Monthly Archives: January 2008

Is Fat On Your Hips Better for Your Brain than Fat On Your Belly?

New research suggests that women with an hourglass figure may on average be brighter and have more clever children.

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A study found that women with large hips and small waists tend to be more intelligent than those with either  apple-shaped  or linear bodies. Such women may also tend to give birth to more intelligent children. One possible reason is the greater percentage of omega 3 fats found on the hips.

The study examined 16,000 women and girls, and found that women with a greater difference between the waist and hips scored significantly higher on cognitive tests, as did their children. Those with a waist-to-hip ratio between 0.6 and 0.7 achieved the highest scores.

Fat around hips and thighs holds higher levels of omega 3 fats, which are essential for the growth of the brain during pregnancy. Fat around the waist may have higher levels of omega 6 fats acids, which are less well suited to brain growth. Waist fat is also more likely to be a contributory factor in diabetes and heart disease.

Sources:
Times Online November 11, 2007
Evolution and Human Behavior January 2008 Volume 29, Issue 1, Pages 26-34

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Embracing Grief

Grief Is Important
Change is something that happens each and every moment in our lives. Since nothing is constant, it may sometimes seem as if we are losing something whenever things do change. Understanding that this is part of our daily existence and that there will not only be gains but also losses in our lives can help us more readily accept and deal with whatever happens.

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Whenever we lose something or somebody we love, it is important for us to take time out for ourselves and truly feel the weight of what we are experiencing. Although it may seem that doing so will push us into a deeper state of sadness, truly giving ourselves permission to be with whatever arises actually creates space for us to begin the healing process. This is because the act of grieving is a natural process, allowing us to sort through the range of emotions that are present in our everyday existence. Even though it may sometimes seem easier to involve ourselves in activities that take our minds off of our sadness, this will only make the route to healing more difficult. Unless we listen to where we are in the moment, the emotions we experience will only grow in intensity, and our feelings will manifest themselves in more powerful and less comfortable ways. Once we consciously acknowledge that these emotions are present, however, we are more able to soothe the sorrow of t! he moment. In so doing, we become more open to our natural ability to heal ourselves.

Grieving doesn’t have to be a process that keeps us rooted in our thoughts of fear and sadness. For the moment we might feel despondent, but by expressing and coping with our true feelings, we face the sadness head-on. When we allow ourselves to accept and deal with our loss fully, we will then be able to continue our life’s journey with a much more positive and accepting outlook. This will make it easier for us to see that our grief is ephemeral and, just like our moments of happiness, it will also come to pass.

Sources:Daily Om

Contact Dermatitis

As its name implies, contact dermatitis is inflammation of the skin caused by contact with a specific substance. there are two types: irritant contact dermatitis, which is caused by primary irritants (substances, such as bleach, that harm anyone’s skin); and allergic contact dermatitis, which occurs when a person comes in contact with a particular substance to which he or she has developed a sensitivity over time.

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substances that commonly trigger irritation or allergic reactions include some cosmetics; the nickel contained in jewelry, buttons, earrings for pierced ears, or watch straps; certain chemicals; drugs in skin creams; and plants, such as poison ivy or ragweed.

It is a term for a skin reaction resulting from exposure to allergens (allergic contact dermatitis) or irritants (irritant contact dermatitis). Phototoxic dermatitis occurs when the allergen or irritant is activated by sunlight.

Contact dermatitis is a localized rash or irritation of the skin caused by contact with a foreign substance. Only the superficial regions of the skin are affected in contact dermatitis. Inflammation of the affected tissue is present in the epidermis (the outermost layer of skin) and the outer dermis (the layer beneath the epidermis).[1] Unlike contact urticaria, in which a rash appears within minutes of exposure and fades away within minutes to hours, contact dermatitis takes days to fade away. Even then, contact dermatitis fades only if the skin no longer comes in contact with the allergen or irritant. Contact dermatitis results in large, burning, and itchy rashes, and these can take anywhere from several days to weeks to heal. Chronic contact dermatitis can develop when the removal of the offending agent no longer provides expected relief.

Types of contact dermatitis
There are three types of contact dermatitis: irritant contact, allergic contact, and photocontact dermatitis. Photocontact dermatitis is divided into two categories: phototoxic and photoallergic.

