Menopause: Hormone Replacement Therapy and NSAIDs

There is currently a great deal of uncertainty regarding the effect of hormone replacement therapy on heart disease in women subsequent to menopause. Premenopausal women are much less likely to experience heart attacks and strokes than men, a difference that does not exist between postmenopausal women and men.

One mechanism that might explain these observations relates to the effect of estrogen, which is thought to have a protective effect on the heart. Hormone replacement therapy consisting of replacement estrogen, and sometimes progesterone as well is often taken by women experiencing symptoms of menopause.

Evidence from observational studies and the Women’s Health Initiative (WHI) trial has suggested that hormone therapy protects against heart disease in the time just before and after menopause in women (perimenopause).

However, researchers have suggested that any beneficial effect of hormone replacement therapy on the heart might be counteracted by the effects of certain types of painkillers also being taken by women involved in the studies.

These painkillers, non-steroidal anti-inflammatory drugs (NSAIDs), prevent production of a molecule called prostacyclin. Prostacyclin plays a role in preventing blood clotting and is therefore thought to be important in protecting the heart.

Estrogen, however, acts to increase production of prostacyclin, and it is therefore theoretically possible that hormone replacement therapy does have a beneficial effect on heart health, but which is counteracted by the negative effects of NSAIDs.

In a 2007 study carried out by researchers in Spain and the United States, researchers wanted to find out whether there was any evidence for an interaction between NSAID use, hormone replacement therapy, and heart disease. Such understanding in turn might help to identify more clearly whether hormone replacement therapy protects against heart disease in specific subgroups of postmenopausal women.

This study was carried out using information from the UK's General Practice Research Database, which is the largest computer database of anonymous medical records from primary care anywhere in the world. It contains information entered by UK general practitioners on their patients' drug prescriptions, diagnoses, referrals to hospital, and other data.

The researchers searched for all individuals from the database who were aged between 50 and 84 years on 1 January 1997, and then followed them up through the database for four years, or until the individual died, reached 85 years of age, or was diagnosed with a heart attack or cancer.
From this search, the researchers found 1,673 women who had heart attacks or who died from coronary heart disease; these were considered “cases.” Then, these 1,673 women were matched against 20,000 “control” women of similar age.

Information was pulled out for each case or control on their use of hormone replacement therapy, NSAIDs (covering 21 different drugs, but most commonly diclofenac, ibuprofen, and naproxen), and various risk factors for heart disease.

The researchers then compared the use of hormone replacement therapy and NSAIDs between the cases and controls, while making statistical adjustments for other risk factors (such as diabetes and smoking, for example).

The researchers found that current use of hormone replacement therapy was associated with a lower risk of heart attack than non-use. The odds ratio (chance of a heart attack among hormone replacement therapy users compared to the chance among non-users of hormone replacement therapy) was 0.78.

However, when looking at women who used NSAIDs at the same time as hormone replacement therapy, the researchers found no suggestion of a reduction in risk of heart attack: the odds ratio for the chance of heart attack among this group of women, as compared to nonusers of both NSAIDs and hormone replacement therapy, was 1.50.

The researchers findings suggest that hormone replacement therapy and NSAIDs might interact, with NSAIDs acting against a role for hormone replacement therapy in preventing heart attacks.

Citation: Editors' Summary: García Rodríguez LA, Egan K, FitzGerald GA (2007) Traditional Nonsteroidal Anti-Inflammatory Drugs and Postmenopausal Hormone Therapy: A Drug–Drug Interaction? PLoS Med 4(5): e157 doi:10.1371/journal.pmed.0040157. Copyright: © 2007 Rodríguez et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License.

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COPD Awareness and Neglect

Chronic obstructive pulmonary disease (COPD) is a major and increasing global health epidemic that has received insufficient attention from the health-care profession, governments, and the pharmaceutical industry. Urgent action is now required to recognise COPD, predicted to soon become one of the major causes of death and disability, and to develop more effective prevention and treatment strategies in the management of COPD.

What Is COPD?

COPD is described by the Global Initiative for Chronic Obstructive Lung Disease as “a preventable and treatable disease characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases”.

This progressive and relentless loss of lung function is caused by emphysema due to destruction of lung parenchyma and by narrowing of small airways as a result of chronic inflammation and fibrosis and loss of elastic recoil. This results in progressive airflow limitation, air trapping, and progressive shortness of breath on exertion.

Despite growing recognition as an important international health problem, COPD has suffered neglect from clinicians, researchers, and the pharmaceutical industry. (Lancet 364: 564–565).

This is largely because COPD is viewed as self-inflicted (by smoking) and also because the underlying disease process is generally perceived to be irreversible. Consequently, there is a fundamental lack of knowledge about the cellular, molecular, and genetic causes of COPD.

Existing therapies for COPD are inadequate and none have been shown to slow the relentless progression of the disease.

In terms of research funding, COPD has been relatively neglected among common diseases, with little investment in research into its underlying cellular and molecular mechanisms.

COPD is now recognised to have the greatest socioeconomic inequality of any common disease. It is also suggested that there are environmental factors other than smoking contributing to the disease.

Indeed, over 10% of patients with a clinical diagnosis of COPD are non-smokers, and this proportion is much higher amongst women in developing countries such as India, where exposure to biomass fuels in an enclosed space is an important cause of COPD. (Proc Natl Acad Sci U S A 97: 13286–13293).

The epidemiological (population) studies of Fletcher and Peto demonstrated that death and disability from COPD were related to an accelerated decline in lung function with time, with a loss of 50–100 ml in forced expiratory volume in one second (FEV1) per year, compared to the normal loss of less than 30 ml per year.

