"at least one of the following lifetime depressive or anxiety disorders:
major depressive disorder (47%), specific phobia (24%), social phobia
(16%), obsessive- compulsive disorder (9%), panic disorder (8%), bipolar
I disorder (6%), generalized anxiety disorder (4%), dysthymic disorder
(3%), and agoraphobia without panic disorder (1%).

The investigators found that major depressive disorder, bipolar I
disorder, panic disorder, specific phobia, and obsessive-compulsive
disorder were significantly more common among SLE subjects than among
other white women."

Hmmm, are you trying to tell us you are really a woman, or are
considering a gender change?  You are on the list for more then one
thing.

On Jun 29, 5:12 am, Janice Duffy <janicejake2...@yahoo.com> wrote:
Comorbid mood disorders impact upon recovery outcomes in a raft of
chronic diseases <<

I'll assume you meant to say ..

"People with lupus have a higher than normal rate of mental illness.
Does the increase of porphyrins in lupus have anything to do with
my being somewhat .. eccentric"

Rather than what I believe you .. really .. meant ..

SLE Patients Prone to Certain Depressive and Anxiety Disorders
NEW YORK (Reuters Health) Jun 25 - Several mood and anxiety disorders
are more common in women with systemic lupus erythematosus (SLE) than
in the general population, according to results of a study published
in the June 15th issue of Arthritis and Rheumatism.

"Although most research has focused on depressed mood or clinical
unipolar depression in people with SLE, other research suggests that
symptoms of anxiety may be equally important in this population," Dr.
Elizabeth A. Bachen, of Mills College, Oakland, California, and
colleagues write.

The researchers examined lifetime prevalence rates of depressive and
anxiety disorders in 326 white women with SLE. The subjects completed
the Composite International Diagnostic Interview (CIDI) for the
assessment of psychiatric disorders. They also completed the Systemic
Lupus Activity Questionnaire (SLAQ) to assess self-reported disease
activity in the last 2 months.

Of the 326 participants, 211 met the criteria for at least one of the
following lifetime depressive or anxiety disorders: major depressive
disorder (47%), specific phobia (24%), social phobia (16%),
obsessive-
compulsive disorder (9%), panic disorder (8%), bipolar I disorder
(6%), generalized anxiety disorder (4%), dysthymic disorder (3%), and
agoraphobia without panic disorder (1%).

The investigators found that major depressive disorder, bipolar I
disorder, panic disorder, specific phobia, and obsessive-compulsive
disorder were significantly more common among SLE subjects than among
other white women.

In contrast, generalized anxiety disorder and dysthymic disorder were
significantly less common in SLE patients.

"In our study, we found that self-reported disease activity in
patients with SLE, but not renal involvement (an important indicator
of disease severity), predicted lifetime diagnoses of major
depressive
disorder and presence of any mood or anxiety disorder," Dr. Bachen's
team reports. "It is possible that disease activity is more closely
tied to mental health outcomes because it reflects symptoms that
interfere with day-to-day activities and quality of life, such as
fatigue, rashes, pain, and swelling."

Arthritis Rheum 2009;61:822-829.

------------------

"PUFA as potential treatment of depressive disorders."

Depression Patients Show Altered Response To Pain
Article Date: 06 Nov 2008 - 0:00 PST

When anticipating pain, the brains of subjects with major depressive
disorder appear to react more strongly, and appear to display altered
functioning of the neural network that moderates pain sensitivity,
according to an article released on November 3, 2008 in Archives of
General Psychiatry, one of the JAMA/Archives journals.

"Chronic pain and depression are common and often overlapping
syndromes," write the authors. More than 75% of patients with
depression also manifest with recurring or chronic pain, while
between
30 and 60% of patients with chronic pain report symptoms of
depression. According to the authors, this association could have
important implications if there is a biological mechanism that can be
attributed. "Understanding the neurobiological basis of this
relationship is important because the presence of comorbid pain
contributes significantly to poorer outcomes and increased cost of
treatment in major depressive disorder," they say.