Chemical irritant contact dermatitis
is either acute or chronic, which is usually associated with strong and weak irritants respectively (HSE MS24). The following definition is provided by Mathias and Maibach (1978): a nonimmunologic local inflammatory reaction characterized by erythema, edema, or corrosion following single or repeated application of a chemical substance to an identical cutaneous site.

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The mechanism of action varies between toxins. Detergents, surfactants, extremes of pH, and organic solvents all have the common effect of directly affecting the barrier properties of the epidermis. These effects include removing fat emulsion, inflicting cellular damage on the epithelium, and increasing the transepidermal water loss by damaging the horny layer water-binding mechanisms and damaging the DNA, which causes the layer to thin. Strong concentrations of irritants cause an acute effect, but this is not as common as the accumulative, chronic effect of irritants whose deleterious effects build up with subsequent doses (ESCD 2006).

Common chemical irritants implicated include solvents (alcohol, xylene, turpentine, esters, acetone, ketones, and others); metalworking fluids (neat oils, water-based metalworking fluids with surfactants); latex; kerosene; ethylene oxide; surfactants in topical medications and cosmetics (sodium lauryl sulfate); alkalies (drain cleaners, strong soap with lye residues).

Physical irritant contact dermatitis
is a less researched form of ICD (Maurice-Jones et al) due to its various mechanisms of action and a lack of a test for its diagnosis. A complete patient history combined with negative allergic patch testing is usually necessary to reach a correct diagnosis. The simplest form of PICD results from prolonged rubbing, although the diversity of implicated irritants is far wider.[citation needed] Examples include paper friction, fiberglass, and scratchy clothing.

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Many plants cause ICD by directly irritating the skin. Some plants act through their spines or irritant hairs. Some plant such as the buttercup, spurge, and daisy act by chemical means. The sap of these plants contains a number of alkaloids, glycosides, saponins, anthraquinones, and (in the case of plant bulbs) irritant calcium oxalate crystals – all of which can cause CICD (Mantle and Lennard, 2001).

Allergic Contact Dermatitis
This condition is the manifestation of an allergic response caused by contact with a substance. A list of common allergens is shown in Table 1 (Kucenic and Belsito, 2002).

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Although less common than ICD, ACD is accepted to be the most prevalent form of immunotoxicity found in humans (Kimble et al 2002). By its allergic nature, this form of contact dermatitis is a hypersensitive reaction that is atypical within the population. The mechanisms by which these reactions occur are complex, with many levels of fine control. Their immunology centres around the interaction of immunoregulatory cytokines and discrete subpopulations of T lymphocytes.

ACD arises as a result of two essential stages: an induction phase, which primes and sensitizes the immune system for an allergic response, and an elicitation phase, in which this response is triggered (Kimble et al 2002). As such, ACD is termed a Type IV delayed hypersensitivity reaction involving a cell-mediated allergic response. Contact allergens are essentially soluble haptens (low in molecular weight) and, as such, have the physico-chemical properties that allow them to cross the stratum corneum of the skin. They can only cause their response as part of a complete antigen, involving their association with epidermal proteins forming hapten-protein conjugates. This, in turn, requires them to be protein-reactive.

The conjugate formed is then recognized as a foreign body by the Langerhans cells (LCs) (and in some cases Dendritic cells (DCs)), which then internalize the protein; transport it via the lymphatic system to the regional lymph nodes; and present the antigen to T-lymphocytes. This process is controlled by cytokines and chemokines – with tumor necrosis factor alpha (TNF-α) and certain members of the interleukin family (1, 13 and 18) – and their action serves either to promote or to inhibit the mobilization and migration of these LCs. (Kimble et al 2002) As the LCs are transported to the lymph nodes, they become differentiated and transform into DCs, which are immunostimulatory in nature.

Once within the lymph glands, the differentiated DCs present the allergenic epitope associated with the allergen to T lymphocytes. These T cells then divide and differentiate, clonally multiplying so that if the allergen is experienced again by the individual, these T cells will respond more quickly and more aggressively.

