pieces and they may find themselves having to pay privately for follow-up surgery here."

Risks

But the British Medical Association said it was against patients being barred from NHS care.

Dr Vivienne Nathanson, head of ethics at the BMA, added: "It is essential that patients are warned about the potential risks of any surgery, and the specific risks of managing complications after having surgery overseas.

"What may seem like a bargain could cost them their health."

Katherine Murphy, of the Patients Association, agreed it would be wrong to withhold treatment.

She said patients needed better information about treatment available abroad.

A spokesman for the Department of Health said it had already made clear that the NHS was only there to deal with emergencies in such cases.

The spokesman added: "People are free to have cosmetic or other private surgery abroad if they wish to.

"However, we strongly advise people to do their research and make sure that they are clear about prices, procedures, recovery times, aftercare and what happens in the event that the treatment goes wrong."

noreply@blogger.com (Sridevi. V, M.A) — Tue, 18 Nov 2008 14:18:00 +0000

Hypertension

Hypertension, also referred to as high blood pressure, HTN or HPN, is a medical condition in which the blood pressure is chronically elevated. In current usage, the word "hypertension"^[ without a qualifier normally refers to arterial hypertension.

Hypertension can be classified either essential (primary) or secondary. Essential hypertension indicates that no specific medical cause can be found to explain a patient's condition. Secondary hypertension indicates that the high blood pressure is a result of (i.e., secondary to) another condition, such as kidney disease or tumours (pheochromocytoma and paraganglioma).

In individuals older than 50 years, hypertension is considered to be present when a person's systolic blood pressure is consistently 140 mm Hg or greater. Beginning at a systolic pressure of 115 and diastolic pressure of 75 (commonly written as 115/75 mm Hg), cardiovascular disease Prehypertension is defined as blood pressure from 120/80 mm Hg to 139/89 mm Hg. Prehypertension is not a disease category; rather, it is a designation chosen to identify individuals at high risk of developing hypertension.Mayo Clinic specifies blood pressure is "normal if it's below 120/80". Patients with blood pressures over 130/80 mm Hg along with Type 1 or Type 2 diabetes, or kidney disease require further treatment. (CVD) risk doubles for each increment of 20/10 mmHg. The

Distinguishing primary vs. secondary hypertension

Once the diagnosis of hypertension has been made it is important to attempt to exclude or identify reversible (secondary) causes.

Over 91% of adult hypertension has no clear cause and is therefore called essential/primary hypertension. Often, it is part of the metabolic "syndrome X" in patients with insulin resistance: it occurs in combination with diabetes mellitus (type 2), combined hyperlipidemia and central obesity.
Secondary hypertension is more common in preadolescent children, with most cases caused by renal disease. Primary or essential hypertension is more common in adolescents and has multiple risk factors, including obesity and a family history of hypertension.

Investigations commonly performed in newly diagnosed hypertension

Tests are undertaken to identify possible causes of secondary hypertension, and seek evidence for end-organ damage to the heart itself or the eyes (retina) and kidneys. Diabetes and raised cholesterol levels being additional risk factors for the development of cardiovascular disease are also tested for as they will also require management.

Blood tests commonly performed :

Creatinine (renal function) - to identify both underlying renal disease as a cause of hypertension and conversely hypertension causing onset of kidney damage. Also a baseline for later monitoring the possible side-effects of certain antihypertensive drugs.
Electrolytes (sodium, potassium)
Glucose - to identify diabetes mellitus
Cholesterol

Additional tests often include:

Testing of urine samples for proteinuria - again to pick up underlying kidney disease or evidence of hypertensive renal damage.
Electrocardiogram (EKG/ECG) - for evidence of the heart being under strain from working against a high blood pressure. Also may show resulting thickening of the heart muscle (left ventricular hypertrophy) or of the occurrence of previous silent cardiac disease (either subtle electrical conduction disruption or even a myocardial infarction).
Chest X-ray - again for signs of cardiac enlargement or evidence of cardiac failure.