Only about 10% of smokers were thought to develop COPD, suggesting that genetic or other environmental factors may play an important role in susceptibility. Apart from FEV1, exercise capacity, exacerbation frequency, and systemic features all indicate a poor prognosis. (N Eng J Med 350: 1005–1012).

A more recent epidemiological (population) study with a longer follow-up (25 years) suggests that over 25% of smokers may develop COPD, with no difference in susceptibility between men and women. (Thorax 61: 935–939).

The implication of this study is that the prevalence of COPD amongst smokers is likely to rise even more as people survive longer.

Smoking cessation strategies have a poor success rate, with the most effective approaches yielding a quit rate of only about 15%. (Lancet 357: 1571–1575).

In any case, stopping smoking as the disease becomes more severe has little impact on its progression. (Am J Respir Crit Care Med 161: 381–390).

Several studies have now shown that smoking cessation fails to reverse the chronic airway inflammation. (Eur Respir J 26: 835–845).

This stresses the need for more effective anti-smoking strategies, including new and more effective drugs for nicotine addiction, and earlier intervention.

Anti-inflammatory drugs, which are used so successfully to manage asthma, have few clear beneficial effects in COPD and there is a very poor response to corticosteroids due to an active resistance against the anti-inflammatory actions of steroids. (Chest 129: 151–155).

Bronchodilators, which are the mainstay of current drug therapy, do not significantly affect the underlying disease process and therefore do not slow disease progression towards respiratory failure and death.

Although progress has recently been made in understanding the molecular, cellular, and genetic mechanisms involved in COPD, far more research is required in this area. This may lead to a better understanding of the mechanisms for disease progression and to the development of effective therapies in the future.

It is clearly necessary to increase awareness of COPD amongst health-care professionals, the general public, and governments.

General practitioners must be educated about how to recognize COPD and institute the most appropriate therapy.

The Global Initiative for Chronic Obstructive Lung Disease plays an important role in raising awareness of COPD amongst health-care professionals and has formulated updated evidence-based guidelines for diagnosis, therapy, and prevention. (Global Initiative for Chronic Obstructive Lung Disease 2006).

Stopping smoking early is very important, particularly for those in the early stages of the disease, in whom smoking cessation has a clear benefit and reduces mortality. (Ann Intern Med 142: 233–239).

More research is needed into the underlying disease mechanisms, to identify the genetics of susceptibility and to identify new targets for treatment. It is increasingly recognised that there is heterogeneity in the disease and more careful phenotyping is required in the future to elucidate disease mechanisms and optimise novel therapies. This will require much more investment from funding bodies and governments.

The attitude that smoking-related lung diseases are self-induced and therefore less worthy of attention needs to be changed; this attitude does not appear to apply to the same extent to ischemic heart disease, diabetes, or obesity.

Non-smoking causes of COPD will require far more attention in the future and the genetic and environmental cofactors that interact with COPD need to be more carefully explored.

Far more research needs to be done in developing countries where non-smoking causes of COPD account for a much greater proportion of COPD than in developed countries.

The striking socioeconomic disparities in COPD prevalence implicate factors other than smoking, but these factors have so far largely been ignored.

In the UK, respiratory disease, which includes COPD, receives less funding in relation to the burden of disease than any other disease area.

COPD will undoubtedly place an increasing burden on health resources and this burden is likely to be particularly severe in developing countries.

Finally, COPD needs to be more prominently featured in peer-reviewed journals that address global health issues - as recently pointed out by the editors of this journal. (PLoS Med 3: e512).

The author of this paper, Peter J. Barnes, is with the Airway Disease Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom.

Reference:
Extracted and adapted from: Barnes PJ (2007) Chronic Obstructive Pulmonary Disease: A Growing but Neglected Global Epidemic. PLoS Med 4(5): e112 doi:10.1371/journal.pmed.0040112. Copyright: © 2007 Peter J. Barnes. This is an open-access article distributed under the terms of the Creative Commons Attribution License.

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Coenzyme Q10: Exercise Duration Is Increased

Coenzyme Q10 appears to increase the duration of exercise to exhaustion in healthy untrained and trained individuals.

Coenzyme Q10 is a vitamin like, fat-soluble substance existing in all cells. Coenzyme Q10 acts as an essential antioxidant and supports the regeneration of other antioxidants. Coenzyme Q10 has been used as a supplementary treatment for chronic diseases such as Chronic Heart Failure (CHF), muscular dystrophies, Parkinson's disease, cancer, and diabetes.

In Chronic Heart Failure patients, a disease characterized by lower than normal Coenzyme Q10 levels, Coenzyme Q10 supplementation has shown to improve stroke volume, ejection fraction and exercise capacity in several double-blind, placebo-controlled studies.

In athletes, Coenzyme Q10 deficiency may also be experienced as metabolic stress and free radical formation is elevated during times of intense training.

Several studies have found that Coenzyme Q10 supplementation (60–100 mg/day for 4–8 weeks) improves aerobic power, anaerobic threshold, exercise performance, and/or recovery after exercise in trained athletes and untrained individuals.

Other studies using similar dosages have found no ergogenic benefit on maximal or submaximal exercise capacity in untrained and trained individuals.

One possible explanation for these inconsistent findings is that the absorption of Coenzyme Q10 into the mitochondrial membrane (part of a cell containing enzymes responsible for producing energy) or non-deficit tissues is rather inefficient.

Coenzyme Q10 is a relatively large, hydrophobic molecule, therefore absorption of Coenzyme Q10 into tissues is often slow and limited. Formulations that could maximize Coenzyme Q10 absorption would not only improve its uptake into the blood plasma, but potentially improve its absorption into the skeletal muscle.

Recently, the bioavailability and absorptive properties of several Coenzyme Q10 preparations were examined (i.e., fast-melt tablet, effervescent tablet, soft gelatin liquid capsule, and a hard shell powdered capsule).