Kimbe et al (2002) explore the complexities of ACD’s immunological reaction in short: It appears that there are two major phenotypes of cytokine production (although there exists a gradient of subsets in between), and these are termed T-helper 1 and 2 (Th1 and Th2). Although these cells initially differentiate from a common stem cell, they develop with time as the immune system matures. Th1 phenotypes are characterised by their focus on Interleukin and Interferon, while Th2 cells action is centred more around the regulation of IgE by cytokines. The CD4 and CD8 T lymphocyte subsets also have been found to contribute to differential cytokine regulation, with CD4 having been shown to produce high levels of IL-4 and IL10 while solely CD8 cells are associated with low levels of IFN?. These two cell subtypes are also closely associated with the cell matrix interactions essential for the pathogenesis of ACD.

White et al have suggested that there appears to be a threshold to the mechanisms of allergic sensitisation by ACD-associated allergens (1986). [10] This is thought to be linked to the level at which the toxin induces the up-regulation of the required mandatory cytokines and chemokines. It has also been proposed that the vehicle in which the allergen reaches the skin could take some responsibility in the sensitisation of the epidermis by both assisting the percutaneous penetration and causing some form of trauma and mobilization of cytokines itself.

Common allergens implicated include the following:

Nickel (nickel sulfate hexahydrate) – metal frequently encountered in jewelry and clasps or buttons on clothing
Gold (gold sodium thiosulfate) – precious metal often found in jewelry
Balsam of Peru (Myroxylon pereirae) – a fragrance used in perfumes and skin lotions, derived from tree resin (see also Tolu balsam)
Thimerosal – a mercury compound used in local antiseptics and in vaccines
Neomycin – a topical antibiotic common in first aid creams and ointments, cosmetics, deodorant, soap and pet food
Fragrance mix – a group of the eight most common fragrance allergens found in foods, cosmetic products, insecticides, antiseptics, soaps, perfumes and dental products
Formaldehyde – a preservative with multiple uses, e.g., in paper products, paints, medications, household cleaners, cosmetic products and fabric finishes
Cobalt chloride – metal found in medical products; hair dye; antiperspirant; metal-plated objects such as snaps, buttons or tools; and in cobalt blue pigment
Bacitracin – a topical antibiotic
Quaternium-15 – preservative in cosmetic products (self-tanners, shampoo, nail polish, sunscreen) and in industrial products (polishes, paints and waxes).

Photocontact Dermatitis
Sometimes termed “photoaggravated”(Bourke et al 2001)[13], and divided into two categories, phototoxic and photoallergic, PCD is the eczematous condition which is triggered by an interaction between an otherwise unharmful or less harmful substance on the skin and ultraviolet light (320-400nm UVA) (ESCD 2006), therefore manifesting itself only in regions where the sufferer has been exposed to such rays. Without the presence of these rays, the photosensitiser is not harmful. For this reason, this form of contact dermatitis is usually associated only with areas of skin which are left uncovered by clothing. The mechanism of action varies from toxin to toxin, but is usually due to the production of a photoproduct. Toxins which are associated with PCD include the psoralens. Psoralens are in fact used therapeutically for the treatment of psoriasis, eczema and vitiligo.

Photocontact dermatitis is another condition where the distinction between forms of contact dermatitis is not clear cut. Immunological mechanisms can also play a part, causing a response similar to ACD.

 

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Symptoms:
Contact dermatitis usually affects the area that has been in direct contact with the substance that triggered the reaction. In irritant contact dermatitis, the skin inflammation develops soon after contact with the substance. the severity of the resulting rash depends both on the concentration of the irritant and on the duration of exposure.

Allergic contact dermatitis usually develops slowly over a period of time, and it is possible to have contact with a substance for several years without any skin inflammation occurring. however, once your skin has become sensitive to the substance, even a small amount of it, or a short exposure time, can trigger an allergic reaction.

In either form of contact dermatitis, the symptoms may include:

* Redness and swelling of the skin.This is the usual reaction. The rash appears immediately in irritant contact dermatitis; in allergic contact dermatitis, the rash sometimes does not appear until 24-72 hours after exposure to the allergen.

* water- or pus-filled blisters that may ooze, drain, or become encrusted. Blisters, welts, and hives often form in a pattern where skin was directly exposed to the allergen or irritant.

* flaking skin, which may develop into raw patches.

* persistent itching…..Itchy, burning skin. Irritant contact dermatitis tends to be more painful than itchy, while allergic contact dermatitis often itches.

