Many of us have experienced that annoying buzzing sound known as tinnitus. It’s thought of as more of a symptom than as a diagnosis. It affects more than a million people worldwide and has been chronicled as far back as the first century AD. Only 20% of people with tinnitus seek treatment. That is most likely due to the fact that most tinnitus comes and goes and is tolerated to a degree in which we can function. Although in the United States, almost one third of patients who request treatment report symptoms that are debilitating.

Tinnitus is variable with the quality and loudness of the buzz, hiss or ringing that is often described. Prevalence increases with age, smoking, male gender and ethnicity, with the non-Latino white population statistically at greater risk. Some conditions such as diabetes and other autoimmune diseases are risk factors for tinnitus. A history of loud sound, which can be recreational (those crazy late night concerts!), occupational or environmental also can predispose a person to tinnitus.

The majority of tinnitus cases are considered Primary which is defined as having no identifiable cause. On the other hand, Secondary tinnitus has an identifiable cause which can include a long list of conditions such as certain medications (NSAIDS, chemotherapy, antibiotics), inner and outer ear disturbances, neurological and vascular causes, infections and nutrient deficiencies. Persistent tinnitus (lasting more than 6 months) can impact ones quality of life and can lead to depression, anxiety, insomnia and neurocognitive decline. It can really be devastating!

The cause of tinnitus is alittle more complicated than we once thought. It is not simply a cochlear (inner ear) phenomenon. It has to do with the damaged stereocilia (inner ear organelles of hair cells) located in the cochlea that exhibit an increase in a spontaneous firing rate in response to lost frequencies which are relayed to higher structures in the brain. It appears to be a maladaptive neural plasticity as it results in increased spontaneous firing rates and synchrony among neurons in central auditory structures, according to research by Shore and colleagues (Shore, SE, Roberts LE, Langgguth B. Maladaptive plasticity in tinnitus- triggers, mechanisms and treatment. Nat Rev Neurol. 2016;12(3):150-160.

So, what to do?
First, lab testing should be done to rule out causes of tinnitus. Imaging is usually unnecessary unless one questions a tumor or vascular cause. When no underlying pathology is identified for tinnitus, then a patient should be sent for a full audiology evaluation. Management involves treatment of perceived loudness and treatment of comorbid symptoms such as depression, anxiety, sleep disturbance, etc.
The leading recommendation made by The American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) is cognitive behavioral therapy (CBT). The sound cannot be eliminated but the patient’s response to the sound can be modified. Tinnitus Retraining therapy (TRT) is another form of habituation therapy that has been successful. Unlike CBT, which is the idea that behaviors are modifiable thoughts that can be changed by teaching coping mechanisms such as relaxation, TRT aims to eliminate the perception of sound. A patient wears a device similar to hearing aids using broadband noise that closes the gap between silence and the perception of tinnitus. This device is worn for 6 hours a day for 12 months.

Other alternative non-medical therapies include Chinese herbal medications such as Ginko biloba, vitamins, zinc, manganese, and melatonin. Cannabinoids, which is a plant that contains hundreds of chemicals that each act differently on the brain may have an inhibitory effect on neurotransmitter release. Other modalities such as yoga, meditation, physical therapy and mindfulness have helped patients feel more relaxed but they had no effect on the severity of tinnitus.

Of course prevention cannot be underestimated. Occupational noise and recreational use of music devices put people at heightened risk for hearing loss and tinnitus. If you are suffering from tinnitus, see a practitioner for evaluation to help your symptoms.

Reference: Gillian Ross, W, Danielsen, R. What’s the Buzz? Treatment Strategies in Chronic Subjective Tinnitus. Clinician Reviews. September/October 2018/Vol 28,NO 10. p. 34-41.

Alcohol use has a complicated association with health. It tends to follow a “U” shape curve. Some research suggests that low levels of alcohol consumption give some protection against heart disease, diabetes and several other conditions. Too much alcohol on the other hand, can lead to adverse effects on organs and tissues leading to injuries, poisoning, potential self-harm or violence. So there’s a “sweet” spot.

The Global Burden of Disease Study 2016 collected data from developed and developing nations, involving 195 countries and territories, from 1990-2016. It is one of the largest studies of its kind looking at the association between population-wide consumption of alcohol to population wide trends. This study published in the Lancet concluded that alcohol consumption is involved in 2.8 million deaths worldwide annually. This makes it the 7th leading risk factor for death and disability.
The bottom line in this study was that alcohol use (10 grams of pure ethyl alcohol = 3.4 ounces of red wine at 13% alcohol, 12 ounces of beer at 3.5% alcohol or 1 ounce of 80-proof whiskey) is a leading risk factor for global disease burden and causes substantial health loss and the level of consumption should be zero!

