Bipolar Disorder – going through intense moods

Do you go through intense moods?  Do you feel very happy and energized some days, and very sad and depressed on other days? Do these moods last for a week or more? Do your mood changes make it hard to sleep, stay focused, or go to work?

Some people with these symptoms have bipolar disorder, a serious mental illness. This brochure will give you more information.

What is bipolar disorder?

Bipolar disorder is a serious brain illness. It is also called manic-depressive illness or manic depression. People with bipolar disorder go through unusual mood changes. Sometimes they feel very happy and “up,” and are much more energetic and active than usual. This is called a manic episode. Sometimes people with bipolar disorder feel very sad and “down,” have low energy, and are much less active. This is called depression or a depressive episode.

Bipolar disorder is not the same as the normal ups and downs everyone goes through. The mood swings are more extreme than that and are accompanied by changes in sleep, energy level, and the ability to think clearly. Bipolar symptoms are so strong that they can damage relationships and make it hard to go to school or keep a job. They can also be dangerous. Some people with bipolar disorder try to hurt themselves or attempt suicide.

People with bipolar disorder can get treatment. With help, they can get better and lead successful lives.

Who develops bipolar disorder?

Anyone can develop bipolar disorder. It often starts in a person’s late teen or early adult years. But children and older adults can have bipolar disorder too. The illness usually lasts a lifetime.

Why does someone develop bipolar disorder?

Doctors do not know what causes bipolar disorder, but several things may contribute to the illness. Family genes may be one factor because bipolar disorder sometimes runs in families. However, it is important to know that just because someone in your family has bipolar disorder, it does not mean other members of the family will have it as well. Another factor that may lead to bipolar disorder is the brain structure or the brain function of the person with the disorder. Scientists are finding out more about the disorder by studying it. This research may help doctors do a better job of treating people. Also, this research may help doctors to predict whether a person will get bipolar disorder. One day, doctors may be able to prevent the illness in some people.

What are the symptoms of bipolar disorder?

Bipolar “mood episodes” include unusual mood changes along with unusual sleep habits, activity levels, thoughts, or behavior. People may have manic episodes, depressive episodes, or “mixed” episodes. A mixed episode has both manic and depressive symptoms. These mood episodes cause symptoms that last a week or two or sometimes longer. During an episode, the symptoms last every day for most of the day.

Mood episodes are intense. The feelings are strong and happen along with extreme changes in behavior and energy levels.

People having a manic episode may:

• Feel very “up” or “high”
• Feel “jumpy” or “wired”
• Have trouble sleeping
• Become more active than usual
• Talk really fast about a lot of different things
• Be agitated, irritable, or “touchy”
• Feel like their thoughts are going very fast
• Think they can do a lot of things at once
• Do risky things, like spend a lot of money or have reckless sex

People having a depressive episode may:

• Feel very “down” or sad
• Sleep too much or too little
• Feel like they can’t enjoy anything
• Feel worried and empty
• Have trouble concentrating
• Forget things a lot
• Eat too much or too little
• Feel tired or “slowed down”
• Have trouble sleeping
• Think about death or suicide

Can someone have bipolar disorder along with other problems?

Yes. Sometimes people having very strong mood episodes may have psychotic symptoms. Psychosis affects thoughts and emotions as well as a person’s ability to know what is real and what is not. People with mania and psychotic symptoms may believe they are rich and famous, or have special powers. People with depression and psychotic symptoms may believe they have committed a crime, they have lost all of their money, or that their lives are ruined in some other way.

Sometimes behavior problems go along with mood episodes. A person may drink too much or take drugs. Some people take a lot of risks, like spending too much money or having reckless sex. These problems can damage lives and hurt relationships. Some people with bipolar disorder have trouble keeping a job or doing well in school.

Is bipolar disorder easy to diagnose?

No. Some people have bipolar disorder for years before the illness is diagnosed. This is because bipolar symptoms may seem like several different problems. Family and friends may notice the symptoms but not realize they are part of a bigger problem. A doctor may think the person has a different illness, like schizophrenia or depression.

People with bipolar disorder often have other health problems as well. This may make it hard for doctors to recognize the bipolar disorder. Examples of other illnesses include substance abuse, anxiety disorders, thyroid disease, heart disease, and obesity.

How is bipolar disorder treated?