Results indicated that the fast-melt tablet and effervescent formulation provided a more rapid delivery of Coenzyme Q10 to the blood, while exhibiting similar pharmacokinetic properties (the process by which a drug is absorbed, distributed, metabolized, and eliminated by the body) compared with the soft gel and hard capsule forms of Coenzyme Q10, suggesting that Coenzyme Q10 in a fast-melt or effervescent form may facilitate Coenzyme Q10 delivery and uptake to the muscle.

Researchers in the United States, reporting in the Journal of the International Society of Sports Nutrition, conducted a study to determine whether acute (single dose) and/or chronic (14-days) supplementation of Coenzyme Q10 would improve anaerobic and/or aerobic exercise performance by increasing blood plasma and muscle Coenzyme Q10 concentrations within trained and untrained individuals. (The above information is extracted from the same study).

The results of their study demonstrated that a fast-melt form of Coenzyme Q10 is a safe and effective supplement that prolongs exercise performance in healthy individuals. Further, acute Coenzyme Q10 supplementation increased total Coenzyme Q10 concentration within the skeletal muscle and lowered blood plasma oxidative stress during and following exercise.

Studies that have reported improvements in aerobic power, anaerobic threshold, and/or recovery following Coenzyme Q10 supplementation have not generally been published in peer-reviewed journals.

The authors of this study stated that, to their knowledge, this is the first study to demonstrate both improvements in exercise performance and increased muscle Coenzyme Q10 concentration in healthy trained and untrained humans following Coenzyme Q10 supplementation.

This study showed a strong trend for increased time to exhaustion following Coenzyme Q10 supplementation. Additionally, acute Coenzyme Q10 supplementation tended to increase Coenzyme Q10 levels within the muscle, albeit not significantly.

Though no significant changes were observed following chronic supplementation, it is evident that muscle Coenzyme Q10 concentration was generally higher at the end of the study, compared to the start of the study, in the Coenzyme Q10-supplemented group compared to the placebo group.

In fact, muscle Coenzyme Q10 levels declined in the placebo group over the 2-week period.

The findings indicate that ingestion of a fast-melt form of Coenzyme Q10 will increase blood plasma availability of Coenzyme Q10 and may also influence muscle concentrations on an acute and/or chronic basis.

The authors concluded that their study demonstrated that a fast-melt Coenzyme Q10 formulation appears to be a safe dietary supplement that tended to increase the duration of exercise to exhaustion in healthy untrained and trained individuals.

Reference:
Extracted and adapted from: Matthew Cooke, Mike Iosia, Thomas Buford, Brian Shelmadine, Geoffrey Hudson, Chad Kerksick, Christopher Rasmussen, Mike Greenwood, Brian Leutholtz, Darryn Willoughby and Richard Kreider. Effects of acute and 14-day coenzyme Q10 supplementation on exercise performance in both trained and untrained individuals. Journal of the International Society of Sports Nutrition 2008, 5:8. © 2008 Cooke et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0).

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Homocysteine Levels: What Lowers Homocysteine Levels Effectively and Safely?

In people who have dramatically elevated levels of homocysteine, different food supplements have been shown to bring down homocysteine levels and to reduce the risk of heart disease and strokes.

A link between high levels of homocysteine, a sulfur-containing amino acid, and heart disease was first suggested in the 1960s, when it became clear that patients with inborn errors of homocysteine metabolism were prone to develop severe cardiovascular disease in their teens and twenties.

Treatment with homocysteine-lowering substances such as folate, vitamin B12, vitamin B6 and betaine reduces the incidence of heart attacks and strokes in these patients.

Homocysteine is an amino acid in the blood (amino acids are the building blocks of proteins). Too much homocysteine in the blood is related to a higher risk of stroke and heart disease. Mildly elevated levels (which are quite common) might promote atherosclerosis (furring up of the arteries), but this link has not been proven yet. Studies are currently under way to test whether reducing homocysteine levels in people who have mildly elevated levels could prevent heart disease or stroke.

Several studies have found higher homocysteine levels in patients with coronary, peripheral, and cerebral vascular disease, particularly in those with vascular disease (vessels of the body, especially the arteries and veins) not readily explained by conventional risk factors such as high low-density lipoprotein (LDL) cholesterol, diabetes, or smoking.

Several studies then sought to determine whether elevated homocysteine levels were a cause or effect of cardiovascular disease, and evidence for a causal relationship is accumulating.

A study conducted in the Netherlands looked at the effects of betaine, folic acid, and phosphatidylcholine on blood lipids (fats) in healthy people. The researchers wanted to study blood lipids (fats), especially “bad” cholesterol (LDL cholesterol), because they are known to influence the risk of heart disease.

“We are keenly awaiting the results from several ongoing trials. In the meantime, our group is trying to determine the risks and benefits associated with different homocysteine-lowering nutrients,” said Margreet Olthof.

She and her colleagues at the Wageningen Centre for Food Science analysed four independent, placebo-controlled, randomized intervention studies that examined the effects of betaine, folic acid, and phosphatidylcholine on blood plasma homocysteine concentrations in healthy volunteers.

They analysed the blood samples (which had previously been used to measure homocysteine) for lipid levels (fats such as cholesterol and triglycerides) from the individual studies and compared changes in blood lipid concentrations between individuals taking homocysteine-lowering nutrients and those taking placebo.

The researchers found that betaine increased the level of “bad” cholesterol. Folic acid did not affect lipid (fat) levels. The data for phosphatidylcholine were not conclusive.

This suggests that the beneficial effects of betaine (which lowers homocysteine) might be undone at least in part by its negative effects on blood lipids.