To investigate the association between major depressive disorder and
brain function in response to pain, Irina A. Strigo, Ph.D., of the
University of California San Diego, La Jolla, and colleagues examined
15 young adults diagnosed with major depressive disorder who were not
taking medication and 15 controls with the same level of education
but
without depression. The depressed patients were given a survey,
examining any tendencies to magnify, ruminate over, or feel helpless
when faced with pain. The study subjects all were studied using
functional magnetic resonance imagine (fMRI) as their arms were
exposed to a device heated to painfully high temperatures, which
averaged 115 to 116ºF (46.4 to 46.9ºC). Visual images were also
applied before any heat was applied: either a green shape, indicating
non-painful warmth, and a red shape, indicating painful warmth.

Patients with depression tended to have increased activation in
specific areas of the brain, including the right amygdala, when they
anticipated painful stimuli, in comparison to the reactions of the
controls. Depressed patients also showed decreased activation in
other
areas, such as those responsible for modifying pain by adjusting
sensitivity, over the course of the painful experience.

The percentage change in activation in the amygdala was then examined
in the context of the survey descriptions of helplessness, rumination
and victimization, to see if this action was associated with passive
coping styles. The authors write that the correlation existed:
"Significant positive correlations were observed in the major
depressive disorder group between greater helplessness scores and
greater activity in the right amygdala during the anticipation of
pain."

The authors indicate that this association could help elucidate the
basis behind the common comorbidity of chronic pain and depression.
"The anticipatory brain response may indicate hypervigilance to
impending threat, which may lead to increased helplessness and
maladaptative modulation during the experience of heat pain," they
write. "This mechanism could in part explain the high comorbidity of
pain and depression when these conditions become chronic."

They conclude: "Future studies that directly examine whether
maladaptive response to pain in major depressive disorder is due to
emotional allodynia [a pain response to a non-painful stimulus],
maladaptive control responses, lack of resilience and/or ineffectual
recruitment of positive energy resources will further our
understanding of pain-depression comorbidity."

Association of Major Depressive Disorder With Altered Functional
Brain
Response During Anticipation and Processing of Heat Pain
Irina A. Strigo, PhD; Alan N. Simmons, PhD; Scott C. Matthews, MD;
Arthur D. (Bud) Craig, PhD; Martin P. Paulus, MD
Arch Gen Psychiatry. 2008;65(11):1275-1284

-------------------

"5 weeks of a PUFA blend containing 70% alpha-linolenic acid"

PUFA induce antidepressant-like effects in parallel to structural and
molecular changes in the hippocampus.
Venna VR, Deplanque D, Allet C, Belarbi K, Hamdane M, Bordet R
Psychoneuroendocrinology 2008 Oct 8.

Epidemiological data suggest that omega-3 polyunsaturated fatty acids
(PUFA) consumption may be inversely correlated to the prevalence and
severity of depression but little is known about the underlying
mechanisms.
In this study, we experimentally investigated whether a chronic
supplementation with PUFA may induce antidepressant-like effects in
mice in parallel to brain structural and molecular changes.
Six weeks feeding with a PUFA-enriched diet induced behavioral
changes
in the Forced Swim Test (FST), the Tail Suspension Test and the
Novelty-Suppressed Feeding Test.
Moreover, more than 5 weeks supplementation with a PUFA blend
containing 70% alpha-linolenic acid induced antidepressant-like
effects in the FST with an increase in both swimming and climbing
behaviors.
The combination of a shorter duration of PUFA supplementation with a
low dose of imipramine also induced an additive effect in the FST.
Finally, PUFA supplementation was associated with an increase in the
hippocampal volume, an over-expression of both synaptophysin and
BDNF,
and a raise in the number of newborn cells.
Besides the possible modulation of brain plasticity, present results
highlight the effectiveness of PUFA given alone or in combination
with
antidepressant drug as potential treatment of depressive disorders.

