You can prevent tinnitus by taking steps and precautions especially if you have bad genetics. It is much easier to prevent tinnitus than it is to cure it. The first step in preventing tinnitus is too avoid exposure to loud noises along with avoiding head and neck trauma. If you know you are going to be exposed to loud noises or high frequencies you should take precautions to protect your hearing. If you already have tinnitus you should take precautions to protect your hearing because it is possible that your tinnitus can get worse. Proper precautions include wearing protective earplugs and earmuffs. It is best to avoid places you know are likely to have loud noises such as concerts and clubs. In the case that you forget to bring your hearing protection do not try to improvise with wadded up tissue or cotton balls. These will not effectively protect your hearing and they have the potential to become lodged in your ear.

Younger and younger cases of tinnitus are being reported and it has been suggested that this is due to the excessive use of iPods. Do not be discouraged from using an iPod just avoid raising the volume so loud to the extent that other people around you can hear it. You can also prevent tinnitus by eliminating alcohol and beverages containing caffeine from your diet along with smoking and tobacco products. Nicotine and tobacco may cause tinnitus by reducing the blood circulation to the structures of your ears. If you already have tinnitus it is suggested that staying within a healthy weight range can help reduce or even stop the ringing in your ears. Statistically it has been shown that tinnitus occurs more frequently in obese adults. Getting your daily amount of vitamins can also significantly decrease your chance of getting tinnitus. Specifically getting enough B12 vitamin in your diet through milk, dairy products, meat, and eggs.

There are easier ways to cure your tinnitus. According to recent advances in science it is suggested that tinnitus can be treated in the comfort of your own home using home remedies. Very few people know about these remedies, but for those who do, it has been proven to be highly effective in treating mild to severe cases of tinnitus. These techniques are quick, cheap, and require only a few minutes a day. They can completely clear your tinnitus within a week and have even been proven to be more effective than most prescribed medications.

If you are concerned about familial breast cancer, the first step is to talk things over with your GP or Genetic Counsellor.

You will be asked about your family history and ethnic background, as well as any blood relatives, on either side of your family, who have had breast or related cancers.

If a faulty breast cancer gene has already been identified in a family member, you may be referred directly to a specialist genetic service.

Once your GP or Genetic Counsellor has taken a full family history, your risk of developing breast cancer can be assessed.

Most women will be at no greater risk than any other woman.

If this is the case your counsellor should discuss this with you and provide you with some written information on being breast aware and lifestyle risks.

However, if you develop any breast changes or if your family history or circumstances alter, it is important to go back and see your GP.

An increased risk

A small number of women may be viewed as having a greater risk of developing breast cancer on the grounds of a strong family history.

If this applies to you, you will be classified as having one of the following:

• a moderate risk
• a high risk.

You will then be referred to either a family history clinic or a specialist in cancer genetics. The type of care you receive will be depending on your risk level.

Screening

Depending on your age, you may be offered a mammogram.

Women between the ages of 40 and 49 will normally be offered annual mammograms.

However, it is currently unclear how effective mammograms are in detecting breast cancer early in women at increased risk - clinical studies are currently researching this issue.

Because of this, women aged 30 to 39 will be offered mammograms only as part of a research study rather than as a matter of routine.

Women under the age of 30 are unlikely to be offered mammograms, as younger women's breast tissue is too dense to produce a clear mammogram picture.

Genetic counselling

If you are considered to be at high risk of developing breast cancer you will be offered specialist genetic counselling.

This will give you more information about your family history, how your lifestyle may affect you, what having a genetic test means, and the options available to you if you choose to go ahead with the test.

You may feel anxious about finding out about your risk of developing breast cancer, but remember that your counsellor is trained to deal with these issues.

Testing

The test (Screening of BRCA1 and BRCA2) is done by Eastern Biotech & Life Sciences, Dubai on a blood sample from a living relative who has already developed breast or ovarian cancer.

The results can take many months to complete, as it is technically very difficult to identify the faulty gene.