Right now, there is no cure for bipolar disorder, but treatment can help control symptoms. Most people can get help for mood changes and behavior problems. Steady, dependable treatment works better than treatment that starts and stops. Treatment options include:

1. Medication. There are several types of medication that can help. People respond to medications in different ways, so the type of medication depends on the patient. Sometimes a person needs to try different medications to see which works best.

Medications can cause side effects. Patients should always tell their doctors about these problems. Also, patients should not stop taking a medication without a doctor’s help. Stopping medication suddenly can be dangerous, and it can make bipolar symptoms worse.

2. Therapy. Different kinds of psychotherapy, or “talk” therapy, can help people with bipolar disorder. Therapy can help them change their behavior and manage their lives. It can also help patients get along better with family and friends. Sometimes therapy includes family members.

3. Other treatments. Some people do not get better with medication and therapy. These people may try electroconvulsive therapy, or ECT. This is sometimes called “shock” therapy. ECT provides a quick electric current that can sometimes correct problems in the brain.

Sometimes people take herbal and natural supplements, such as St. John’s wort or omega-3 fatty acids. Talk to your doctor before taking any supplement. Scientists aren’t sure how these products affect people with bipolar disorder. Some people may also need sleep medications during treatment.

Getting Help

If you’re not sure where to get help, call your family doctor. You can also check the phone book for mental health professionals. Hospital doctors can help in an emergency. Finally, the Substance Abuse and Mental Health Services Administration (SAMHSA) has an online tool to help you find mental health services in your area. You can find it here: https://findtreatment.samhsa.gov .

How can I help myself if I have bipolar disorder?

You can help yourself by getting treatment and sticking with it. Recovery takes time, and it’s not easy. But treatment is the best way to start feeling better. Here are some tips:

• Talk with your doctor about your treatment.
• Stay on your medication.
• Keep a routine for eating and sleeping.
• Make sure you get enough sleep.
• Learn to recognize your mood swings.
• Ask a friend or relative to help you stick with your treatment.
• Be patient with yourself. Improvement takes time.

How can I help someone I know with bipolar disorder?

Help your friend or relative see a doctor to get the right diagnosis and treatment. You may need to make the appointment and go to the doctor together. Here are some helpful things you can do:

• Be patient.
• Encourage your friend or relative to talk, and listen carefully.
• Be understanding about mood swings.
• Include your friend or relative in fun activities.
• Remind the person that getting better is possible with the right treatment.

I know someone who is in crisis. What do I do?

If you know someone who might hurt himself or herself, or if you’re thinking about hurting yourself, get help quickly. Here are some things you can do:

• Do not leave the person alone.
• Call your doctor.
• Call 911 or go to the emergency room.
• Call the National Suicide Prevention Lifeline, toll-free:
  1-800-273-TALK (8255). The TTY number is 1-800-799-4TTY (4889).

How does bipolar disorder affect friends and family?

When a friend or relative has bipolar disorder, it affects you too. Taking care of someone with bipolar disorder can be stressful. You have to cope with the mood swings and sometimes other problems, such as drinking too much. Sometimes the stress can strain your relationships with other people. Caregivers can miss work or lose free time.

If you are taking care of someone with bipolar disorder, take care of yourself too. Find someone you can talk to about your feelings. Talk with the doctor about support groups for caregivers. If you keep your stress level down, you will do a better job, and it might help your loved one stick to his or her treatment.

For More Information

National Institute of Mental Health
Office of Science Policy, Planning, and Communications
Science Writing, Press, and Dissemination Branch
6001 Executive Boulevard
Room 6200, MSC 9663
Bethesda, MD 20892-9663
Phone: 301-443-4513 or 1-866-615-NIMH (6464) toll-free
TTY: 301-443-8431 or 1-866-415-8051 toll-free
Fax: 301-443-4279
Email: nimhinfo@nih.gov
Website: http://www.nimh.nih.gov

U.S. Department of Health and Human Services
National Institutes of Health
National Institute of Mental Health

November 2015
NIH Publication Number TR 15-3679

Source:  https://www.nimh.nih.gov/health/publications/bipolar-disorder/index.shtml

Scientists at the University of Utah have found a link between short-term exposure to pollution and suicide – particularly for middle-aged men.

Examining the deaths of more than 1,500 men and women in Salt Lake City, Utah between 2000 and 2010, the findings draw an association between suicide and exposure to elements that exist in polluted air – nitrogen dioxide and fine particulate matter, small particles that can range from dust to combustible sources that float invisibly in the air.

The study, published yesterday in The American Journal of Epidemiology, was conducted by Amanda Bakian, an assistant professor of psychiatry at the university, and colleagues in the health sector.

