Monday, May 21, 2018

Acute Ischemic Stroke and High-Risk TIA

Combination antiplatelet therapy with clopidogrel and aspirin may reduce the rate of recurrent stroke during the first 3 months after a minor ischemic stroke or transient ischemic attack (TIA). A trial of combination antiplatelet therapy in a Chinese population has shown a reduction in the risk of recurrent stroke. We tested this combination in an international population.

A total of 4881 patients were enrolled at 269 international sites. The trial was halted after 84% of the anticipated number of patients had been enrolled because the data and safety monitoring board had determined that the combination of clopidogrel and aspirin was associated with both a lower risk of major ischemic events and a higher risk of major hemorrhage than aspirin alone at 90 days. Major ischemic events occurred in 121 of 2432 patients receiving clopidogrel plus aspirin and in 160 of 2449 patients receiving aspirin plus a placebo, with most events occurring during the first week after the initial event. Major hemorrhage occurred in 23 patients receiving clopidogrel plus aspirin and 10 patients receiving aspirin plus placebo.

In summary, patients with minor ischemic stroke or high-risk TIA, those who received a combination of clopidogrel and aspirin had a lower risk of major ischemic events but a higher risk of major hemorrhage at 90 days than those who received aspirin alone.

My Take:
The accompanying editorial points out that most of the benefit of this combination therapy is during the first week following a minor stroke or TIA. Limiting the use of both drugs to three weeks was recommended.

The use of aspirin as secondary prevention (after an ischemic event) is well established as a medical standard. However, the common practice of taking an aspirin daily as primary prevention is not. Several studies have demonstrated that the side effects of daily aspirin, including major hemorrhage and death, exceed any benefit in preventing an initial event. Again, the odds favor the use of aspirin after a patient has suffered a heart attack, stroke, or TIA.

The Bottom Line:
If you are taking an aspirin daily, even a low-dose or “baby” aspirin for primary prevention, please review this practice with your primary care physician. It is not the standard of care. If you have had a vascular event and are taking a daily aspirin with another blood thinner (combination therapy), like this study, please review this practice with your health care provider. Although still an accepted practice, the long term risks involved outweigh the benefits.

Source: May 16, 2018 New England Journal of Medicine

Friday, May 18, 2018

Do Nightshade Vegetables Make Arthritis Worse?

Nightshade foods contain solanine, a chemical which some people believe may aggravate arthritis pain and inflammation. The Arthritis Foundation say that his is not true. However, if a person feels that certain foods trigger their arthritis symptoms, including nightshades, they should avoid these foods.

Nightshade vegetables are part of the plant family Solanaceae. Some species are toxic, including the belladonna plant, which is also called deadly nightshade. Other species are commonly cultivated and eaten by humans. Common nightshade vegetables include white potatoes, tomatoes, eggplant, bell peppers, cayenne pepper and paprika.

Solanine is found in trace amounts in potatoes and is normally safe, though the leafy stalks of the potato plant and green potatoes are toxic, and solanine poisoning has been reported from eating green potatoes.

A person may be allergic to one or more nightshade vegetables if they experience the following symptoms shortly after eating them: hives or a skin rash, shortness of breath, wheezing, coughing, tightness of the throat, pale skin, and anaphylaxis.

Nightshade vegetables are excellent sources of nutrition, and no research to date has linked them specifically to increased inflammation or other symptoms of arthritis. A person should speak with a dietitian if they are concerned about the effects of a particular food on their health.

My Take:
Nightshades are the fifth most common food allergy I find clinically. Only wheat, dairy, soy and corn test positive more often. They are a weird group of foods because the common link is the presence of solanine not their appearance or use in the diet.

Wednesday, May 16, 2018

Wisdom Wednesday: Fibromyalgia vs Rheumatoid Arthritis


Fibromyalgia and rheumatoid arthritis share some symptoms, such as pain and exhaustion. If a person has both conditions, the symptoms may be difficult to distinguish. However, fibromyalgia and rheumatoid arthritis (RA) are unrelated and have different causes.