If it is found that you do carry the faulty gene, although you will not necessarily develop breast cancer, you do have a higher risk of doing so.

In Ashkenazi Jewish women, specialists already know that there are three specific gene faults in a large proportion of the families where breast and ovarian cancer is common.

This means that testing may be offered to relatives at high risk without needing to carry out the gene search.

Depression is a severe illness affecting the lives of not only the sufferers but also their families. Anyone can suffer from depression, young or old, male or female. Most causes of mood and anxiety disorders remain unknown and neuropsychiatric disorders are complex.

But it's known that stress is a risk factor for the onset of many psychiatric disorders. A strong genetic predisposition is often blamed for mental illnesses as it is seen that depression run in families. But there is evidence to show that environmental influences can cause increased susceptibility. For example, stressful situations in early life contribute to major risk factors for the subsequent development of depression. Stressful events later in life such as family loss, divorce or financial problems can also cause considerable increase in depression. Ongoing stressful circumstances such HIV patients are more likely to suffer from depression and psychological stress. The early onset of stress, mood problems and depression also has an inclination to continue throughout adult life. Therefore stressful and unhappy home environmental in childhood that affect the developing brain are associated with increased risk of depression in later life.

This suggests that a combination of genetics, early life stress, and on-going stress situations cause and determine individuals to respond to stress and become vulnerable to major depression, panic disorder, posttraumatic stress disorder and other psychiatric disorders. One example of genetic factors of depression is the dysfunctions in neurotransmitter systems such as in the dopamine, serotonin and noradrenaline that have been shown to cause several disorders such addiction, bipolar disorder, and depression. For example, lack of serotonin-1A receptor shows increased depression and anxiety related behaviour but normal behaviour is restored if the receptor is genetically or pharmacologically. However, in recent years other candidate genes have appeared to be connected with depression in humans. In recent years compounds or agonists (designed to selectively interact with the serotonin-1A receptor in the brain) that target this receptor have been approved for anxiety and major depression.

Depression like behaviors is seen in organisms artificially manipulated by either environmental stress or through genetic/pharmacological factors. Therefore these carefully and ethically constructed scientific studies including volumetric brain imaging techniques and genetics; coupled with screening programmes will allow us to understand the complex correlation of nature and nurture in the development of mood disorders. As depression costs the health service a huge amount of money there is still a great need to understand the disease and identify the "risk gene" of depression. Its about time researchers discovered a genetic test for depression. In the meantime, the best way to keep away from stress and depression is to keep physically healthy.

Although many diagnosed with diabetes have the disease somewhere in their family medical history, diabetes is not a disease that is inherited in any simple pattern.

First of all, Type 1 and Type 2 diabetes do not have the same causes. However, there are two factors that are involved in both: there must be an inherent predisposition for the disease and there must be a trigger for it.

Proof that genes alone are not enough to get diabetes can be found in the case of identical twins. Identical twins have identical genes, yet in cases where one twin is diagnosed with Type 1 diabetes there is only a 50% chance that the other twin will also develop the Type 1 diabetes. If the diagnosis is Type 2 diabetes, then the risk goes to 3 out of four for chance. A mixture of nature and environmental factors make it impossible to determine who will get diabetes and who will not.

Type 1 Diabetes

When it comes to Type 1 diabetes, people generally need to inherit risk factors from both sides of their family. These risk factors are very prevalent in Caucasian segments of the population. Still, even those who are at risk do not always get diabetes, prodding researchers to dig deeper into what possible environmental triggers there are that set off the disease.

Type 1 diabetes is known to occur more often in winter than in summer and therefore has researchers believing that cold weather is a possible trigger. Viruses are also suspected as a trigger as well as other auto-immune diseases. (Diseases in which the immune system attacks the body's tissues.)