Prevention

Drug-free Treatment of Hypertension

Lifestyle modification (nonpharmacologic treatment)

Weight reduction and regular aerobic exercise (e.g., jogging) are recommended as the first steps in treating mild to moderate hypertension. Regular mild exercise improves blood flow and helps to reduce resting heart rate and blood pressure. These steps are highly effective in reducing blood pressure, although drug therapy is still necessary for many patients with moderate or severe hypertension to bring their blood pressure down to a safe level.
Reducing dietary sugar intake
Reducing sodium (salt) in the diet may be effective: it decreases blood pressure in about 33 percent of people (see above). Many people choose to use a salt substitute to reduce their salt intake.
Additional dietary changes beneficial to reducing blood pressure includes the DASH dietdietary approaches to stop hypertension), which is rich in fruits and vegetables and low fat or fat-free dairy foods. This diet is shown effective based on research sponsored by the US National Institutes of Health. In addition, an increase in daily calcium intake has the benefit of increasing dietary potassium, which theoretically can offset the effect of sodium and act on the kidney to decrease blood pressure. This has also been shown to be highly effective in reducing blood pressure. (
Discontinuing tobacco use and alcohol consumption has been shown to lower blood pressure. The exact mechanisms are not fully understood, but blood pressure (especially systolic) always transiently increases following alcohol and/or nicotine consumption. Besides, abstention from cigarette smoking is important for people with hypertension because it reduces the risk of many dangerous outcomes of hypertension, such as stroke and heart attack. Note that coffee drinking (caffeine ingestion) also increases blood pressure transiently, but does not produce chronic hypertension.
Reducing stress, for example with relaxation therapy, such as meditation and other mindbody relaxation techniques, by reducing environmental stress such as high sound levels and over-illumination can be an additional method of ameliorating hypertension. Jacobson's Progressive Muscle Relaxation and biofeedback are also used, particularly, device-guided paced breathing, although meta-analysis suggests it is not effective unless combined with other relaxation techniques.

The aim of treatment should be blood pressure control to <140/90 style="text-decoration: underline;"> Each added drug may reduce the systolic blood pressure by 5-10 mmHg, so often multiple drugs are necessary to achieve blood pressure control.

Commonly used drugs :

ACE inhibitors such as creatine captopril, enalapril, fosinopril (Monopril), lisinopril quinapril, ramipril (Altace) (Zestril),
Angiotensin II receptor antagonists: eg, telmisartan (Micardis, Pritor), irbesartan losartan (Cozaar), valsartan (Diovan), candesartan (Amias) (Avapro),
Alpha blockers such as prazosin, or terazosin. Doxazosin has been shown to increase risk of heart failure, and to be less effective than a simple diuretic^[29], so is not recommended.
Beta blockers such as atenolol, labetalol, metoprolol (Lopressor, Toprol-XL), propranolol.
Calcium channel blockers such as nifedipine (Adalat)^[30] amlodipine (Norvasc), diltiazem, verapamil
Direct renin inhibitors such as aliskiren (Tekturna)
Diuretics: eg, bendroflumethiazide, chlortalidone, hydrochlorothiazide (also called HCTZ)
Combination products (which usually contain HCTZ and one other drug)

Complications

While elevated blood pressure alone is not an illness, it often requires treatment due to its short- and long-term effects on many organs. The risk is increased for:

Cerebrovascular accident (CVAs or strokes)
Myocardial infarction (heart attack)
Hypertensive cardiomyopathy (heart failure due to chronically high blood pressure)
Hypertensive retinopathy - damage to the retina
Hypertensive nephropathy - chronic renal failure due to chronically high blood pressure
Hypertensive encephalopathy - confusion, headache , convulsion due to vasogenic edema in brain due to high blood pressure.

noreply@blogger.com (Sridevi. V, M.A) — Tue, 18 Nov 2008 13:55:00 +0000

Drug-resistant ward bug concern

Acinetobacter does not usually pose a threat to healthy people

Hospitals need to be vigilant against an emerging drug-resistant bacterium Acinetobacter baumannii, infection control experts have warned.

Like MRSA and Clostridium difficile, the bacterium poses the greatest risk to seriously ill patients.