Psychoneuroendocrinology [Psychoneuroendocrinology]

---------------
---------------

"Alpha-linolenic acid elevates eicosapentaenoic acid"

Omega-3 Fatty Acids May Benefit Adults and Children
with Depression

Summary:
In a review of 3 studies investigating the effects of omega-3 fatty
acids in the treatment of patients with depression - unipolar,
bipolar, and childhood - supplementation with omega-3 fatty acids,
specifically EPA (eicosapentaenoic acid) was found to have
beneficial effects.
In one study which involved 20 patients with unipolar recurrent
major depression, significant improvements were found after 3 weeks
of daily supplementation with EPA (in addition to antidepressant
drug therapy) as compared to a placebo.
In another study, involving 12 bipolar depression outpatients with
depressive symptoms, supplementation with 1.5 to 2.0 g/d EPA
for up to 6 months was found to reduce Hamilton depression scores
by at least 50% in 8 of the 10 subjects who completed at least 1
month of follow-up.
In the third study, involving 28 children between the ages of 6 and
12 with "childhood major depression," omega-3 fatty acids were
found to have significant benefits, according to ANOVA.
The authors conclude, "Omega-3 fatty acids were shown to be more
effective than placebo for depression in both adults and children in
small controlled studies and in an open study of bipolar
depression."

Keywords: DEPRESSION, CHILDHOOD MAJOR DEPRESSION,
BIPOLAR DEPRESSION, UNIPOLAR DEPRESSION - Omega-3
Fatty Acids, EPA, Eicosapentaenoic Acid, DHA, Fish Oil
Reference: "Omega-3 fatty acids in depression: a review of three
studies," Osher Y, Belmaker RH, CNS Neurosci Ther, 2009 Summer;
15(2): 128-33. (Address: Ministry of Health Beer Sheva Mental Health
Center, Faculty of Health Sciences, Ben Gurion University of the
Negev,
Beer Sheva, Israel.
E-mail: y...@bgu.ac.il ).
----------------

"Amounts that are easily achieved by dietary modification"
"Alpha-linolenic acid for 12 wk was sufficient to elevate erythrocyte
EPA"

Flaxseed oil and fish-oil capsule consumption alters human red blood
cell n-3 fatty acid composition: a multiple-dosing trial comparing 2
sources of n-3 fatty acid.
Am J Clin Nutr. 2008 Sep;88(3):801-9.
Barceló-Coblijn G, Murphy EJ, Othman R, Moghadasian MH, Kashour T,
Friel JK.
Department of Pharmacology, University of North Dakota, Grand Forks,
ND, USA.

BACKGROUND:
An increase in plasma n-3 fatty acid content, particularly
eicosapentaenoic acid (20:5n-3; EPA) and docosahexaenoic acid
(22:6n-3; DHA), is observed after consumption of fish oil-enriched
supplements.
Because alpha-linolenic acid (18:3n-3; ALA) is the direct precursor
of EPA and DHA, ALA-enriched supplements such as flax may have a
similar effect, although this hypothesis has been challenged because
of reported low conversion of ALA into DHA. OBJECTIVE:
To address this question, we designed a clinical trial in which flax
oil, fish-oil, and sunflower oil (placebo group) capsules were given
to firefighters (n = 62), a group traditionally exposed to
cardiovascular disease risk factors.
DESIGN:
Firefighters were randomly divided into 6 experimental groups
receiving 1.2, 2.4, or 3.6 g flax oil/d; 0.6 or 1.2 g fish oil/d; or
1 g sunflower oil/d for 12 wk.
Blood was drawn every 2 wk, and the total phospholipid fatty acid
composition of red blood cells was determined.
RESULTS:
As expected, fish oil produced a rapid increase in erythrocyte DHA
and total n-3 fatty acids.
The consumption of either 2.4 or 3.6 g flax oil/d (in capsules) was
sufficient to significantly increase erythrocyte total phospholipid
ALA, EPA, and docosapentaenoic acid (22:5n-3) fatty acid content.
There were no differences among groups in plasma inflammatory markers
or lipid profile.
CONCLUSIONS:
The consumption of ALA-enriched supplements for 12 wk was sufficient
to elevate erythrocyte EPA and docosapentaenoic acid content, which
shows the effectiveness of ALA conversion and accretion into
erythrocytes.
The amounts of ALA required to obtain these effects are amounts that
are easily achieved in the general population by dietary
modification.