Based on these results, folic acid would be a better choice for people who want to lower their homocysteine levels, since folic acid doesn't cause a rise in “bad” cholesterol.

References:
Olthof MR, van Vliet T, Verhoef P, Zock PL, Katan MB (2005) Effect of Homocysteine-Lowering Nutrients on Blood Lipids: Results from Four Randomised, Placebo-Controlled Studies in Healthy Humans. PLoS Med 2(5): e135 doi:10.1371/journal.pmed.. Copyright: © 2005 Olthof et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License.

(2005) Comparison of Homocysteine-Lowering Drugs. PLoS Med 2(5): e145 doi:10.1371/journal.pmed..

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Heart Health and Healthy Eating Habits

The health consequences of eating one large meal a day compared with eating three meals a day has not been established. Now two recently published journal articles are among the first to report the effects of meal skipping on key health outcomes, based on a study involving a group of normal-weight, middle-aged adults.

For the study, a small group of male and female volunteers participated in two eight-week meal-treatment periods.

The study's crossover design meant that each volunteer completed both of the treatment diets, enabling them to serve as their own controls.

Volunteers were divided into one of two groups during each treatment period.

They consumed either all of their required weight-maintenance calories in one meal a day or in three meals a day.

Agricultural Research Service physiologists David Baer and William Rumpler and National Institute on Aging neuroscientist Mark Mattson designed the study.

The first study analysis showed that consuming a one-meal-per-day diet, rather than a traditional three-meal-per-day diet, is feasible for a short duration. It showed that when the volunteers were "one-mealers," they had significant increases in total cholesterol, LDL "bad" cholesterol and in blood pressure, compared to when they were "three-mealers."

The changes in cardiovascular disease risk factors occurred despite the fact that the one- mealers saw slight decreases in their weight and fat mass in comparison to when they were three-mealers.

Those findings were published in the April 2007 issue of the American Journal of Clinical Nutrition.

Further analysis of the study group showed that when the volunteers were one-mealers, they had higher morning fasting blood sugar levels, higher and more sustained elevations in blood sugar concentrations, and a delayed response to the body's insulin, compared to when they were "three-mealers."

Insulin is required to lower blood sugar levels.

Those findings were published in the December 2007 issue of Metabolism.

Reference:
Rosalie Marion Bliss, U.S. Department of Agriculture, Agricultural Research Service February 15, 2008.

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Dealing With Depression During Pregnancy – Part 6

Whether or not to take antidepressants drugs was a difficult decision.

Stage 2. Gaining knowledge.

Hearing the diagnosis.
Receiving a definitive diagnosis, while difficult for some women, created a sense of relief and hope, and was a turning point for the women: it signified an identifiable, manageable disorder, justified and explained how they were feeling, and created a sense of relief, comfort, and hope upon hearing that they were “not the only one” to feel this way.

Many of the women had knowledge of postpartum depression, but few knew that depression could occur during pregnancy. One woman summed up this turning point as follows:

So, it's sort of almost a relief to find out that you are not the only
one, and there are actually reasons behind it. (#20) (Note: As mentioned in Part 1, confidentiality was maintained by assigning each participant a code number).

Although many of the women were embarrassed and ashamed, they were not surprised to be diagnosed with depression; it confirmed what they “already knew”. This was expressed by one participant as:

It was one of those things that you kind of know, but you don't
really admit it to anyone, even to yourself. (#19)

Seeking information
The question that was paramount to the women was whether or not to take antidepressants. The experiences of women varied considerably in their quest for information. Some found their family physician helpful:

But, he [family physician] was very open, probably because I
came with some informed sort of knowledge already, but he was
very willing, he did research on it as well, and he brought a
couple of studies to my attention. (#7)

Others reported that their family doctor "wasn’t really equipped to deal with the question” of antidepressant use. However, all women received information about depression and its management from the psychiatrist which was “really helpful”, and which many found sufficient.

She told me everything, and she also told me I could call
Motherisk and ask them. I didn’t call them, because I
thought about it, and her information was good. (#21)

Motherisk is a teratogen information counseling service based in Toronto, Canada. This program offers women who are pregnant, planning, or breastfeeding, a phone-in help service to answers questions about the risk or safety of medication use.

Others “wanted to check it out” for themselves and actively engaged in obtaining information via the Internet. One woman described her search for information as follows:

I started off with Motherisk and then medical journals online and
abstracts. I've definitely read stuff like on Safe Parent Web Site,
or Baby Centre Web Site. I tend to not trust them as much….. I
don't go into the whole journals, but usually just reading the
abstracts is enough to get a summary. (#7)

Stage 3. Taking control

The process of taking control, which is grounded in the personal and social context of the women’s lives, has three interrelated properties, making a plan, assessing progress, and balancing the risks. It is important to note that the properties making a plan, assessing progress and balancing the risks are not unidirectional, that is, the information flow and subsequent actions, may occur in either direction. As the depressive symptoms change over time, the assessment is updated, and the plan is reformulated. Nevertheless, the overall process is cyclical and moves in a clockwise direction. This is signified in the text and in Figure 1 by preceding the first word of each property with (Re).

(Re)Making a plan
Women spoke of “making a plan” in collaboration with their psychiatrist for managing their depression. Making a plan was informed by the women’s recently acquired knowledge, pragmatic knowledge, and their own and their husband’s values and beliefs about medication use. All women actively participated in, and took responsibility for, the management decision.

Although influenced by their husband’s concerns and beliefs, none of the women relinquished control of the management decisions to their husband. The act of doing so afforded the women a sense of regaining control over themselves and their lives and gave hope when they had been without hope.