Rates of resistance to antibiotics that halt the bug currently stand at 30%, Lancet Infectious Diseases reports.

The journal report authors said the infection was a growing public health worry across the world.

Measures in the UK to control MRSA and other "hospital-acquired infections" should also bring down Acinetobacter rates, experts said.

It is important that Trusts remain vigilant in their treatment of this and all healthcare associated infections

A spokeswoman for the Health Protection Agency

Acinetobacter shares many of the "superbug" properties of MRSA and Clostridium difficile, such as survival on surfaces and resistance to disinfectants. This makes it difficult to eradicate from wards once it is there, experts say.

Typically, the bacterium causes bloodstream infections, pneumonia or infection of a wound.

It can be carried on the skin of healthy people and can be passed to patients by poor hand hygiene.

It also survives in dust and on objects such as bedding for months, making rigorous cleaning of wards essential to control its spread.

The strains of Acinetobacter that are resistant to standard treatments can be treated with other antibiotics, however, and the bug does not usually pose a threat to healthy people.

Vigilance

Strict hygiene compliance and more thorough research into drug choice, especially those for multidrug-resistant Acinetobacter baumannii, are vital to prevent major outbreaks, say the report authors Professor Matthew Falagas and Dr Drosos Karageorgopoulos, of the Alfa Institute of Biomedical Sciences in Athens, Greece.

In the UK, the numbers of Acinetobacter bloodstream infections reported to the Health Protection Agency via its voluntary surveillance scheme increased by 5.4% between 2003 and 2007 to 1,187 reports.

We mustn't be complacent but currently its impact can be geographically constrained

Dr Andrew Berrington, a consultant microbiologist at Sunderland Royal Hospital

But the HPA says this increase could be due to increased awareness and reporting rather than a true rise in infection rates.

A spokeswoman for the Health Protection Agency said: "Acinetobacter can cause problems in those who are already seriously ill with weakened immune systems.

"Although we do see some outbreaks of this infection in the UK, numbers of cases are fortunately small.

"Transmission of this infection can be reduced by careful attention to infection control procedures such as cohort nursing groups, hand hygiene and environmental cleaning. It is important that trusts remain vigilant in their treatment of this and all healthcare associated infections."

She said the HPA had no plans to make the reporting of cases mandatory, largely because it is not deemed to be as great a threat as the notifiable hospital-acquired infections such as MRSA and C.difficile.

Professor Richard James, director of the Centre for Healthcare Associated Infections at Nottingham University, said: "If we could overnight solve the problems of hospital infections caused by C.difficile and MRSA then there are other potential superbugs like Acinetobacter baumannii lying in wait.

"Hospitals are full of sick patients and very fit bacteria that will spread from patient to patient unless infection control measures are up to the challenge.

"Acinetobacter baumannii, multidrug resistant tuberculosis (MDR-TB) and extremely drug resistant tuberculosis (XDR-TB) are examples of new threats to public health that are already causing serious problems in other countries."

Dr Andrew Berrington, a consultant microbiologist at Sunderland Royal Hospital, said there was little evidence to suggest outbreaks of Acinetobacter were becoming more common in the UK.

"We mustn't be complacent but currently its impact can be geographically constrained - some hospitals struggle to control outbreaks, others see very little of it."

noreply@blogger.com (Sridevi. V, M.A) — Mon, 17 Nov 2008 00:21:00 +0000

Tooth decay

Young people are particularly vulnerable

Tooth decay, known technically as dental caries, is one of the most common health complaints in the world.

It is particularly common in children and young adults, and rates have been fuelled by an increase in sugars in the diet, and poor dental hygiene.

What causes tooth decay?

The problem is caused by sticky deposits called plaque that collect, in particular, around the gum line, the edges of fillings and the grooved surfaces of the teeth.

Plaque is made up of food debris, saliva and the bacteria that are normally present in the mouth, and convert food into acids.

If plaque is allowed to collect over time it will harden into a substance called tartar.

Both tartar and plaque contain acids which, over time, can dissolve away the protective, hard enamel coating of the tooth, and create holes, or cavities.