PMID: 18779299

---------------

Alpha-Linolenic Acid: An Underappreciated Omega-3
6/18/2009 7:55:00 AM

Kelley Fitzpatrick, M.Sc., Contributing Editor

The inclusion of omega-3 fatty acids from flax oil and fish oil
are increasingly popular as food manufacturers seek to improve
the nutrient value of their products.
Flax contains the omega-3 fatty acid alpha-linolenic acid (ALA).
Fish oils are sources of the longer-chain omega-3s
eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).
Despite the positive attributes expounded for the category, and
omega-3s’ increasing presence in the marketplace, there is also
confusing messaging around the health effects of the specific
omega-3s, in particular the physiological significance of ALA vs.
fish-based EPA and DHA.
Recent headlines have warned consumers not to “confuse” the
benefits of these omega-3s and have downplayed the significance
of ALA for health.
However, ALA has an important role in reducing chronic disease
through conversion to EPA and DHA, as well as through its own
unique metabolic activities.
Additionally, what many fail to understand is the critical need for
both plant- and fish-based omega-3s, especially considering the
increasing predominance of omega-6 fatty acids in the diet.
ALA is the true “essential” omega-3 fatty acid, because it is the
parent fatty acid of the omega-3 family and must be obtained from
foods.
1 ALA’s essential nature is reflected in the federal government’s
dietary recommendations.
The current recommended Adequate Intake (AI), which represents
the average usual intake of a nutrient by healthy people, is based
on ALA, not EPA or DHA.
2 Diets deficient in ALA result in impaired vision in monkeys,
learning
deficits in rats and, in humans, very low levels of omega-3 fatty
acids
in plasma and red blood cells, as well as nervous system
abnormalities
such as numbness, weakness and pain in the legs.3

Fast conversion facts
ALA and its counterpart omega-6 essential fatty acid, linoleic acid
(LA),
are converted to longer-chain fatty acids by a series of alternating
desaturations and elongations.
Conversion is dependent upon a number of factors.
Estimates of the amount of ALA converted to EPA range from 0.2% to
8%, with young women showing a conversion rate as high as 21%.
4,5 Conversion of ALA to DHA appears limited in humans, with most
studies showing a conversion rate of about 0.05%, although one study
reported a figure of 4%, and a conversion rate of 9% was reported in
young women.
5 The large differences in the rates of ALA conversion reflect major
differences in study methodologies.
The impact that LA has on reducing ALA’s health benefits is often
overlooked. Diets rich in LA can reduce the conversion of ALA to
EPA and DHA.
For example, in a study of 22 healthy men, an LA-rich diet reduced
the EPA content of plasma phospholipids significantly after four
weeks
compared to a low-LA diet, even though both diets contained the same
amount of ALA.6
The absolute amounts of ALA and LA in the diet also affect ALA
conversion.
Decreasing the intake of LA has been found to increase the proportion
of dietary ALA converted into EPA, while increasing ALA intake can
increase the absolute amount of DHA synthesized.7

Healthy discoveries
Research indicates ALA consumption may reduce the risk of heart
disease and other inflammatory diseases by reducing inflammatory
compounds called cytokines and eicosanoids.
LA is converted to longer-chain omega-6 fatty acids, in particular,
arachidonic acid (AA), the precursor of eicosanoids, several of which
promote blood platelet aggregation, the clotting of blood within
blood
vessels (thrombosis) and inflammatory reactions.
ALA dampens inflammation by blocking the formation of the compounds
that promote it.
Inflammation is a feature of many chronic diseases,such as heart
disease, type 2 diabetes, metabolic syndrome, obesity, cancer and
Alzheimer’s disease.
In addition, ALA interferes with the conversion of LA to AA—acting
as a “nutritional brake” to block further synthesis of AA to its
pro-inflammatory eicosanoids.
For example, in a study of healthy men who consumed 1.75
tablespoons of flax oil daily for four weeks, the TXB2 (an inactive
metabolite of TXA2) concentration in immune cells decreased by
30%.
8 TXA2 is one of the most-potent known promoters of both
inflammation and platelet aggregation.
Similarly, concentrations of the pro-inflammatory cytokines TNF-α
and IL-1β in immune cells decreased 26% and 28%, respectively.
In another study, serum levels of TNF-α decreased by 43%, and
the production by immune cells of TNF-α and IL-1β decreased
between 18% and 22% in 23 people with high cholesterol levels
who consumed a diet rich in ALA compared with the average
American diet, further supporting the anti-inflammatory aspects
of ALA.9
ALA, EPA and DHA have all been shown to prevent sudden
death from arrhythmias in animals and reduce the risk of sudden
cardiac death in humans.
10,11,12 Arrhythmias are abnormal rhythms of the heart muscle
that can lead to sudden death.
ALA assists in achieving a normal heart rhythm by decreasing
the heart muscle recover time after a heart beat and by maintaining
a steady heart beat.13 In the Nurses’ Health Study, women who
consumed as little as 1.2 grams of ALA daily (the amount found
in less than 1 teaspoon of flax oil) had a 40% lower risk of sudden
cardiac death than women with a low-ALA diet.12
Epidemiological studies and, increasingly, clinical work support
the beneficial effects of ALA in minimizing the risk of heart disease
and for anti-inflammatory effects.
ALA is the main, if not only, omega-3 in the diet of at least one
billion vegetarians worldwide; despite not consuming fish,
vegetarians do not have a higher prevalence of chronic diseases
than nonvegetarians.
There is no doubt that EPA and DHA are beneficial, as these fatty
acids have been the subjects of thousands of clinical trials.
In Sept. 2004, FDA approved a qualified health claim for reduced
risk of coronary heart disease on conventional foods that contain
EPA and DHA.
This claim, however, does not extend to ALA, because ALA was
not a part of the petition process.
The FDA has never assessed nor denied a qualified health claim
for ALA.