It was comforting, and prepared me to say okay, how far am I
willing to go, not only medication, but therapy wise. I think that
set me in motion to say I am taking control over my moods, my
disorder. (#16)

Re(Assessing) progress
Assessments of the women’s mood were formally undertaken by the psychiatrist, and informally by the women themselves. If a woman’s mood worsened, or if she saw herself as “stagnating”, the plan was modified.

Changes included increased frequency of counseling sessions, incorporation of antidepressants in a management strategy that had been free of antidepressants, or, for those already taking antidepressants, an increase in dose.

She was doing that test, the EPDS. She would check the score each
time. It was very high in the beginning, and then slowly when I
started taking the medication, it became low. (#21)

(Re)Balancing the risks
In order to determine an acceptable management plan the majority of women undertook a risk assessment of the available management options. Accepting psychotherapy or counseling was not problematic for any of the women. However, for many women, whether or not to take antidepressants was a difficult and multifaceted decision. The women lamented the fact that there were no “black and white” answers, and struggled with what they perceived to be a complex decision.

The women considered: the risk of untreated depression to the fetus and to themselves; the likelihood of developing postpartum depression (PPD) and the associated risk to the baby, themselves and their family; and the potential risks to the baby of antidepressant use during pregnancy.

One woman articulated her concerns as follows:

You want to put the baby first, but, at the same time, you’re just
balancing out what is the risk to the baby of having a mom who is on
Prozac versus what is the risk to the baby of having a mom who is,
really can’t cope and is falling apart. I kind of got to the point where
I was like, well, I can only do the best I can as a mom. (#7)

Women tried to decrease the perceived risk to the fetus by taking as low an antidepressant dose as possible. For example, “I was kind of just teetering on, like I was trying to take the lowest dosage possible to treat my symptoms.” (#18).

Part 7 will be published soon - Consequences of Becoming the best mom that I can – Regrounding self and regaining control.

The researchers were Heather Bennett, Heather Boon, Sarah Romans and Paul Grootendorst. The above is a partially modified reproduction of their research. Also their references have been omitted for ease of reading.

Reference:
Bennett HA, Boon HS, Romans SE, Grootendorst P. Becoming the best mom that I can: women's experiences of managing depression during pregnancy – a qualitative study. BMC Women's Health 2007, 7:13 (11 September 2007). © 2007 Bennett et al., licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0).

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Foods High in Antioxidants

We’ve all read about the foods high in antioxidants but few studies have been aimed at investigating how well our bodies use these antioxidant-rich foods, and whether or not their ORAC (oxygen radical absorbance capacity) scores really translate into practical, disease-fighting capabilities in humans.

The ORAC method, which was developed and refined by ARS scientists, measures the capacity of a food to mop up the destructive free radicals that are generated when we engage in such everyday activities as eating, breathing, and exercising. Our bodies also stir up these unstable molecules when we’re battling a cold or a disease - or are exposed to pollution, cigarette smoke, or the sun’s ultraviolet rays.

So, to combat such oxidative assaults, is it enough to just feast on foods that researchers tell us are high in antioxidants?
Not necessarily. According to Ronald Prior, a chemist at USDA’s Arkansas Children’s Nutrition Center in Little Rock, to be clear about which foods offer the best antioxidant delivery system, we need a better understanding of how our bodies absorb and metabolize the many phytochemicals found in richly colored fruits and veggies.

“These plant compounds really vary in their bioavailability and may influence our bodies’ biological processes in many different ways,” he says.

And while several studies have linked the increased consumption of fruits and vegetables to a lower incidence of cancer and other diseases, Prior says that scientists haven’t really been able to pinpoint which components in foods are responsible for the beneficial effects.

To learn more, Prior and colleagues recently investigated how various fruits, all known for their impressive antioxidant content, affected the blood antioxidant levels of volunteers.

Collaborators included researchers at the USDA Human Nutrition Research Center on Aging at Tufts University in Boston, Massachusetts; the USDA Western Human Nutrition Research Center in Davis, California; and the University of Maine in Orono.

Volunteers were asked to eat varying amounts of the fruits, which included Bing cherries, dried plums, kiwifruit, red grapes, strawberries, and wild blueberries. Most of the servings were relatively large.


For instance, volunteers in the cherry study popped down 45 of the small fruits; those enlisted in the kiwi study ate 4 entire fruits. Then, using the ORAC method, Prior and colleagues analyzed each volunteer’s blood levels for the fruit’s antioxidant capacity.

The grapes, kiwifruit, and wild blueberries were the best performers, according to Prior, whose findings were reported in the April 2007 issue of the Journal of the American College of Nutrition.

Wild blueberries are certainly one of the most-heralded antioxidant-rich fruits. But the study revealed that a larger serving of the berries - at least a half-cup to more than one cup - was needed to register a real spike in volunteers’ blood antioxidant levels. A so-called high dose, equalling one and one-third cups of the berries, triggered the most significant leap.

“The predominant phytochemicals in blueberries are anthocyanins, which aren’t readily absorbed or perhaps are unstable in the body and are degraded in the gastrointestinal tract before they are absorbed,” says Prior. But there’s still more to learn about the digestibility of this important class of compounds, he notes, since at least 27 different anthocyanins are found in wild blueberries.

Kiwifruit also drove up volunteers’ blood antioxidant capacity. “But we’re not really sure which compounds were responsible,” says Prior. “At least part of the increase can be attributed to the high vitamin C content of kiwis. That goes for strawberries as well.”

Plums, on the other hand, were a bit of a disappointment. Despite their inherently high levels of an antioxidant called “chlorogenic acid,” they didn’t induce an uptick in volunteers’ antioxidant levels. That’s because the pure form of chlorogenic acid isn’t readily absorbed by the human body.

The study yielded a few surprises, including the finding that blueberries and cherries increased volunteers’ lipophilic, or fat-soluble, antioxidant capacity. “We didn’t expect that,” says Prior, “since fruits and berries don’t contain a large amount of lipophilic antioxidants.”