Fibromyalgia usually causes pain, stiffness, and tenderness in muscles and connective tissues throughout the body. RA tends to cause pain, swelling, and tenderness in certain joints. Other shared symptoms include pain mirrored on both sides of the body, stiffness that is worse in the morning, chronic exhaustion, reduced mobility and range of motion in muscles and joints, depression and anxiety.

While the effects may be similar, these conditions have different causes. Fibromyalgia changes the way the brain and nervous system process and interpret pain. People with the condition tend to feel amplified pain when they experience everyday injuries, such as strains.

RA is an autoimmune condition. It causes the immune system to harm the synovial tissues, which line the joints. This leads to inflammation and pain. Over time, RA can cause permanent damage to the bones and connective tissues in the joints. Inflammation may also spread to the lungs, skin, and eyes.

The medical community currently does not believe that fibromyalgia causes inflammation. However, recent research indicates that fibromyalgia may induce a type of inflammation that is not detected by routine blood tests. No evidence suggests that this inflammation causes joint or muscle damage like RA, and there may be no visible signs.

Though the conditions are unrelated, having RA may increase a person’s likelihood of developing fibromyalgia. An estimated 20-30% of people with RA also have fibromyalgia. Researchers suggest that the chronic inflammation and pain associated with RA may make the nervous system hypersensitive over time, leading to fibromyalgia.

Monday, May 14, 2018

Melatonin for Migraine Headache Prophylaxis

Interest in using melatonin for headache disorders has been developing for decades. Over the years, several clues have emerged to suggest that melatonin plays a role in a variety of headache disorders, including migraine, cluster, and tension. In patients with migraine headaches, for instance, some research shows that melatonin levels are lower on days when migraines occur. Patients with chronic migraine also appear to have lower melatonin levels than those with episodic migraine. Nighttime melatonin levels are also lower in patients with migraine compared with those without.

Imaging studies provide additional evidence for melatonin’s role in migraine prevention. During migraine attacks, the hypothalamus is activated. Given the presence of melatonin receptors within the suprachiasmatic nucleus of the hypothalamus, it is conceivable that melatonin’s binding and action in the hypothalamus could play a role in these headaches.

Melatonin might also affect headaches through direct effects on pain and inflammation. Animal studies show that melatonin can reduce pain perception in models of inflammation and neuropathic pain, possibly by binding receptors in the spinal cord or through a variety of other pathways.

Clinical research evaluating melatonin in patients with migraine headaches has focused on migraine prophylaxis. Most studies have found beneficial effects from melatonin on headache frequency; however, some of these studies also have serious methodologic limitations. Several uncontrolled studies found that taking melatonin over a period of 2-6 months significantly reduced migraine headache frequency in both adults and children. In these studies, about 62-78% of patients had a greater than 50% reduction in migraine frequency at the end of the trial compared with at the beginning.

In all clinical trials, melatonin was well tolerated, with sleepiness being the most commonly reported side effect. Less common side effects included fatigue, dizziness, constipation, stomach upset, and dry mouth. In the placebo-controlled trials, side effects were comparable to those of placebo and less common compared with either amitriptyline of sodium valproate.

Friday, May 11, 2018

A ‘Metabolic Switch’ May Explain Why Fasting Boosts Gut Health

Fasting for 24 hours can reverse the loss of stem cell function in the gut that accompanies aging, according to a study of mice.
Intestinal stem cells are crucial for tissue repair and regeneration, and their decline as we age means that it becomes harder to recover from gastrointestinal conditions and infections.

The researchers, who were led by a team from Massachusetts Institute of Technology (MIT) in Boston, discovered that fasting for 24 hours boosted regeneration of gut stem cells in younger and older mice. They found that fasting exerted this effect by means of a metabolic switch that causes cells to break down fatty acids instead of carbohydrates such as glucose. They also discovered a molecule that can activate the same switch – a finding that might lead to drugs that boost older people’s recovery from gastrointestinal infections or chemotherapy.