Assessing intake
The current AI of ALA for men is 1.6 grams of ALA per day; for
women who are not pregnant or breastfeeding, it is 1.1 grams
of ALA per day.
Of these amounts, about 10%—160 mg per day for men and 110
mg per day for women—can come from a combination of EPA
plus DHA.2
Canadian children consume 1.2 grams of ALA and 92 mg of EPA
plus DHA on average every day.
Although their average omega-3 intake appears to be adequate,
only 61% of the children met the AI for ALA and only 22% met the
AI for EPA plus DHA.14
Some experts believe higher intakes of omega-3 fatty acids are
needed for health: an intake of 2.2 grams per day for ALA; an EPA
plus DHA intake of 500 mg per day to decrease the risk of coronary
heart disease; and an EPA plus DHA intake of 1,000 mg (or 1 gram)
per day for adults with diagnosed heart disease.15
Clinical studies suggest that 3.6 grams of ALA (found in less than
1.5 teaspoon of flax oil) can be converted by the body to 500 to 540
mg of long-chain omega-3s, bringing current intakes closer to that
recommended for reducing the risk of heart disease.16,17
It is unfortunate that in the “omega-3 debate” there are those who
choose to downplay the importance of ALA in the diet and simply
ignore the omega-6 side of the metabolic equation.
The typical North American diet is “deficient” in omega-3 fatty acids
and overly rich in omega-6 fatty acids.
The omega-6 to omega-3 ratio may be as high as 17:1 in some
Western diets.
In the Women’s Health Study, some women ate diets with a ratio
of 33:1.18 The omega-6 to omega-3 ratio recommended by
international nutrition agencies ranges from 4:1 to 10:1.19
The best route to improving one’s omega-6 to omega-3 ratio is
by decreasing the intake of omega-6 fats and increasing the
intake of the omega-3 fats ALA, EPA and DHA in whole foods,
flax, fortified foods and supplements.

Kelley Fitzpatrick is the director of health and nutrition for
Flax Canada 2015.
She has a Master of Science in nutrition and close to 20
years of experience linking agriculture to the disciplines of food
and health through research, marketing and promotion activities.
She can be reached at kell...@shaw.ca .
For more information about Flax Canada, log on to fc2015.ca or
healthyflax.com.