Eating Is Stressful - Antioxidants Can Help

Making wise food choices is hard enough work. But who knew that the mere act of eating can leave our bodies’ cells battered and beleaguered?

In the process of breaking down and metabolizing food, our bodies generate a lot of free radicals. “And without any antioxidants present, like those from colorful fruits and vegetables, for instance, there’s nothing to counteract this detrimental effect,” says Prior.

Antioxidants can almost be viewed as an antidote to the body’s problematic, not-100-percent-effective, energy-processing system.

This cause-and-effect relationship between consumption of foods lacking in antioxidants and decrease in antioxidant blood levels was backed up by the study ARS conducted.

In it, volunteers who drank a shake containing carbohydrates, protein, and fat, but no antioxidants, produced blood samples with a reduced ability to counter noxious free radicals.

“We’re learning that antioxidants should be consumed with every meal,” says Prior. “And if you routinely skip antioxidants in your diet, over time, the excess number of free radicals being produced may begin damaging cellular components, ultimately leading to atherosclerosis, cancer, and other diseases.”

Eventually, Prior would like to make preliminary projections of antioxidant needs based on a person’s energy intake or calorie consumption. Of course, other factors - such as age, health, and environmental exposures to damaging oxidants - all influence an individual’s bodily antioxidant status.

In the meantime, most Americans can do their bodies good by eating the recommended amount of fruits and veggies every day.

Reference:Erin K. Peabody (formerly with ARS), U.S. Department of Agriculture, Agricultural Research Service. Photo courtesy ARS, USDA.

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Foods That Lower Cholesterol, Triglycerides and Prevent Cancer - Muscadine Grapes

Muscadine grapes are a natural food source for lowering both total cholesterol and LDL (bad) cholesterol levels, blood pressure, triglycerides and also protects against coronary heart disease, gastrointestinal diseases, and colon cancer.

Research conducted by ARS horticulturist James B. Magee and Mississippi State nutritionist Betty J. Ector predicts that the muscadine will not only be an alternative crop for growers in the Southeast, but a new health food as well.

Magee and Ector have found significant amounts of resveratrol the compound in French red and white wines that is being touted as an agent for lowering cholesterol levels and the risk of coronary heart disease - in the skin, pulp, and seeds of these grapes.

In a study reported January 1997 in Science, researchers at the University of Illinois at Chicago purified resveratrol from grape sources and showed it to have anticarcinogenic activity, meaning that it inhibits tumor promotion.

Muscadines also contain ellagic acid, a natural organic compound thought to inhibit the start of cancer caused by certain chemicals.

Muscadines are now marketed as juice, jellies, jams, preserves, syrups, and dessert toppings.
In processing muscadines, about 900 to 1,000 pounds of waste come from each ton.

Muscadines have tough, thick skins and yield less juice than other grapes, leaving the skin, pulp, and seeds as waste, or pomace. Some of this is used as fertilizer and livestock feed. But most remains to be disposed of in an environmentally acceptable way.

Betty J. Ector has big plans for the muscadine. In research jointly funded by USDA, the Mississippi State University nutritionist found that a puree of muscadine skins and pulp is an excellent source of resveratrol, dietary fiber, and some essential minerals and is high in carbohydrates and low in fat and protein.

"We found that powdered muscadine puree has more dietary fiber than oat or rice bran," Ector says. "And we know that high fiber consumption lowers blood pressure, serum triglycerides, and both total and LDL (bad) cholesterol levels.

It also protects against coronary heart disease, gastrointestinal diseases, and colon cancer.

Soluble fiber has extra benefits for diabetics by delaying glucose absorption and increasing the sensitivity of skeletal muscles to insulin."

In a study at Mississippi State University in which rats were fed diets containing three levels of powdered muscadine pomace puree, Ector found that those eating the muscadine showed significantly lower LDL cholesterol levels and higher HDL (good) levels than a control group.

Statistics show that French consumers drink a lot of wine and eat a lot of dietary fat, yet have low incidence of coronary heart disease. Researchers say that resveratrol in red wine probably accounts for this.

Resveratrol is a phytochemical in grapes and other plants that helps protect them from attack by pests or diseases.

"If you don't drink wine, try some jam or a muffin made from muscadines," says Ector. "They're an even better source of resveratrol.

One-half serving (2 fluid ounces) of unfiltered muscadine juice, one serving of muscadine jam, one medium muffin, or one-tenth serving of muscadine sauce contains about the same amount of resveratrol as 4 fluid ounces of red wine.

"We're also trying it as additive to beef patties containing 15 to 20 percent fat," Ector reports. "Eating foods made with muscadine products is a good way to get a significant amount of resveratrol in the average diet. And they taste great!"

Reference:
Doris Stanley, USDA, Agricultural Research Service. Photo courtesy UDSA, ARS.

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Natural Remedies for ADHD Children - Zinc

Most notable among ADHD studies are the ones particularly examining the relation between zinc and ADHD. Indeed, zinc is basic for the production and modulation of melatonin, which helps regulate dopamine function, supposed to be an important factor in ADHD and its treatment.

Therefore, ADHD children with zinc deficiency might benefit from a change in diet or from a therapeutic trial with zinc supplementation.

The present study shows the Parent and Teacher Rating Scale scores improved with zinc sulfate over this 6-week, double blind and placebo controlled trial. The efficacy of zinc sulfate to obtain a better improvement in children with ADHD seems to support the role of zinc deficiency in the etiopathogenesis [the cause and development] of ADHD.

The present study is in line with the recent trial that suggests a beneficial effect of zinc sulfate in the treatment of ADHD. (BMC Psychiatry 2004, 4:9).