Researchers found that there was a 20% increase in the odds of suicide in people who had short-term exposure to nitrogen dioxide in the two or three days prior to their deaths. A 5% increase in the odds was found in those who had exposure to high concentrations of fine particulate matter within that same time frame.

However, research shows that men were 25% more likely to commit suicide after being exposed to nitrogen dioxide and 6% more likely to do so after having exposure to fine particulate matter, a rate that increased by 20% for middle-aged men following nitrogen dioxide exposure, and 7% after being exposed to fine particulate matter.

“We examined the method of suicide, whether it was violent non-violent, the person’s gender, and the season in which they committed suicide,” Bakian says, “and there was a strong relationship between air pollutants and odds of suicide in men aged 36 to 64 who committed suicide in the spring time, as well as by individuals who died by violent methods.”

The reason is unclear, but Bakian says that there is potential that men in that age group have different exposure levels to air pollutants or have characteristics that are unique to them at that time in their life.

However, Bakian clearly states that research does not prove that pollution causes people to commit suicide. Rather, exposure to higher levels of pollution may increase the odds of suicide through the interaction with a variety of other factors at play.

She emphasises that suicide is complex, and believes that further research needs to be done before a definitive reason for the link can be made. “Clearly not everyone is uniformly susceptible to the effects of air pollution,” she says. “The exposure required to affect the odds varies across individuals and in some individuals, even low to moderate levels of exposure can result in poor outcomes.”

Bakian says there could be personal characteristics that increase the risk, co-occurring medical issues, lifestyle factors or a combination of different characteristics that are unique to men. Alternatively, Bakian says that men may just get more exposure to pollution than women.

According to Bakian, suicide is the eighth cause of death in Utah and the tenth in the United States.

“It is a preventable outcome,” she says. “We hope that finding out more about the correlation may help lead to its prevention, as well as interventions in public health.” Funding for the research provided in part by the university’s Program for Air Quality, Health and Society programme has been expanded to run state-wide.

Source:  BY CATHERINE PHILLIPS ON 2/13/15 AT 1:28 PM     

Particulate aerosols & Suicide copy .      

http://www.newsweek.com/study-finds-link-between-pollution-and-suicide-306706

DIRTY MEDICINE

May 15, 2013: 9:03 AM ET The epic inside story of long-term criminal fraud at Ranbaxy, the Indian drug company that makes generic Lipitor for millions of Americans. By Katherine Eban

1. The assignment FORTUNE

On the morning of Aug. 18, 2004, Dinesh Thakur hurried to a hastily arranged meeting with his boss at the gleaming offices of Ranbaxy Laboratories in Gurgaon, India, 20 miles south of New Delhi. It was so early that he passed gardeners watering impeccable shrubs and cleaners still polishing the lobby’s tile floors. As always, Thakur was punctual and organized. He had a round face and low-key demeanor, with deep-set eyes that gave him a doleful appearance.

His boss, Dr. Rajinder Kumar, Ranbaxy’s head of research and development, had joined the generic-drug company just two months earlier from GlaxoSmithKline, where he had served as global head of psychiatry for clinical research and development. Tall and handsome with elegant manners, Kumar, known as Raj, had a reputation for integrity. Thakur liked and respected him.

Like Kumar, Thakur had left a brand-name pharmaceutical company for Ranbaxy. Thakur, then 35, an American-trained engineer and a naturalized U.S. citizen, had worked at Bristol-Myers Squibb (BMY) in New Jersey for 10 years. In 2002 a former mentor recruited him to Ranbaxy by appealing to his native patriotism. So he had moved his wife and baby son to Gurgaon to join India’s largest drugmaker and its first multinational pharmaceutical company.

When he stepped into Kumar’s office that morning, Thakur was surprised by his boss’ appearance. He looked weary and uneasy, his eyes puffy and dark. He had returned the previous day from South Africa, where he had met with government regulators. It was clear that the meeting had not gone well.

The two men strolled into the hall to order tea from white-uniformed waiters. As they returned, Kumar said, “We are in big trouble,” and motioned for Thakur to be quiet. Back in his office, Kumar handed him a letter from the World Health Organization. It summarized the results of an inspection that WHO had done at Vimta Laboratories, an Indian company that Ranbaxy hired to administer clinical tests of its AIDS medicine. The inspection had focused on antiretroviral (ARV) drugs that Ranbaxy was selling to the South African government to save the lives of its AIDS-ravaged population.