Most cavities form over a period of months, or even years.

They are usually painless, but they can grow very large, and damage the much softer internal structures of the tooth such as the dentin and the pulp, which is found at the core.

If they remain untreated, they can kill the nerve and blood vessels of the tooth, and ultimately the tooth itself.

What are the symptoms?

The most obvious sign of tooth decay is toothache, particularly after hot or cold foods or drinks. However, pain may not be present until decay has reached an advanced stage.

Pits or holes may also be visible in the teeth.

Most tooth decay is discovered at an early stage during a routine check up.

A serious complication can be the development of a tooth abscess - the build up of pus resulting from a bacterial infection of the centre of the tooth.

Infection may spread out from the root of the tooth and to the bones supporting the tooth.

Plaque and tartar also irritate the gums, and lead to a gum disease called gingivitis.

Is diet a factor?

Yes. Eating a diet rich in sugar and starch increases the risk of tooth decay, and sticky foods can be a particular problem because they are more likely to remain on the surface of the teeth.

Frequent snacking also increases the amount of time that acids are in contact with the teeth.

In the absence of good oral hygiene, it doesn't take long for damage to begin. The acids generated by the breakdown of food stuff in the mouth can begin to attack the tooth enamel within 20 minutes of a meal.

It is thought that tooth decay only became a widespread problem with the establishment of sugar plantations in the 18th century, and worsened with the subsequent widespread cultivation of sugar beet in Europe .

How do you prevent decay?

The best way to keep your teeth in health condition is to ensure that you clean them regularly to get rid of any plaque build up.

Most dentists recommend that you clean your teeth at least twice a day. Using a toothpaste containing fluoride is probably a good idea as this provides the teeth with added protection from the effects of acid.

Flossing between the teeth is also a good idea, as is rinsing out your mouth after eating sticky foods.

It is also important to have a regular check up at the dentist - most suggest once every six months to a year.

Unfortunately, even good oral hygiene does not prevent decay as the bacteria congregate in areas inaccessible to brushes and floss.

How is decay treated?

Once the structure of a tooth has been damaged by decay, there is no way to repair it.

However, if decay is picked up at an early stage its progression can be blocked.

Decayed material can be removed, and replaced with a restorative material such as silver alloy, or plastic. This is known as a filling.

If the decay is more extensive, then another option is a crown. The decayed or weakened area is removed and repaired and a covering jacket - the crown - is fitted over the remainder of the tooth.

If the nerve in a tooth has died, either from decay or a blow, then a dentist will consider root canal work.

This involves removing the centre of the tooth, including the nerve and blood vessel tissue.

The root is then filled with a sealing material, and the process is completed with either filling, and possibly a crown।

Prevention

Oral hygiene

Personal hygiene care consists of proper brushing and flossing daily. The purpose of oral hygiene is to minimize any etiologic agents of disease in the mouth. The primary focus of brushing and flossing is to remove and prevent the formation of plaque. Plaque consists mostly of bacteria. As the amount of bacterial plaque increases, the tooth is more vulnerable to dental caries. A toothbrush can be used to remove plaque on most surfaces of the teeth except for areas between teeth. When used correctly, dental floss removes plaque from areas which could otherwise develop proximal caries. Other adjunct hygiene aids include interdental brushes, water picks, and mouthwashes.

Professional hygiene care consists of regular dental examinations and cleanings. Sometimes, complete plaque removal is difficult, and a dentist or dental hygienist may be needed. Along with oral hygiene, radiographs may be taken at dental visits to detect possible dental caries development in high risk areas of the mouth.

Dietary modification

For dental health, the frequency of sugar intake is more important than the amount of sugar consumed. In the presence of sugar and other carbohydrates, bacteria in the mouth produce acids which can demineralize enamel, dentin, and cementum. The more frequently teeth are exposed to this environment, the more likely dental caries are to occur. Therefore, minimizing snacking is recommended, since snacking creates a continual supply of nutrition for acid-creating bacteria in the mouth. Also, chewy and sticky foods (such as dried fruit or candy) tend to adhere to teeth longer, and consequently are best eaten as part of a meal. Brushing the teeth after meals is recommended. For children, the American Dental Association and the European Academy of Paediatric Dentistry recommend limiting the frequency of consumption of drinks with sugar, and not giving baby bottles to infants during sleep. Mothers are also recommended to avoid sharing utensils and cups with their infants to prevent transferring bacteria from the mother's mouth.