…this group, least expected to have marginal zinc deficiency and with a nutritionally adequate diet by the Food Frequency Questionnaire, showed an involvement of zinc levels in ADHD symptoms. The data reported here suggest that zinc nutrition is involved in symptoms of inattention and, therefore, improving zinc nutritional status might improve inattentive symptoms. (J Child Adolesc Psychopharmacol. 2005 Aug;15(4):628-36).

Zinc supplements may exert their positive effects by helping to regulate the function of the neurotransmitter dopamine.

…a dopamine deficiency may underlie ADHD. Nora Volkow, M.D., a psychiatrist with Brookhaven National Laboratory in Upton, N.Y., and her colleagues found that intravenous injections of the drug most often prescribed to treat ADHD - methylphenidate (Ritalin) - increased dopamine levels in the brain. This result suggests that methylphenidate counters ADHD by increasing brain levels of dopamine. (Psychiatric News 16/3/2001 Volume 36 Number 6).

In a study led by scientists with USDA’s Agricultural Research Service, daily zinc supplements helped Chinese schoolchildren with very low body zinc levels to score better in perception, memory, reasoning and psychomotor skills such as eye-hand coordination.

Findings of the study with 372 Chinese schoolchildren - conducted in three poor, urban areas of China - support previous adult studies and have important implications for countries where low zinc intakes are common. They could also apply to the 10 percent of U.S. grade-school-age girls and 6 percent of boys who get less than half the Recommended Dietary Allowance of zinc through their diets. The RDA for this age group is 10 milligrams daily.

The Chinese children, age 6 to 9 years, were divided into three groups. One group took a 20-milligram zinc supplement daily for 10 weeks. A second group took the zinc supplement plus a micronutrient supplement containing all essential vitamins and minerals, except for zinc and four other minerals known to interfere with its absorption. A control group got only the micronutrients to alleviate any other deficiency that could affect performance on the psychological tests.

Before and after the supplement period, each child took a series of computer-administered tasks developed by the ARS psychologist. The tasks measured attention, perception, memory, reasoning and motor and spatial skills necessary for successful school performance.

The children who got the zinc supplement or zinc plus the micronutrients had the most improved performance, especially in perception, memory and reasoning skills.

In addition to peanuts, popcorn and whole wheat products, the most common source of zinc is red meat. Oysters are the richest source. (Judy McBride, USDA’s Agricultural Research Service).

References:

Shahin Akhondzadeh, Mohammad-Reza Mohammadi and Mojgan Khademi. Zinc sulfate as an adjunct to methylphenidate for the treatment of attention deficit hyperactivity disorder in children: A double blind and randomized trial [ISRCTN64132371]. BMC Psychiatry 2004, 4:9doi:10.1186/1471-244X-4-9. © 2004 Akhondzadeh et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL. http://www.biomedcentral.com/1471-244X/4/9

Judy McBride, USDA’s Agricultural Research Service.

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A Natural Remedy for Depression - Alleviating Sleep Apnea?

Could correcting sleep apnea remedy depression? Studies link sleep apnea and depression, therefore the correction of sleep apnea may be a remedy for depression. For more than twenty years studies have suggested the existence of a relationship between depression and obstructive sleep apnea in the general population.

A researcher at Stanford University found that in the general population of the United Kingdom, Germany, Italy, Portugal, and Spain about 800 of 100,000 individuals have both a breathing-related sleep disorder and a major depressive disorder with nearly 20% of the subjects who had one of these disorders also having the other. (J Clin Psychiatry 2003, 64:1195-200; quiz, 1274-6).

In clinical practice, the presence of depressive symptoms is often considered in patients with obstructive sleep apnea although sleep problems and specifically obstructive sleep apnea are rarely assessed on a regular basis in patients with a depressive disorder.

It is speculated that obstructive sleep apnea might not only be associated with a depressive syndrome, but its presence may also be responsible for failure to respond to pharmacological treatment and that undiagnosed obstructive sleep apnea might be exacerbated by antidepressant medications, such as benzodiazepines.

Although the benzodiazepines (central nervous system depressant drugs) may reduce sleep fragmentation, their long-term use may also cause health problems, such as complete obstructive sleep apnea in heavy snorers…(Am J Med. 1990 Mar 2;88(3A):25S-28S).

Obstructive sleep apnea is the most common form of sleep disordered breathing and is defined by frequent episodes of obstructed breathing during sleep. It is characterized by sleep-related decreases or pauses in respiration.

The prevalence of obstructive sleep apnea is higher in men than in women and is found in all age groups but its prevalence increases with age. In children, the prevalence of obstructive sleep apnea is less well known and has been estimated to be between 2-8%.

The estimated prevalence of sleep-disordered breathing in people between the ages of 30 to 60 years old was 9 percent for women and 24 percent for men. Male sex and obesity were strongly associated with the presence of sleep-disordered breathing. (N Engl J Med. 1993 Apr 29;328(17):1230-5).

Abnormal respiratory events are the hallmark of obstructive sleep apnea and are generally accompanied by heart rate variability and arousals from sleep, with frequent arousals being the most important factor resulting in excessive daytime sleepiness.

The extent to which daytime functioning is affected generally depends on the severity of obstructive sleep apnea. Symptoms other than excessive daytime sleepiness which greatly impact daytime functioning are neuropsychological symptoms such as irritability, difficulty concentrating, cognitive impairment, depressive symptoms, and other psychological disturbances. Therefore obstructive sleep apnea can easily mimic symptoms of a major depressive episode.

In 1997 researchers studied the relation between obstructive sleep apnea and depression and reported that 24% of 25 male patients with obstructive sleep apnea had previously seen a psychiatrist for anxiety or depression. (Arch Intern Med. 1977 Mar;137(3):296-300).