*See Full Article:  Dirty medicine – Fortune Features copy (4)

Use B-Complex Vitamins and DHA to Keep Your Brain Sharp as You Age

If you want to keep your marbles as you grow older, it may be worthwhile focusing on two nutrients: B-complex vitamins and docosahexaenoic acid (DHA), one of the omega-3 fats found in fish oils. Three recent studies have found that these nutrients play major roles in keeping the brain sharp.

In the first study, A. David Smith, PhD, of Oxford University, England, and his colleagues analyzed data from 168 men and women they treated with either B-vitamins or placebos. The subjects’ brain changes were also tracked with MRIs (magnetic resonance images) of the brain.

The supplements consisted of 800 mcg of folic acid, 500 mcg of vitamin B12, and 20 mg of vitamin B6 daily, which the subjects took for two full years. The study participants had been diagnosed with mild cognitive impairment and brain atrophy – problems likely to develop into Alzheimer’s disease. Smith also measured the subjects’ blood levels of homocysteine, one of the markers of B-vitamin deficiency and a risk factor for cardiovascular disease and Alzheimer’s. People taking the B vitamins experienced an average of 30 percent less brain shrinkage, but some of the patients had more than a 50 percent reduction in brain shrinkage, compared with those in the placebo group. Homocysteine levels also decreased significantly among those taking B vitamins, and the rate of response was related to initial homocysteine levels. People with higher homocysteine levels were more likely to benefit from the B vitamins.

In the second study, Giuseppe Astarita, DSc, of the University of California, Irvine, and his colleagues compared brain and liver levels of DHA in 37 people with Alzheimer’s and 14 without the disease. All of the tissues samples were obtained post mortem. People with Alzheimer’s had lower levels of DHA, which is a precursor for neuroprotective compounds. “There were statistically detectable differences in DHA content in all [brain] regions examined,” Astarita wrote.

Astarita determined that the low levels of DHA were related to a defect in the liver’s ability to convert tetracosahexaenoic acid (THA) to DHA. THA is the immediate metabolic precursor to DHA, and the conversation requires “D-bifunctional protein.” People with Alzheimer’s appear to lack the ability to make this particular protein. The finding “led us to hypothesize that the alteration in brain DHA might result from a systemic deficiency in the biosynthesis of this fatty acid,” Astarita wrote. Although Astarita did not explicitly suggest it, his research left open the possibility of using DHA supplements to bypass this defect.

Finally, Matthew F. Muldoon, MD, of the University of Pittsburgh in Pennsylvania and his colleagues measured blood levels of three omega-3 fats – alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and DHA – in 280 people between the ages of 35 and 54 years. None of the subjects had been taking omega-3 supplements.

People with higher levels of DHA performed better on tests given to gauge reasoning, mental flexibility, memory, and vocabulary. Muldoon wrote that the omega-3s are “emerging as important nutrients for optimal brain development and for possible protection against brain senescense…it is plausible that insufficient dietary intake is related to relatively poor cognitive abilities or performance throughout the lifespan…”

SOURCE: Nutrition Reporter,  Jack Challem. Nov. 2010 Vol.21 No.11

References: Smith DA, Smith SM, de Jager CA, et al. Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment: a randomized controlled trial. PLoS One, 2010;5:e12244. Astarita G, Jung KM, Berchtold NC, et al. Deficient liver biosynthesis of docosahexaenoic acid correlates with cognitive impairment in Alzheimer’s disease. PLoS One, 2010;5:e12538. Muldoon MF, Ryan CM, Sheu L, et al. Serum phospholipid docosahexaenoic acid is associated with cognitive functioning during middle adulthood. Journal of Nutrition, 2010;140:848-853. !

A Review of the Evidence

Pharmacogenetic Testing in Clinical Psychiatry

While the review of landmark observational and clinical trials that assessed supplementation with ω-3 fatty acids such as docosahexaenoic acid (DHA),revealed it was not beneficial in symptomatic AD, several observational and clinical trials of ω-3 supplementation in the pre-dementia stage of AD suggested it may slow early memory decline in APOE4 carriers, reported Hussein Yassine, MD, of the Keck School of Medicine at the University of Southern California in Los Angeles, and colleagues.

Results were mixed in patients with mild or no cognitive impairment, they wrote in JAMA Neurology.

DHA is critical to the formation of neuronal synapses and membrane fluidity, the authors explained.