It has been found that milk and certain kinds of cheese like cheddar can help counter tooth decay if eaten soon after the consumption of foods potentially harmful to teeth., chewing gum containing xylitol (wood sugar) is widely used to protect teeth in some countries, being especially popular in the Finnish candy industry. Xylitol's effect on reducing plaque is probably due to bacteria's inability to utilize it like other sugars. Chewing and stimulation of flavour receptors on the tongue are also known to increase the production and release of saliva, which contains natural buffers to prevent the lowering of pH in the mouth to the point where enamel may become demineralised।

Common dentistry trays used to deliver fluoride.

Other preventive measures

The use of dental sealants is a means of prevention. A sealant is a thin plastic-like coating applied to the chewing surfaces of the molars. This coating prevents the accumulation of plaque in the deep grooves and thus prevents the formation of pit and fissure caries, the most common form of dental caries. Sealants are usually applied on the teeth of children, shortly after the molars erupt. Older people may also benefit from the use of tooth sealants, but their dental history and likelihood of caries formation are usually taken into consideration.

Fluoride therapy is often recommended to protect against dental caries. It has been demonstrated that water fluoridation and fluoride supplements decrease the incidence of dental caries. Fluoride helps prevent decay of a tooth by binding to the hydroxyapatite crystals in enamel. The incorporated fluoride makes enamel more resistant to demineralization and, thus, resistant to decay. Topical fluoride is also recommended to protect the surface of the teeth. This may include a fluoride toothpaste or mouthwash. Many dentists include application of topical fluoride solutions as part of routine visits.

Furthermore, recent research shows that low intensity laser radiation of argon ion lasers may prevent the susceptibility for enamel caries and white spot lesions. Also, as bacteria are a major factor contributing to poor oral health, there is currently research to find a vaccine for dental caries. As of 2004, such a vaccine has been successfully tested on animals, and is in clinical trials for humans as of May 2006.

noreply@blogger.com (Sridevi. V, M.A) — Sun, 16 Nov 2008 03:42:00 +0000

Common Cold

What is the common cold, and what causes it?

The common cold, also known as a viral upper respiratory tract infection, is a self-limited contagious illness that can be caused by a number of different types of viruses. More than 200 different types of viruses are known to cause the common cold. Because so many different viruses can cause a cold and because new cold viruses constantly develop, the body never builds up resistance against all of them. For this reason, colds are a frequent and recurring problem. In fact, children in preschool and elementary school can have three to 12 colds per year while adolescents and adults typically have two to four colds per year. The common cold is the most frequently occurring illness in the world, and it is a leading cause of doctor visits and missed days from school and work.

What are the symptoms of the common cold?

Symptoms of the common cold include nasal stuffiness or drainage, sore or scratchy throat, sneezing, hoarseness, cough, and perhaps a fever and headache. Many people with a cold feel tired and achy. These symptoms will typically last anywhere from three to 10 days.

How is the common cold spread?

The common cold is usually spread by direct hand-to-hand contact with infected secretions or from contaminated surfaces. For example, if a person with a cold blows or touches their nose and then touches someone else, that person can subsequently become infected with the virus. Additionally, a cold virus can live on objects such as pens, books, telephones, computer keyboards, and coffee cups for several hours and can thus be acquired from contact with these objects.

Does it have anything to do with exposure to cold weather?

Though the common cold usually occurs in the fall and winter months, the cold weather itself does not cause the common cold। Rather, it is thought that during cold-weather months people spend more time indoors in close proximity to each other, thus facilitating the spread of the virus. For this same reason, children in day care and school are particularly prone to acquiring the common cold.

What is the difference between the common cold and influenza (the flu)?