In 1989 researchers at the University of California Irvine Medical Center, found 67% of patients who presented to a major sleep disorders center reported an episode of depression within the previous 5 years, and 26% described themselves as depressed at presentation. (J Clin Psychol. 1989 Jan;45(1):51-60).

Of 50 patients who had severe obstructive sleep apnea most patients showed cognitive impairment; 76% had suspected or mild to severe deficits in terms of thinking, perception, memory, communication, or the ability to learn new information, resulting in a greater potential for being distractible, confused, and irritable. (J Chronic Dis. 1985;38(5):427-34).

In 1992 researchers in Spain found elevations in several depression scores in 23 obstructive sleep apnea patients (moderate to high severity) compared to 17 controls. Depression, schizophrenia, and hypochondriasis [chronic and abnormal anxiety about imaginary symptoms and ailments] were the highest scales. (Int J Neurosci. 1992 Feb;62(3-4):173-95).

Compared to patients who snore but do not have apnea, those with obstructive sleep apnea have more intense depressive symptoms (e.g., pessimism, inactivity, guilt) and somatic [physical] concerns. However, patients who snore but do not have apnea show psychological maladjustment that is in quality similar, but in quantity less severe, than those with obstructive sleep apnea. (Sleep. 1999 May 1;22(3):355-9).

Contradictory Research with Due to Limitations:

Researchers at the University of Kentucky, Department of Medicine, conducted a 5-year study of 95 normal older persons and did not find any significant depressive symptoms in elderly patients with a relatively mild obstructive sleep apnea, when compared to a control group without obstructive sleep apnea. (Chest. 1996 Sep;110(3):654-8).

However, there are multiple limitations to this study, besides a relatively small sample size for group comparisons and a non-representative study population.

Obstructive sleep apnea was only assessed at the start of the study, but not repeated at the five-year follow-up, i.e. neuropsychological data were compared between two groups based on obstructive sleep apnea status five years earlier.

Second, obstructive sleep apnea severity was mild even in the obstructive sleep apnea group.

Third, the groups differed significantly by age, with the obstructive sleep apnea group being older than the control group.

Finally, the drop out rate over the five years was very high with only 42 out of the initial 95 subjects completing the follow-up assessment. (Annals of General Psychiatry 2005, 4:13).

In 1998 researchers in Israel conducted a study comprising 2,271 patients (1,977 men, 294 women) with suspected Sleep Apnea Syndrome. They did not observe any association between respiratory disturbances and Symptom Check List 90 psychiatric questionnaire. (Chest. 1998 Sep;114(3):697-703).

However, the SCL-90 psychiatric questionnaire was developed as a screening tool for psychiatric patients, and not for a normal study population. Therefore, it might be a less sensitive tool with regards to milder forms of mood disturbances than other scales. (Annals of General Psychiatry 2005, 4:13).

However, the researchers in the abovementioned study did observe that among the minority of women in the study, those with severe obstructive sleep apnea had higher depression scores than those with mild obstructive sleep apnea. (Chest. 1998 Sep;114(3):697-703).

Fewer studies have focused on the screening for obstructive sleep apnea in primarily depressed study groups.

Sleep apnea was found in 42.9% of demented patients, 17.6% of depressives, and 4.3% of controls. A significant association between sleep apnea and dementia of the Alzheimer type was found in women but not in men. Moreover, severity of dementia was significantly correlated with apnea index. (J Clin Psychiatry. 1985 Jul;46(7):257-61).

All of the above suggests that obstructive sleep apnea might be an important confounding factor for studies on mood disorders in general, as its presence is not routinely determined in either research studies examining mood or clinical settings.

More studies are required to assess the prevalence of obstructive sleep apnea in primarily depressed patients, particularly as it can be suspected from existing studies that obstructive sleep apnea is greatly under diagnosed in depressed patients.

Reference: Adapted from: Schröder CM, O'Hara R. Depression and Obstructive Sleep Apnea (OSA). Annals of General Psychiatry 2005, 4:13 (27 June 2005). Review. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0).

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Do Leptin Supplements Help Burn More Calories?

Leptin has become a hot area for obesity research since the discovery of a mutation in the mouse leptin gene that increases the animals' appetite while lowering their metabolic rate.

New findings, however, dampen the prospect that this hormone-like signal may explain differences in body fat among people.

The research was done at the Human Nutrition Research Center on Aging at Tufts, Boston. The center is funded by the Agricultural Research Service, USDA’s chief scientific agency.

The researchers found no relationship between the amount of leptin circulating in the blood of 61 men and women and the total number of calories they burned each day or their metabolic rate while resting or after eating.

The study volunteers ranged in age from 18 to 81, and none were obese.

The researchers concluded in the September issue of Obesity Research that leptin doesn't influence energy regulation in adults by increasing their energy expenditure.

In a study by others, young children with higher leptin levels reportedly burned more calories during physical activity. But the recent study indicates adults apparently lose their responsiveness to this signal.

Maintaining a stable body weight is a matter of burning as many calories as we consume.

In people whose weight control mechanism is working properly, the body's metabolic rate automatically revs up after periods of overeating and slows down after periods of undereating to maintain this balance.

Similarly, appetite automatically adjusts by decreasing or increasing. This process of energy regulation is controlled by a sequence of metabolic signals. But the details of that sequence are still sketchy.

To better understand leptin's role, Susan B. Roberts, who heads energy metabolism studies at the Boston center, and her colleagues examined how leptin might affect metabolic rate in adults.

Because leptin is produced by fat cells, the volunteers who had more body fat also had higher blood leptin levels. But that didn't prompt them to burn more calories.

Reference:
Agricultural Research Service, USDA’s chief scientific agency.

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