“We hypothesize that DHA supplementation in APOE4 carriers can result in beneficial outcomes if the timing of the intervention precedes the onset of dementia. Given the safety profile, availability, and affordability of DHA, refining an interventional prevention study in APOE4 carriers is warranted,” they noted, adding that advanced brain imaging techniques could be used to identify optimal timing of DHA supplementation and treatment efficacy could be evaluated using specific biomarkers.

Their review of original articles, systematic reviews, and meta-analyses of ω-3 studies in AD showed that most associated higher levels of seafood, ω-3 consumption, or ω-3 blood levels with decreased incidence of AD, better cognitive measures, or preserved brain volume in AD-vulnerable regions.

One summary of 21 studies in a meta-analysis of of 181,580 participants, with 4,438 dementia cases identified over follow-up of 2 to 21 years, concluded that a single weekly serving of fish was associated with significantly lower risk for AD dementia.

A 2015 meta-analysis concluded that ω-3 supplementation significantly improved episodic memory in cognitively healthy older individuals.

“These studies indicate that APOE4 is a modifiable AD risk factor, and that the effect of APOE4 on AD pathologic changes can be attenuated with DHA supplementation,” Yassine’s group said.

Individuals with a single ε4 allele are three to four times more likely to develop AD as those without an ε4 allele, and people with two ε4 alleles have a 12-fold higher risk of developing AD, the researchers pointed out.

In an email to MedPage Today, Yassine stressed that the review was not intended to act as a recommendation for DHA supplementation. It was done “to stimulate interest in refining the role of high-dose DHA supplementation in a population at increased risk of AD using appropriately designed interventions. We think that long-term high-dose DHA supplementation in APOE4 carriers who are not avid seafood consumers may result in reducing AD incidence. This is evident from some of the epidemiology studies, but was difficult to demonstrate in randomized clinical trials given the limitations of trial designs.”

His group proposed that APOE4 carriers be classified into three stages based on disease severity.

In the earliest pre-dementia phase of the disease (stage I), participants would have evidence of brain imaging changes in areas vulnerable to AD. However, no cognitive changes, or only subtle ones, would be detectable.

“In this stage, brain DHA metabolism is altered by APOE4, and brain imaging or CSF biomarkers can be used to select at-risk individuals and monitor the efficacy of supplementation,” they explained.

It is for patients in an early prodromal stage of disease (stage II) that long-term high dose DHA supplementation could slow cognitive decline, the researchers stated. Patients in this group would have evidence of memory and/or executive decline but no significant impairment in activities of daily living.

Stage III would represent clinical AD with impairments in multiple cognitive domains. DHA supplementation would probably not be beneficial in this group.

Steven DeKosky, MD, of the McKnight Brain Institute in Gainesville, Fla., agreed that “it is almost surely correct that DHA won’t help much if at all in people with full-blown disease.”

But he cautioned that “the jury is still out on pre-AD. There isn’t much to say to clinicians about how they should act on this information other than to know that we somehow have to get a trial going to prove if it does help or not,” he told MedPage Today.

“This frequently gets translated into ‘My doctor said I should take DHA supplements,'” noted DeKosky, who was not involved in the review.

Calling the hypothesis “thoughtful,” DeKosky predicted that getting “evidence [of DHA supplementation’s value] for the jury” would not be easy. Such a study would have to run long enough to demonstrate the DHA supplementation is effective in delaying onset or emergence of signs or symptoms of AD, he stated.

“Given that DHA is not patented, no pharma will fund a study that long since many companies could sell it,” DeKosky said. “But that would be the evidence we would need.”

Yassine’s group plan to identify whether APOE4 carriers in the pre-dementia stage have measurable changes in brain DHA homeostasis, using novel imaging methods or cerebrospinal fluid DHA levels as an index of brain DHA. Then they will test to see whether high-dose DHA supplementation can offset these changes before the onset of AD dementia, Yassine explained.

by Kristin Jenkins 
Contributing Writer, MedPage Today January 16, 2017            

While the review of landmark observational and clinical trials that assessed supplementation with ω-3 fatty acids such as docosahexaenoic acid (DHA),revealed it was not beneficial in symptomatic AD, several observational and clinical trials of ω-3 supplementation in the pre-dementia stage of AD suggested it may slow early memory decline in APOE4 carriers, reported Hussein Yassine, MD, of the Keck School of Medicine at the University of Southern California in Los Angeles, and colleagues.

Results were mixed in patients with mild or no cognitive impairment, they wrote in JAMA Neurology.

