Bipolar disorder more likely to cause premature death than smoking, study warns


 An alarming new study reveals people with bipolar disorder are significantly more likely to die prematurely. Researchers from the University of Michigan are showcasing a stark reality faced by individuals with this serious mental illness, which is characterized by extreme mood swings ranging from manic highs to depressive lows.

For the study, researchers analyzed data from two different groups. They found that people with bipolar disorder were four to six times more likely to die early than those without the disorder. This contrasted sharply with smokers, who were found to be only twice as likely to die prematurely, regardless of their bipolar status.

cigarette smoking

Utilizing data from 1,128 individuals, including 847 with bipolar disorder, the study began in 2006 and revealed that nearly all of the 56 deaths recorded were among those with the condition. The analysis, adjusted for statistical factors, showed that a diagnosis of bipolar disorder increased the likelihood of dying within a 10-year period sixfold compared to those without the disorder.

The team then corroborated these findings with another data set from over 18,000 patients at Michigan Medicine, the University of Michigan’s academic medical center. This larger pool included over 10,700 people with bipolar disorder and more than 7,800 without any psychiatric disorder. Here, they discovered that individuals with bipolar disorder were four times as likely to die during the study period than those without the disorder. Notably, high blood pressure was the only factor associated with a higher chance of dying during this period.

“Bipolar disorder has long been seen as a risk factor for mortality, but always through a lens of other common causes of death,” says study lead author Dr. Anastasia Yocum, data manager of the research program at the Heinz C. Prechter Bipolar Research Program, in a university release. “We wanted to look at it by itself in comparison with conditions and lifestyle behaviors that are also linked to higher rates of premature death.”

depression mental illness

The study’s findings highlight the urgent need for more action in the medical and public health communities to address the factors contributing to this heightened risk of death among people with bipolar disorder.

“To our major surprise, in both samples we found that having bipolar disorder is far more of a risk for premature death than smoking,” says study co-author Dr. Melvin McInnis, a professor of psychiatry at the University of Michigan Medical School. “Over the years there have been all kinds of programs that have been implemented for smoking prevention and cardiovascular disease awareness, but never a campaign on that scale for mental health.”

Other differences observed in the study included a higher likelihood of people with bipolar disorder to have ever smoked and a greater prevalence of females in this group. Additionally, the Prechter cohort with bipolar disorder was more likely to suffer from conditions like asthma, diabetes, high blood pressure, migraines, fibromyalgia, and thyroid issues.

“We need to know more about why people with bipolar have more illnesses and health behaviors that compromise their lives and lifespan and do more as a society to help them live more healthily and have consistent access to care,” concludes Dr. McInnis.

How Turmeric Can Save the Aging Brain From Dementia and Premature Death


How Turmeric Can Save the Aging Brain From Dementia and Premature Death

Presently, there are no pharmaceutical interventions that effectively slow, and certainly not reverse, age-related cerebrovascular pathologies linked to conditions such as Alzheimer’s disease and stroke. A new study on turmeric extract, however, indicates that a natural curative agent already exists and is close to the everyday consumer as their spice rack. 

A promising study published in Cellular Physiology and Biochemistry titled, “Dietary Curcumin Ameliorates Aging-Related Cerebrovascular Dysfunction through the AMPK/Uncoupling Protein 2 Pathway,”[i] reveals the primary polyphenol in turmeric known as curcumin (which gives it its golden hue) may provide what the study authors describe as an “effective therapeutic strategy to reverse age-related cerebrovascular dysfunction.”

Age-related cerebrovascular dysfunction is occurring on an epidemic scale in Western countries and include, “stroke, cerebral amyloid angiopathy, cognitive decline and neurodegenerative diseases.”  Presently, very few if any conventional medical interventions are capable of providing effective solutions, and none have been found to reverse underlying pathologies in conditions whose trajectories are generally characterized as ‘incurable.’ All the more reason why the new study holds so much promise in providing an evidence-based natural solution that is safe, effective, affordable and easily accessible as a familiar food ingredient.

The study was conducted using a rat model. 24-month old male rodents were given dietary curcumin (.2%), with young control rodents 6-months of age.  After one month of curcumin treatment, the researchers observed a ‘remarkable restoration’ of the impaired cerebrovascular endothelium-dependent vasorelaxation (i.e. the ability of the blood vessels to naturally relax) in the aging rats. They observed three distinct ‘molecular’ ameliorative effects:

  • Curcumin promoted eNOS and AMPK phosphylation: Increasing nitric oxide (NO) bioavailability enables the inner lining of the blood vessels (endothelium) to fully dilate, reducing cardiovascular risk factors such as hypertension and associated damage to the arteries. Increased 5′-AMP activated protein kinase (AMPK) activity is also associated with improved age-related endothelial function.
  • Curcumin upregulated mitochondrial uncoupling protein 2 (UCP2): UCP2 plays an important role in mitochondrial homeostasis and its optimal functionaing has been associated with increased lifespan.
  • Curcumin reduced Reactive Oxygen Species (ROS) production: ROS reduction is associated with decreased oxidative stress and related cellular damage.