While either form of contact dermatitis can affect any part of the body, irritant contact dermatitis often affects the hands, which have been exposed by resting in or dipping into a container (sink, pail, tub) containing the irritant.


Causes:

In North/South America, the most common causes of allergic contact dermatitis are plants of the Toxicodendron genus: poison ivy, poison oak, and poison sumac. Common causes of irritant contact dermatitis are harsh (highly alkaline) soaps, nickel, detergents, and cleaning products and rubbers.

Treatment:

Self-care at Home
Immediately after exposure to a known allergen or irritant, wash with soap and cool water to remove or inactivate most of the offending substance.
– Weak acid solutions [lemon juice, vinegar] can be used to counteract the effects of dermatitis contracted by exposure to basic irritants [phenol etc.].

If blistering develops, cold moist compresses applied for 30 minutes 3 times a day can offer relief.
Calamine lotion and cool colloidal oatmeal baths may relieve itching.
Oral antihistamines such as diphenhydramine (Benadryl, Ben-Allergin) can also relieve itching.
For mild cases that cover a relatively small area, hydrocortisone cream in nonprescription strength may be sufficient.
Avoid scratching, as this can cause secondary infections.

What might be done?
Your doctor will want to know when the skin inflammation developed and whether you have any known allergies. the site of the reaction is often a clue to its cause. For example, a patch of dermatitis on the wrist may be caused by an allergic to nickel in a watch or watch strap. people who handle chemicals at work often develop irritant or allergic contact dermatitis on their hands.

Your doctor may prescribe a topical corticosteroid to relieve itching and inflammation. however, even with treatment, contact dermatitis may take a few weeks to clear up.

If you handle chemicals at work, it is particularly important to find the cause of your skin allergy. If the cause cannot easily be identified, you may need to have patch testing.

Once the trigger has been identifies, you should avoid it as much as possible. If you cannot do so, you may need to use creams, protective clothing, or gloves whenever you come into contact with the trigger.

Medical Care
If the rash does not improve or continues to spread after 2-3 of days of self-care, or if the itching and/or pain is severe, the patient should contact a dermatologist or other physician. Medical treatment usually consists of lotions, creams, or oral medications.

Corticosteroids. A corticosteroid medication similar to hydrocortisone may be prescribed to combat inflammation in a localized area. This medication may be applied to your skin as a cream or ointment. If the reaction covers a relatively large portion of the skin or is severe, a corticosteroid in pill or injection form may be prescribed.
Antihistamines. Prescription antihistamines may be given if nonprescription strengths are inadequate.

Prevention
Since contact dermatitis relies on an irritant or an allergen to initiate the reaction, it is important for the patient to identify the responsible agent and avoid it. This can be accomplished by having patch tests, a method commonly known as allergy testing. The patient must know where the irritant or allergen is found to be able to avoid it. It is important to also note that chemicals sometimes have several different names.

Summary
The distinction between the various types of contact dermatitis is based on a number of factors. The morphology of the tissues, the histology, and immunologic findings are all used in diagnosis of the form of the condition. However, as suggested previously, there is some confusion in the distinction of the different forms of contact dermatitis (Reitschel 1997). Using histology on its own is insufficient, as these findings have been acknowledged not to distinguish (Rietschel, 1997), and even positive patch testing does not rule out the existence of an irritant form of dermatitis as well as an immunological one. It is important to remember, therefore, that the distinction between the types of contact dermatitis is often blurred, with, for example, certain immunological mechanisms also being involved in a case of irritant contact dermatitis.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://en.wikipedia.org/wiki/Contact_dermatitis
http://www.charak.com/DiseasePage.asp?thx=1&id=149

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Depression Risk ‘Highest In 40s’

Life may begin at 40, but research suggests that 44 is the age at which we are most vulnerable to depression.....CLICK & SEE..

CLICK & SEE->.Realistic aspirations may be the key to happiness

.Data analysis on two million people from 80 countries found a remarkably consistent pattern around the world.

The risk of depression was lowest in younger and older people, with the middle-aged years associated with the highest risk for both men and women.

The study, by the University of Warwick and Dartmouth College in the US, will feature in Social Science & Medicine.

The only country which recorded a significant gender difference was the US, where unhappiness reached a peak around the age of 40 for women, and 50 for men.