DHA is critical to the formation of neuronal synapses and membrane fluidity, the authors explained.

“We hypothesize that DHA supplementation in APOE4 carriers can result in beneficial outcomes if the timing of the intervention precedes the onset of dementia. Given the safety profile, availability, and affordability of DHA, refining an interventional prevention study in APOE4 carriers is warranted,” they noted, adding that advanced brain imaging techniques could be used to identify optimal timing of DHA supplementation and treatment efficacy could be evaluated using specific biomarkers.

Their review of original articles, systematic reviews, and meta-analyses of ω-3 studies in AD showed that most associated higher levels of seafood, ω-3 consumption, or ω-3 blood levels with decreased incidence of AD, better cognitive measures, or preserved brain volume in AD-vulnerable regions.

One summary of 21 studies in a meta-analysis of of 181,580 participants, with 4,438 dementia cases identified over follow-up of 2 to 21 years, concluded that a single weekly serving of fish was associated with significantly lower risk for AD dementia.

A 2015 meta-analysis concluded that ω-3 supplementation significantly improved episodic memory in cognitively healthy older individuals.

“These studies indicate that APOE4 is a modifiable AD risk factor, and that the effect of APOE4 on AD pathologic changes can be attenuated with DHA supplementation,” Yassine’s group said.

Individuals with a single ε4 allele are three to four times more likely to develop AD as those without an ε4 allele, and people with two ε4 alleles have a 12-fold higher risk of developing AD, the researchers pointed out.

In an email to MedPage Today, Yassine stressed that the review was not intended to act as a recommendation for DHA supplementation. It was done “to stimulate interest in refining the role of high-dose DHA supplementation in a population at increased risk of AD using appropriately designed interventions. We think that long-term high-dose DHA supplementation in APOE4 carriers who are not avid seafood consumers may result in reducing AD incidence. This is evident from some of the epidemiology studies, but was difficult to demonstrate in randomized clinical trials given the limitations of trial designs.”

His group proposed that APOE4 carriers be classified into three stages based on disease severity.

In the earliest pre-dementia phase of the disease (stage I), participants would have evidence of brain imaging changes in areas vulnerable to AD. However, no cognitive changes, or only subtle ones, would be detectable.

“In this stage, brain DHA metabolism is altered by APOE4, and brain imaging or CSF biomarkers can be used to select at-risk individuals and monitor the efficacy of supplementation,” they explained.

It is for patients in an early prodromal stage of disease (stage II) that long-term high dose DHA supplementation could slow cognitive decline, the researchers stated. Patients in this group would have evidence of memory and/or executive decline but no significant impairment in activities of daily living.

Stage III would represent clinical AD with impairments in multiple cognitive domains. DHA supplementation would probably not be beneficial in this group.

Steven DeKosky, MD, of the McKnight Brain Institute in Gainesville, Fla., agreed that “it is almost surely correct that DHA won’t help much if at all in people with full-blown disease.”

But he cautioned that “the jury is still out on pre-AD. There isn’t much to say to clinicians about how they should act on this information other than to know that we somehow have to get a trial going to prove if it does help or not,” he told MedPage Today.

“This frequently gets translated into ‘My doctor said I should take DHA supplements,'” noted DeKosky, who was not involved in the review.

Calling the hypothesis “thoughtful,” DeKosky predicted that getting “evidence [of DHA supplementation’s value] for the jury” would not be easy. Such a study would have to run long enough to demonstrate the DHA supplementation is effective in delaying onset or emergence of signs or symptoms of AD, he stated.

“Given that DHA is not patented, no pharma will fund a study that long since many companies could sell it,” DeKosky said. “But that would be the evidence we would need.”

Yassine’s group plan to identify whether APOE4 carriers in the pre-dementia stage have measurable changes in brain DHA homeostasis, using novel imaging methods or cerebrospinal fluid DHA levels as an index of brain DHA. Then they will test to see whether high-dose DHA supplementation can offset these changes before the onset of AD dementia, Yassine explained.

The study was supported by the National Heart, Lung, and Blood Institute, the Alzheimer’s Association, the National Institute on Aging, the LK Whittier Foundation, and Huntington Medical Research Institute.

Donald Rauh M.D., Ph.D., FAPA

BACKGROUND

SOURCE:   Fish OIl & Asthma NEJM

N Engl J Med 2016; 375:2530-2539December 29, 2016DOI: 10.1056/NEJMoa1503734