The authors summarized their findings as follows:

“In summary, our findings provide the first evidence that chronic pharmacological AMPK/UCP2 pathway activation by curcumin treatment may be an effective therapeutic strategy to reverse age-related cerebrovascular dysfunction. Curcumin administration may represent a promising lifestyle intervention for preventing age-related cerebrovascular disturbances.”

A Massive Body of Research On Curcumin’s Brain Protective Properties

GreenMedInfo.com houses a database of over 3,000 abstracts from the National Library of Medicine on the health value of turmeric and/or curcumin in over 900 health conditions. View them all here: turmeric health benefits.  Of the 280 distinct beneficial physiological actions documented within this literature, 276 of them concern the spice’s neuroprotective properties. View them here: neuroprotective properties of turmeric.

While this latest study, and most of the research on our turmeric database is preclinical, there are reports of turmeric causing significant improvements in cerebrovascular dysfunction diseases such as Alzheimer’s. In a previous article titled, “Turmeric Produces ‘Remarkable’ Rocvery iin Alzheimer’s Patients,” we reported on the ability of turmeric to produce dramatic improvement in patients suffering from behavioral and psychological symptoms of dementia.

As we discussed in the article, other documented Anti-Alzheimer’s disease mechanisms of turmeric include:

  • Anti-inflammatory: Curcumin has been found to play a protective role against β-amyloid protein associated inflammation.[11]
  • Anti-oxidative: Curcumin may reduce damage via antioxidant properties.[12]
  • Anti-cytotoxic: Curcumin appears to protect against the cell-damaging effects of β-amyloid proteins.[13] [14]
  • Anti-amyloidogenic: Turmeric contains a variety of compounds (curcumin, tetrahydrocurcumin, demethoxycurcumin and bisdemethoxycurcumin) which may strike to the root pathological cause of Alzheimer’s disease by preventing β-amyloid protein formation.[15] [16] [17] [18]
  • Neurorestorative: Curcuminoids appear to rescue long-term potentiation (an indication of functional memory) impaired by amyloid peptide, and may reverse physiological damage by restoring distorted neurites and disrupting existing plaques.[19] [20]
  • Metal-chelating properties: Curcumin has a higher binding affinity for iron and copper rather than zinc, which may contribute to its protective effect in Alzheimer’s disease, as iron-mediated damage may play a pathological role.[21] [22]

Turmeric, of course, is not the only natural substance that has been proven to have value in neurodegenerative conditions.  For those looking for additional research on food and spice-based natural alternatives that are evidence based, here are additional substances that may be of value:

  • Coconut Oil: This remarkable substance contains approximately 66% medium chain triglycerides by weight, and is capable of improving symptoms of cognitive decline in those suffering from dementia by increasing brain-boosing ketone bodies, and perhaps more remarkably,within only one dose, and within only two hours.[23]
  • Cocoa: A 2009 study found that cocoa procyanidins may protect against lipid peroxidation associated with neuronal cell death in a manner relevant to Alzheimer’s disease.[24]
  • Sage: A 2003 study found that sage extract has therapeutic value in patients with mild to moderate Alzheimer’s disease.[25]
  • Folic acid: While most of the positive research on this B vitamin has been performed on the semi-synthetic version, which may have unintended, adverse health effects,  the ideal source for this B vitamin is foliage, i.e. green leafy vegetables, as only foods provide folate. Also, the entire B group of vitamins, especially including the homocysteine-modulating B6 and B12,[26] may have the most value in Alzheimer’s disease prevention and treatment. 
  • Resveratrol: this compound is mainly found in the Western diet in grapes, wine, peanuts and chocolate. There are 16 articles on our website indicating it has anti-Alzheimer’s properties.[27]
  • Gingko biloba: is one of the few herbs proven to be at least as effective as the pharmaceutical drug Aricept in treating and improving symptoms of Alzheimer’s disease.[28] [29]
  • Melissa offinalis: this herb, also known as Lemon Balm, has been found to have therapeutic effect in patients with mild to moderate Alzheimer’s disease.[30]
  • Saffron: this herb compares favorably to the drug donepezil in the treatment of mild-to-moderate Alzheimer’s disease.[31]