Many people confuse the common cold with influenza (the flu). Influenza is caused by the influenza virus, while the common cold generally is not. While some of the symptoms of the common cold and influenza may be similar, patients with the common cold typically have a milder illness. Patients with influenza are usually sicker and have a more abrupt onset of illness with fever, chills, headache, body aches, dry cough, and extreme weakness.

Though differentiating between the common cold and influenza can be difficult, there is laboratory testing available to confirm the diagnoses of influenza.

What is the treatment for the common cold?

There is no cure for the common cold. Home treatment is directed at alleviating the symptoms associated with the common cold and allowing this self-limiting illness to run its course.

Supportive measures for the common cold include rest and drinking plenty of fluids. Over-the-counter medications such as throat lozenges, throat sprays, cough drops, and cough syrups may also help bring relief. Decongestants such as pseudoephedrine (Sudafed) or antihistamines may be used for nasal symptoms. Saline sprays and a humidifier may also be beneficial.

Acetaminophen (Tylenol and others) and ibuprofen (Advil and others) can help with fever, sore throat, and body aches.

WARNING: The United States Food and Drug Administration (FDA) recommends that over-the-counter cough and cold medications not be used in children younger than 2 years of age because serious and potentially life-threatening side effects can occur.

Do not use aspirin or aspirin containing medications in children or teenagers because it has been associated with a rare potentially fatal condition called Reye's syndrome।

Are antibiotics a suitable treatment for the common cold?

No. Antibiotics play no role in treating the common cold. Antibiotics are effective only against illnesses caused by bacteria, and colds are caused by viruses. Not only do antibiotics not help, but they can also cause allergic reactions that can be fatal (1:40,000). Furthermore, using antibiotics when they are not necessary has led to the growth of several strains of common bacteria that have become resistant to certain antibiotics (including one that commonly causes ear infections in children). For these and other reasons, it is important to limit the use of antibiotics to situations in which they are medically indicated.

Though occasionally a bacterial infection, such as sinusitis or a middle ear infection, can develop following a cold, treatment with antibiotics should be left at the discretion of your physician or health-care practitioner.

When should a doctor or other health-care practitioner be consulted?

Generally speaking, the common cold can be treated at home and managed with over-the-counter medications. However, if you develop more severe symptoms such as shaking chills, high fever (greater than 102 F), severe headache or neck stiffness, nausea, vomiting, difficulty breathing or chest pain, you should consult your physician or health-care practitioner immediately.

If you have a sore throat and a fever with no other cold symptoms, you should also be seen by your physician. This illness may be strep throat, a bacterial infection requiring treatment with antibiotics.

Finally, if you notice facial pain or yellow/green drainage from your nose accompanied by a fever, it is possible that you have a sinus infection (sinusitis) that would benefit from a medical evaluation and a possible course of antibiotics।

How do you prevent the common cold?

The most important measure to prevent the common cold is frequent hand washing, as this can destroy viruses that you have acquired from touching contaminated surfaces. Also, try to avoid sharing utensils and try to use disposable items (such as disposable cups) if someone in your family has a cold. Finally, lifestyle modifications such as smoking cessation and stress management may decrease your susceptibility to acquiring the common cold.

Health Tip: Caught a Cold?

You shouldn't treat a cold -- always caused by a virus -- with antibiotics, since these medicines are meant to treat bacterial infections. But there are things you can do to feel better while the cold runs its course.

The University of Virginia Health System offers these suggestions:

Try over-the-counter medications, such as an antihistamine, decongestant or cough medicine.
Get plenty of sleep.
Increase the amount of fluids you drink.
Take a pain reliever to control headache and fever.
Soothe a sore throat by gargling with warm salt water.
Apply petroleum jelly to sore, dry skin around the nose and lips.
Use a warm steam to ease congestion।

noreply@blogger.com (Sridevi. V, M.A) — Sun, 16 Nov 2008 03:21:00 +0000

Back pain

Back pain is a common problem

Back pain is one of the most common ailments in the UK.

It is thought more than 17 million Britons suffer from the problem, and the Health and Safety Executive estimates that it is responsible for nearly 5 million lost working days a year.