OK…so that doesn’t sit well with many of us. So lets look deeper in the study.
First of all, the researchers relied on sales of alcohol and surveys to estimate the prevalence of drinking in each country. They linked consumption data to 23 health outcomes which included car accidents, suicides, tuberculosis, liver cirrhosis, cardiovascular disease and cancers.
Rates of alcohol consumption vary greatly by country. Plus, this was a meta-analysis, which means it is a collection of many observational studies in which the data is then combined into mathematical models to predict the harm from alcohol consumption worldwide. The problem is, observational data can miss other causes of the problem. Examples are: Do those who drink have other health problems, such as smoking tobacco? Do those that drink alcohol have an unhealthy diet or live in poorer neighborhoods? These could be more of the cause of death and disability, and the studies that were analyzed did not look at these variables.

Second, looking at the health outcome of tuberculosis (TB) is interesting. According to the World Health Organization, over 95% of cases and deaths of TB are in developing countries and those that are infected with HIV are 20-30 times more likely to develop active TB. Again, this could be a confounding factor as I described above because the causes of death in developing countries are different than in developed nations. TB was the major cause of death in young adults, and we know alcohol can raise the risk for TB activation. This may show a statistical significant change in the data but gives an overall bias in the clinical importance.

Third, this is a world wide study, but the results are being interpreted at an individual level. The 23-alcohol related health issues are not experienced at the same rate. For instance, the rate of heart disease and diabetes actually go down with light or moderate drinking. The risks for cancer and tuberculosis can go up for some people (depending on many circumstances). It’s not clear that everyone is at the same risk in real life.
So if 0 drinks is ideal, what is the risk at 1 drink per day? Well, if you don’t drink, 914 for every 100,000 people can expect to experience one of the 23-alcohol related problems in any given year. Having 1 drink per day, that number goes to 918 per 100,000. That means 99,082 are unaffected. So the risks in the study present themselves as much bigger than they really are. Don’t get me wrong…I’m not advocating drinking, but there is a balance and we shouldn’t interpret these results individually to induce panic or fear to change policy. We have enough of that right now.

So we need better studies. More likely a large randomized control trial looking at light to moderate drinking, to get the best perspective on the harms and benefits of alcohol consumption. This may give us more answers on the way most people consume alcohol and perhaps give us insight on more specifics such as cultural, age and gender differences.

https://www.nytimes.com/2018/08/27/health/alcohol-drinking-health.html

The prescription anti-nausea medication Ondansetron (Zofran) is the first line drug for nausea in the emergency department (ED) for non-cancer patients. Now, an alternative option, inhaled isopropyl alcohol, has shown promise. Yes, this is your typical rubbing alcolhol that you may have in your bathroom cabinet.

A recent trial involved 120 ED adult patients with nausea and vomiting who did not need IV (intravenous) medications or fluids. They were randomized to receive inhaled isopropyl alcohol in the form of alcohol swabs plus 4 mg of oral ondansetron, inhaled isopropyl alcohol plus an oral placebo, or inhaled saline plus 4 mg oral ondansetron. Patients could sniff the alcohol or saline repeatedly.

Results showed a significant decrease in nausea in the alcolhol/ondansetron and alcohol/placebo groups than in the saline/ondansetron group. Patients in the alcohol groups also had better nausea control at the time of discharge.

For patients who do not require IV therapy, consider repeated inhalations of isopropyl alcohol swabs (which you can buy at your local pharmacy). We don’t know the mechanism of action, but it is simple and safe to try. Call your doctor or get to the ED if your symptoms worsen. And maybe don’t eat the old leftovers in the frig next time…

Reference: April MD et al. Aromatherapy vs oral ondansetron for antiemetic therapy among adult emergency department patients. A randomized control trial. Ann Emerg Med 2018 Aug; 72-:184.
Photo by Internet Archive Book Images

Photo by Internet Archive Book Images

There may be some new discoveries in Alzheimers disease.

This article explains some of the new insights into the causes of the most common type of dementia, Alzheimers disease.
Scientists have reviewed years of research and have noticed the virus herpes, appears to interact with human genes known to increase Alzheimers risk. This is not the sexually transmitted disease herpes but other types known as HHV-6 and HHV-7.
This combination of genetic and infectious influence can cause an overactive immune system.

The amyloid protein theory may still play a part in contributing to this disease but it has been losing ground in the thought that it was the only cause of Alzheimers.

Strong consideration of microbes actually being the initial seed that provokes a toxic turmoil is being looked at. This amyloid protein has the potential to build up to fight infection which then begins to impair function of neurons in the brain. The excess amyloid causes another protein called tau, to form tangles which can damage more brain cells and produce inflammation that stimulates the immune system. It is this inflammation, according to Harvard neuroscientist, Rudolph Tanzi, that does the most damage and causes a neurotoxic mess to the Alzheimer’s-afflicted brain. Scientific research has for the past few decades, clearly demonstrated that inflammation is a fundamental process that underlies the development of Alzheimer’s disease.

Tanzi explains that microbes may be the initial seed for the complex pathology of Alzheimer’s but that genetics and environmental factors also come into play.

In my opinion, we will find that the microbiome plays an important role in this discovery since its genetic makeup can regulate gene expression as well as modulate inflammation in the immune system.

https://www.npr.org/sections/health-shots/2018/09/09/645629133/infectious-theory-of-alzheimers-disease-draws-fresh-interest