References

1. Whitney E, Rolfes, SR. 2005. Understanding Nutrition.
Belmont, CA: Wadsworth; p. 7.
2. Institute of Medicine. 2002. Dietary Reference Intakes
for Energy, Carbohydrate, Fiber, Fat, Fatty Acids,
Cholesterol, Protein, and Amino Acids, National
Academies Press, Washington, DC, pp. 7-1 to 7-69
(dietary fiber), 8-1 to 8-97 (fat and fatty acids).
3. Anderson GJ, Connor WE. 1989. On the demonstration
of ω-3 essential-fatty-acid deficiency in humans.
Am J Clin Nutr. 49:585-587.
4. Burdge GC, Calder PC. Conversion of α-linolenic acid
to longer-chain polyunsaturated fatty acids in human adults.
2005. Reprod. Nutr. Dev. 45:581-597.
5. Burdge GC, Wootton SA. 2002. Conversion of α-linolenic
to eicosapentaenoic, docosapentaenoic and docosahexaenoic
acids in young women. Br. J. Nutr. 88:411-420.
6. Liou YA, King DJ, Zibrik D, Innis SM. 2007. Decreasing
linoleic acid with constant α-linolenic acid in dietary fats
increases (n-3) eicosapentaenoic acid in plasma phospholipids
in healthy men. J. Nutr. 137:945-952.
7. Goyens PLL, Spilker ME, Zock PL, et al. 2006. Conversion
of α-linolenic acid in humans is influenced by the absolute
amounts of α-linolenic acid and linoleic acid in the diet and
not by their ratio. Am. J. Clin. Nutr. 84:44-53.
8. Caughey GE, Mantzioris E, Gibson RA, Cleland LG,
James MJ. 1996. The effect on human tumor necrosis
factor α and interleukin 1β production of diets enriched
in n-3 fatty acids from vegetable oil or fish oil. Am. J.
Clin. Nutr. 63:116-22.
9. Zhao G, Etherton TD, Martin KR, et al. 2007. Dietary
alpha-linolenic acid inhibits proinflammatory cytokine
production by peripheral blood mononuclear cells in
hypercholesterolemic subjects. Am. J. Clin. Nutr. 85:385-91.
10. Ander BP, Weber AR, Rampersad PP, et al. 2004.
Dietary flaxseed protects against ventricular fibrillation
induced by ischemia-reperfusion in normal and
hypercholesterolemic rabbits. J Nutr. 134:3250-3256.
11. Billman GE, Kang JX, Leaf A. 1999. Prevention of
sudden cardiac death by dietary pure ω-3 polyunsaturated
fatty acids in dogs. Circulation. 99:2452-2457.
12. Albert CM, Oh K, Whang W, et al. 2005. Dietary
α-linolenic acid intake and risk of sudden cardiac death
and coronary heart disease. Circulation. 112:3232-3238.
13. Christensen JH, Schmidt EB, Mølenberg D, Toft E. 2005.
Alpha-linolenic acid and heart rate variability in women
examined for coronary artery disease. Nutr Metab Cardiovasc
Dis. 15:345-351.
14. Madden SMM, Garrioch CF, Holub BJ. 2009. Direct diet
quantification indicates low intakes of (n-3) fatty acids in
children 4 to 8 years old. J Nutr. 139:1-5.
15. Gebauer SK, Psota TL, Harris WS, Kris-Etherton PM.
2006. n-3 Fatty acid dietary recommendations and food
sources to achieve essentiality and cardiovascular benefits.
Am J Clin Nutr. 83(suppl):1526S-1535S.
16. Burdge GC, Jones AE, Wootton SA. 2002.
Eicosapentaenoic and docosapentaenoic acids are
the principal products of α-linolenic acid metabolism
in young men. Br J Nutr. 88:355-363.
17. Emken EA, Adlof RO, Gulley RM. 1994. Dietary
linoleic acid influences desaturation and acylation of
deuterium-labeled linoleic and linolenic acids in young
adult males. Biochim Biophys Acta. 1213:277-288.
18. Miljanović B, Trivedi KA, Dana MR, et al. 2005.
Relation between dietary n-3 and n-6 fatty acids and
clinically diagnosed dry eye syndrome in women.
Am. J. Clin. Nutr. 82:887-893.
19. Gebauer SK, Psota, TL, Harris, WS, Kris-Etherton
PM. 2006. n-3 Fatty acid dietary recommendations and
food sources to achieve essentiality and cardiovascular
benefits. Am. J. Clin. Nutr. 83:1526S-1535S.

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh

Man Is A Herbivore!
http://tinyurl.com/4rq595

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

Most diets seem to be deficint in ALA