Type 2 Diabetes

Of the two types of diabetes, Type 2 has the stronger genetic base but depends a great deal more on environmental factors. The genetic predisposition for Type 2 diabetes mixed with those living in a Western lifestyle is an infamous cocktail for developing this disease. As is such with the great majority of the Western diet and lifestyle, too much fat and refined carbohydrates and not enough fiber coupled with inactivity has birthed this disease into epidemic proportions. As obesity rises, so do reports of diabetes. In comparison, those living in areas of the world that are not Westernized do not develop Type 2 diabetes despite their high genetic risk.

Gestational Diabetes

Gestational diabetes, diabetes that develops during pregnancy, has no clear genetic or environmental triggers. Although women who develop the disease are more likely to have a family history of diabetes, it is unclear what other non-genetic factors play a role. Women who put off having children until their later years and women who are overweight seem to be the most common groups to be diagnosed but this is not always the case.

So what is the conclusion here? You can have the genetic risk, environment, and the lifestyle triggers, and still not develop diabetes. The other side is also true. Diabetes can develop without many of the triggers.

The only thing that we as a human race can do is limit the triggers for diabetes as much as we can. Eat healthy, exercise regularly, keep our weight under control and hope that our genes are in our favor.

It seems that some people are destined to be skinny. They have never known being fat, and they make being thin look easy. Others of us are in the opposite situation. It is a struggle to lose weight, and being thin seems impossible. Could it be that our genes have something to do with it? As it turns out, there are several genes that play a role in obesity. Defects in some of these genes cause certain syndromes to develop. Not everything is known about the genetics of obesity, but our knowledge is expanding.

A part of the brain called the hypothalamus controls several functions of the body. One of these is the regulation of the sense of hunger. There is an interplay between various chemical messengers and the hypothalamus. This interplay is called the hypothalamic leptin-melanocortin system. Our fat cells make a signal called leptin. The more fat we have, the more leptin is produced. It binds to the leptin receptor in the hypothalamus. The hypothalamus senses a minimal amount of leptin which tells the brain that the body has at least the required amount of fat to function. Once the receptor is activated, a protein called proopiomelanocortin (POMC) is made. POMC is then cut into smaller parts by enzymes. One of these enzymes is proenzyme convertase 1 (PC-1). One of the smaller proteins produced by PC-1 is called alpha-MSH which binds another receptor in the hypothalamus called MC4R. Once MC4R is turned on, it triggers some intracellular signals that end up telling your brain that you are not as hungry. Got all that?! Check out the link at the end of this article and go to the "Genetics" tab. On the "leptin" page, there is a diagram that explains it.

A defect in the genes for any of the signals, enzymes, and receptors mentioned above can lead to an increased appetite. The most common of these mutations is a defect in MC4R. However, it is not the most severe, and some people with a defective MC4R gene are still thin. Mutations in other genes cause a voracious appetite in very young children, and they are nearly destined to eat far more than their bodies will ever need. In addition to becoming very obese, associated problems can include: small ovaries and testicles, thyroid dysfunction, decreased immunity, and low functioning adrenal glands. Fortunately, these more severe conditions are rare with only a handful of known cases. There are treatments for a few, like replacing leptin with shots. For others, like MC4R, there are to treatments.

A few genes that aid in the development of the hypothalamus are also associated with obesity. The SIM1 gene encodes signals that come from the MC4R receptor. One case of a young girl with a SIM1 mutation was obese and also tall. In addition to development of the hypothalamus, the tropomysin-related kinase B (TrkB) receptor and the chemical signal called brain-derived neutrotrophic factor (BDNF) play roles in memory, behavior, and intellect. Defects in either of these two can cause obesity and memory problems.

In the reward center of the brain, dopamine is released when we eat food. People who have mutations in a stretch of DNA called TaqIA have fewer dopamine receptors and thus need to eat more to feel the same sense of reward. This lends weight to the fact that some people may literally be addicted to food, and the sweeter the food, the stronger the addiction.

There are also several genetic syndromes associated with obesity that involve more than one gene. They are too complex for this article, but here is a list of some of them: Prader-Willi, Bardet-Biedl, Ahlstrom, Cohen, and Carpenter syndromes.