How is the back made up?

The major feature is the spine. This is a highly complex and delicate structure which is made up of 33 small bones called vertebrae.

In between each vertebra is a disc which acts as a shock absorber, and stops the bones rubbing together.

The discs are made up of a jelly like substance, which is protected by a tough, fibrous outer casing.

The spine is supported by specialised back muscles, and an array of ligaments, nerves and tendons.

What causes back pain?

As the spine is such a complex structure, it can often be difficult to pin down the exact cause of back pain.

Probably the most common cause is when the back muscles begin to spasm.

This can often occur after strenuous activity, or can be a reaction to repetitive strain.

The muscle is damaged, or irritated, and goes into spasm to protect the area from further injury.

This can be extremely painful, and can lead to muscle tears if undue stress is exerted.

Other causes of back pain include arthritis, fractures and infections.

In many cases experts believe back pain is a manifestation of emotional upset, rather than a physical problem.

More serious causes can include a prolapsed disc, or degenerative diseases of the spine - but these are relatively rare.

Are certain parts of the back more vulnerable?

Yes. The lower - or lumbar - region of the back is particularly prone to injury.

This because it bears the entire weight of the upper body, and is twisted and bent more than other parts.

As a result it inevitably suffers more wear and tear.

Why is back pain on the increase?

Experts believe that a major factor is the modern tendency to lead a sedentary lifestyle, both at work and home.

Spending long stretches of time sitting in one position - often with the back not properly supported - is not good for the spine.

The reliance on comfy soft furnishing may seem appealing - but often it encourages us to adopt a poor posture.

Back pain is much less common in places such as India, where many more people are used to sitting on the floor, which is thought to allow the back muscles to find their own natural position.

What is the treatment?

For most cases of back pain the only treatment is pain relief, often through the use of non-steroidal anti-inflammatory drugs such as aspirin.

Physiotherapy, heat therapy, massage and hydrotherapy can help.

How can you minimise the risk?

The spine is naturally curved into an S shape. The best way to keep it healthy is to try to maintain this shape as much as possible.

This is particularly important when performing tasks, such as lifting, that carry an increased risk of injury.

Strengthening the back muscles, keeping fit by taking regular exercise, and maintaining a healthy weight can all help to minimise the risk of back pain.

It is also important to have a mattress that properly supports the body while you are asleep.

If you do have a bad back probably the worst thing you can do is take to your bed.

Experts believe that it is best to stay as active as you possibly can.

Could there be another explanation for back pain?

Some lumbar and lower spinal pain is caused by patients having one leg longer than the other.

This puts the pelvis out of alignment causing pain, which without correction leads to long term compensatory problems such as back pain.

In this case it might be wise to consult a podiatrist who will measure the patient's limbs and if required provide either an orthoses - an orthopedic appliance used to support, align, prevent, or correct deformities - or arrange to modify the patients shoe to correct the difference.

noreply@blogger.com (Sridevi. V, M.A) — Sun, 16 Nov 2008 03:18:00 +0000

Amnesia

Amnesia can take many forms

Amnesia is a term used to cover the partial or complete loss of memory. It is most often a temporary condition and covers only a part of a person's experience, such as immediate memory. The causes of amnesia range from psychological trauma to brain damage caused by a blow to the head or conditions such as a brain tumour, a stroke or swelling of the brain. There are many definitions covering the different types of amnesia.

What is amnesia?

The main types of amnesia are:

Anterograde amnesia: People who find it hard to remember ongoing events after suffering damage to the head. They do not tend to forget their childhood or who they are, but have trouble remembering day-to-day events.

Retrograde amnesia:People who find it hard to retrieve memories prior to an incident in which they suffer damage to the head. Sometimes people never remember the seconds leading up to the incident.

Korsakoff's psychosis: Memory loss caused by alcohol abuse. The person's short-term memory may be normal, but they will have severe problems recalling a simple story, lists of unrelated words, faces and complex patterns.

This tends to be a progressive disorder and is usually accompanied by neurological problems, such as uncoordinated movements and loss of feeling in the fingers and toes. If these symptoms occur, it may be too late to stop drinking.