Finally, it is of utmost importance to understand that turmeric contains a wide range of therapeutic biomolecules and not to get fixated on simply curcumin. There are also water and alcohol soluble components of the plant that you won’t find in extracts standardized simply to curcuminoid content. For example, a fat soluble component known as aromatic turmerone has been found to be especially important for brain regeneration, capable as it is of stimulating the regeneration of neural stem cells and their subsequent differentation into functional and fully differentiated neurons. To learn more about the remarkable healing properties of aromatic tumerone and whole turmeric read my previous article on the topic: How WHOLE Turmeric Heals The Damaged Brain.


References

[i] Yunfei Pu, Hexuan Zhang, Peijian Wang, Yu Zhao, Qiang Li, Xing Wei, Yuanting Cui, Jing Sun, Qianhui Shang, Daoyan Liu, Zhiming Zhu. Dietary curcumin ameliorates aging-related cerebrovascular dysfunction through the AMPK/uncoupling protein 2 pathway. Cell Physiol Biochem. 2013 ;32(5):1167-77. Epub 2013 Nov 11. PMID: 24335167

Short-term exposure to low levels of air pollution linked with premature death among US seniors


 air pollution
Credit: CC0 Public Domain

Short-term exposures to fine particulate air pollution and ozone—even at levels well below current national safety standards—were linked to higher risk of premature death among the elderly in the U.S. according to a new study from Harvard T.H. Chan School of Public Health.

The risk was even higher among elderly who were low-income, female, or Black.

The study will be published December 26, 2017 in the Journal of the American Medical Association (JAMA).

“This the most comprehensive study of short-term exposure to pollution and mortality to date,” said Francesca Dominici, professor of biostatistics, co-director of the Harvard Data Science Initiative, and senior author of the study. “We found that the mortality rate increases almost linearly as  increases. Any level of air pollution, no matter how low, is harmful to human health.”

Studies have shown that fine inhalable particles (PM2.5) and —particularly ‘warm-season ozone,’ which occurs from April to September—are linked with increased mortality rates. Under the National Ambient Air Quality Standards (NAAQS) set by the U.S. Environmental Protection Agency (EPA), long-term exposures to PM2.5 are considered safe if they average 12 micrograms per cubic meter of air (12 μg/m3) or less per day over the course of a year. The 24-hour standard is 35 μg/m3. For warm-season ozone there is no annual standard; the 8-hour standard is 70 parts per billion (ppb).

The researchers assessed daily air pollution exposures using prediction models that provided accurate estimates of PM2.5 and ozone for most of the U.S., including unmonitored areas. They then linked the  with mortality data from the entire U.S. Medicare population residing in 39,182 zip codes (93% of all the zip codes in the U.S.), over a 13-year period from 2000-2012.

During the study period, 22 million people in the study population died. The study found that, for each 10 μg/m3 daily increase in PM2.5 and 10 ppb daily increase in warm-season ozone, the daily mortality rate increased by 1.05% and 0.51%, respectively. While this may seem a small increase, the public health impact is enormous if it’s applied to the whole U.S. population of seniors, according to the study authors. For example, an increase of just 1 μg/m3 in daily PM2.5 over the course of one summer in the U.S. would lead to 550 extra deaths per year and 7,150 extra deaths over the course of the 13-year study period. An increase of just 1 ppb in daily ozone over the summer would lead to 250 extra deaths per year or 3,250 extra deaths over 13 years.

Certain subgroups were particularly vulnerable to short-term air pollution. Among Medicaid-eligible (a proxy for low income) recipients, the mortality increase linked with increased PM2.5 was three times higher than that of people not eligible for Medicaid. Women and nonwhites also faced a mortality risk that was 25% higher than those who were male or white. Poverty, unhealthy lifestyle, or poor access to healthcare may play a role in such disparities, the researchers speculated.

A June 2017 study by some of the same Harvard Chan researchers found that long-term exposure to air pollution was linked with an increased risk of premature death, even at levels below the national standards for long-term exposures. Those results are playing a key role in a current review of the annual NAAQS by the EPA. Joel Schwartz, professor of environmental epidemiology at Harvard Chan School, said that the new findings about the short-term  risk from air pollution suggest that the EPA should re-evaluate the daily NAAQS as well.

“No matter where you live—in cities, in the suburbs, or in rural areas—as long as you breathe air , you are at risk,” said Qian Di, lead author of the study and a PhD student in the Department of Environmental Health.