Stem cells are immature cells that have remarkable properties. For instance, they can replicate almost indefinitely and develop into virtually any type of cell in the body, forming an essential source of new cells for growth and repair in many tissues. In the gut, they maintain and repair tissue lining, which ‘renews itself’ about every 5 days.

Now published in the journal Cell Stem Cell, co-senior author Omer H. Yilmaz – an assistant professor of biology at MIT – explains that diet is known to have a “profound effect” on the ability of tissue to regenerate itself. There is also evidence that intermittent fasting can benefit health and age-related decline in tissue function.

Wednesday, May 9, 2018

Wisdom Wednesday: These Common Drugs May Raise Your Risk of Dementia


A landmark study has linked the long-term use of certain anticholinergic drugs to a higher risk of dementia later on. This investigation is believed to be the “largest and most detailed” study to date into long-term anticholinergic use and dementia risk.

Anticholinergics work by blocking a chemical messenger, or neurotransmitter, called acetylcholine that carries brain signals for controlling muscles. They are used to treat a variety of conditions, from Parkinson’s disease and loss of bladder control to asthma, chronic obstructive pulmonary disease, and depression.

Anticholinergics for depression, such as amitriphtyline, dosulepin, and paroxetine, have previously been liked to higher risk of dementia, even when they were used up to 20 years beforehand. Some studies have also suggested that use of any anticholinergic is linked to raised risk of dementia.

But the new study – which was led by the University of East Anglia (UES) in the United Kingdom and is now published in The BMJ – discovered that long-term use of only certain types of anticholinergics is linked to higher dementia risk. It confirms the link to long-term use of anticholinergics for depression, and for Parkinson’s disease and loss of bladder control. However, the study found no link between increased dementia risk and other anticholinergic drugs, such as antihistamines and medications for abdominal cramps.

For their investigation, the researchers used data from the Clinical Practice Research Database, which contains anonymized records for more than 11 million people across the U.K. The researchers used a system called the Anticholinergic Cognitive Burden (ACB) scale to score the anticholinergic effect of the drugs that the patients had been prescribed. An ACB score of 1 meant that a drug was “possibly anticholinergic,” whereas a score of 2 or 3 meant that it was “definitely anticholinergic.” Altogether, they analyzed more than 27 million prescriptions.

Monday, May 7, 2018

Melatonin for Migraine Headache Prophylaxis

Interest in using melatonin for headache disorders has been developing for decades. Over the years, several clues have emerged to suggest that melatonin plays a role in a variety of headache disorders, including migraine, cluster, and tension. In patients with migraine headaches, for instance, some research shows that melatonin levels are lower on days when migraines occur. Patients with chronic migraine also appear to have lower melatonin levels than those with episodic migraine. Nighttime melatonin levels are also lower in patients with migraine compared with those without.

Imaging studies provide additional evidence for melatonin’s role in migraine prevention. During migraine attacks, the hypothalamus is activated. Given the presence of melatonin receptors within the suprachiasmatic nucleus of the hypothalamus, it is conceivable that melatonin’s binding and action in the hypothalamus could play a role in these headaches.

Melatonin might also affect headaches through direct effects on pain and inflammation. Animal studies show that melatonin can reduce pain perception in models of inflammation and neuropathic pain, possibly by binding receptors in the spinal cord or through a variety of other pathways.

Clinical research evaluating melatonin in patients with migraine headaches has focused on migraine prophylaxis. Most studies have found beneficial effects from melatonin on headache frequency; however, some of these studies also have serious methodologic limitations. Several uncontrolled studies found that taking melatonin over a period of 2-6 months significantly reduced migraine headache frequency in both adults and children. In these studies, about 62-78% of patients had a greater than 50% reduction in migraine frequency at the end of the trial compared with at the beginning.

In all clinical trials, melatonin was well tolerated, with sleepiness being the most commonly reported side effect. Less common side effects included fatigue, dizziness, constipation, stomach upset, and dry mouth. In the placebo-controlled trials, side effects were comparable to those of placebo and less common compared with either amitriptyline of sodium valproate.