Traumatic amnesia: This follows brain damage caused by a severe non-penetrative blow to the head, such as in a road accident. It can lead to anything from a loss of consciousness for a few seconds to coma.

Infantile/childhood amnesia:This refers to a person's inability to recall events from early childhood. There are many theories on this, for example, Freud put it down to sexual repression. Others say it could be linked to language development or the fact that some areas of the brain linked to memory are not fully mature.

Hysterical amnesia (also known as fugue amnesia):This covers episodes of amnesia linked to psychological trauma. It is usually temporary and can be triggered by a traumatic event with which the mind finds it difficult to deal. Usually, the memory slowly or suddenly comes back a few days later, although memory of the trauma may remain incomplete.

Treatment varies according to the type of amnesia and the suspected cause.

Anyone suffering any symptoms of amnesia should seek medical attention.

noreply@blogger.com (Sridevi. V, M.A) — Sun, 16 Nov 2008 03:09:00 +0000

Peppermint Oil, Fiber Can Fight Irritable Bowel

For some patients, the best therapy for irritable bowel syndrome (IBS) may be older, cheaper drugs such as fiber, antispasmodics and peppermint oil, a new study finds.

According to researchers, these simple treatments have fallen out of favor because of the availability of newer (and more expensive) drugs, some of which have been taken off the market due to safety concerns.

But more traditional therapies should become first-line treatments in guidelines for the treatment of IBS, the experts say.

"IBS can be difficult for physicians to treat," noted lead researcher Dr. Alex Ford, from McMaster University, Health Sciences Centre in Ontario, Canada.

"New drugs are always being developed, but recent ones such as alosetron and tegaserod have been withdrawn, and are now only available on a restricted basis, and renzapride has not been shown to be effective," he said. On the other hand "older drugs, which are cheap, safe, and in some cases available over the counter, appear to be effective in IBS."

The report is published in the Nov. 14 online edition of the BMJ.

As many as 45 million Americans may have IBS, the International Foundation for Functional Gastrointestinal Disorders reports. Between 60 percent and 65 percent of IBS sufferers are women.

In addition to pain and discomfort, people with IBS experience chronic or recurrent constipation or diarrhea -- or bouts of both. While the exact cause of the condition isn't known, symptoms seem to result from a disturbance in the interaction of the gut, brain and nervous system, according to the foundation.

For the study, Ford's team reviewed trials that compared IBS treatment with fiber antispasmodics and peppermint oil to a placebo or no treatment. The trials included more than 2,500 IBS patients.

The researchers found that fiber, antispasmodics and peppermint oil were effective treatments for IBS. Specifically, that meant that to prevent IBS symptoms in one patient, 11 needed to be treated with fiber, five with antispasmodics, and 2.5 with peppermint oil.

There were no serious side effects associated with any of these treatments, the researchers note.

Peppermint oil appeared to be the most effective therapy of those reviewed, the researchers found.

In trials comparing fiber with placebo, insoluble fiber such as bran was not effective. Instead, only soluble fiber, such as ispaghula husk, reduced symptoms. For antispasmodics, the most effective was hyoscine. This should be used first among antispasmodics, Ford's group advised.

"Physicians, particularly those in primary care, who are being asked to take increasing responsibility for the management of IBS, should consider the use of these agents as first-line therapies for IBS," Ford said.

Dr. Roger Jones, from Kings College London and author of an accompanying journal editorial, welcomed the study.

"These treatments might be slightly more effective than recently thought and they are worth trying," Jones said.

For some patients with pain and diarrhea the antispasmodics may be useful. Patients with constipation should try fiber and for other patients, peppermint oil may be helpful, Jones said.

"If you have IBS which is not under reasonably good control or you are not happy with your symptom profile, you should see your primary-care doc or gastroenterologist for review and perhaps remind them that there is new evidence about the effectiveness of these traditional medicines and you would like to give it a go," Jones said.

"Alternatively, if you feel sufficiently well-informed and confident, you can go do it yourself and get these treatments at the pharmacy," Jones added.

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