Previous research has suggested that the risk of unhappiness and depression stays relatively constant throughout life.

However, the latest finding – of a peak risk in middle age – was consistent around the globe, and in all types of people.

Researcher Professor Andrew Oswald, an economist at the University of Warwick, said: “It happens to men and women, to single and married people, to rich and poor, and to those with and without children.”

He said the reason why middle age was a universally vulnerable time was unclear.

Count your blessings
However, he said: “One possibility is that individuals learn to adapt to their strengths and weaknesses, and in mid-life quell their infeasible aspirations.

Another possibility is that a kind of comparison process is at work in which people have seen similar-aged peers die and value more their own remaining years. Perhaps people somehow learn to count their blessings.”

Professor Oswald said for the average person, the dip in mental health and happiness comes on slowly, not suddenly in a single year.

Only in their 50s do most people emerge from the low period.

“But encouragingly, by the time you are 70, if you are still physically fit then on average you are as happy and mentally healthy as a 20-year-old.

“Perhaps realizing that such feelings are completely normal in midlife might even help individuals survive this phase better.”

Marjorie Wallace, chief executive of the mental health charity Sane, said: “This study raises intriguing questions about the processes that lead to depression in mid-life, as well as indicating what a common experience it is worldwide.

“Depression is a complex and challenging condition that remains poorly understood, with as many as one in ten people with severe depression taking their own life.

“We welcome any scientific contribution to our understanding of this illness, particularly if the research can aid the development of better treatments, both therapeutic and pharmaceutical.”

Andy Bell, of the Sainsbury Centre for Mental Health, said mental health problems were extremely common – but he stressed they could occur at any time in life.

.
“One possibility is that individuals learn to adapt to their strengths and weaknesses, and in mid-life quell their infeasible aspirations”
By Professor Andrew Oswald
University of Warwick

“Depression is a complex and challenging condition that remains poorly understood ”
By Marjorie Wallace
SANE

Sources: BBC NEWS, 29TH. JAN’08

Why Some Can’t Kick The Butt

Mark Twain‘s claimed unsuccessful attempts to quit smoking a hundred times over might be explained not through lack of will, but proteins in the brain.
Blame it on brain

A genetic study of 14,000 people in Europe and the US has shown that variations in segments of two proteins that serve as gateways for nicotine entry into brain cells can predict the risk of addiction.

The study by US and Canadian scientists has shown that people with specific gene sequence coding for these proteins are more likely to be addicted to nicotine than people whose sequences are subtly different.

The two proteins called alpha-3 and alpha-5 form sites on brain cells which are activated during the process of addiction. The findings were published today in the journal Molecular Psychiatry.

“Pharmaceutical companies can now study these targets and develop new drugs that could help people quit (smoking),” Wade Berrettini, professor of psychiatry at the University of Pennsylvania Medical School and lead investigator in the study, told The Telegraph.

Existing anti-nicotine medications are not always effective.

Previous studies from Australia, North America, Scandinavia and China had indicated that the tendency for habitual heavy smoking — up to 20 cigarettes a day — was influenced by the genetic makeup.

Researchers have estimated that two-thirds of the risk of heavy smoking is genetic — believed to be a combination of several genes, each of which contributes to a small amount of the risk.

In the new study, the American-Canadian team found that variations in alpha-3 and alpha-5 could be used to predict the number of cigarettes per day during the period of heaviest smoking.

Existing medications, including nicotine replacement patches, are effective only for a few months in heavy smokers. “We could also use the genetic variations of alpha-3 and alpha-5 to determine whether they can predict the ability of people to quit using existing drugs,” Berrettini said.

The findings also raise the possibility — although there is no evidence for this yet — that people with certain variations in the alpha-3 and alpha-5 genes might find it easier to quit smoking than others.

“This could be confirmed through analysis of genetic variations between people who have quit successfully and those who repeatedly return to nicotine after trying to quit,” Berrittini said.

Public health specialists believe that many people around the world, aware of the health risks of tobacco, are trying to quit but are unable to do so. They’re in the league of the American writer Mark Twain who is said to have once quipped: “Quitting smoking is easy, I’ve done it a hundred times.”

Sources:The Telegraph (Kolkata, India)