- quote -

Choline is quite helpful for autoimmune gut inflammation. If she's
allergic to soy, she can try the brand from Perque.

On Jun 12, 10:26 pm, Zubby <exubera...[at]rcn.com> wrote:
- quote -

I would either reduce carbohydrate intake or start some exercise, not
both at the same time. Also add just one thing at a time and wait cup
of days to see how things turn out.

- quote -

First thing I would do is to stop any Omega-3s, then add some
saturated fat in reasonable amounts (coconut oil, butter, palm kernel
oil), next reduce the sugar/carbohydrates or start some exercise
program appropriate for her condition and last add some AA slowly
watching for any "systemic inflammation" symptoms. Muscle "doms"
after exercise are OK. I wouldn't take any other lipids in a
supplemental form, just make sure all basic nutrients are available
through normal diet (protein, minerals, vitamins). Eating nutrient
dense foods like eggs, organ meat, nutritional yeast and fruit &
vegetables could help. Also proper regeneration, hot baths and high
quality sleep.

Taka

On Jun 11, 10:05 am, Taka <taka0...[at]gmail.com> wrote:
- quote -

I appreciate your thoughts & time about this! She's going to try it.
I will stress the sugar/diet caution. She's fairly sedentary (long
work hours at sit down job).... you think she should use this with
walking? She's been taking Omega 3's so she'll stop that. She also
was taking phosphatidyl choline & another supp of mixed phosphatidyl
lipids. If you think she should stop that too, please let me know.
She thought the phosphatidyl lipids could help the liver. We thought
the problem could in the liver too. Early on she tried MCT's via
coconut oil, but gave this up as it didn't see to have any effect.
Zubby

On Jun 11, 9:30 pm, Zubby <exubera...[at]rcn.com> wrote:
- quote -

I have written a lot about this AA supplement called X-Factor on
Monty's forum:

http://tinyurl.com/29tvpj

It's used in bodybuilding where BTW the need for cholesterol is also
higher ... Can be dangerous in sedentary metabolic syndrome type
people consuming high sugar diet though, so be careful. Also I
believe most of the cholesterol doesn't come from ingested fat but is
manufactured by liver from sugar/carbohydrates. So consistently low
cholesterol should signal a liver problem and liver can be damaged by
oxidative stress which is exacerbated by dietary PUFAs such as
Omega-3s. But the mentioned PLA2 defect leading to AA deficiency
could hamper the proper signaling needed for cholesterol production
(up)regulation in liver. If she gets sore muscles next day after some
physical work her AA release is probably OK and doesn't need to
supplement IMO unless different type of PLA2/AA release mechanism is
used in liver and muscles (not sure about this).

Taka

On Jun 10, 4:00 am, Taka <taka0...[at]gmail.com> wrote:
- quote -

This was fascinating! Given her celiac type condition, this idea is
quite conceivable. I'm going to try to find this supplement - worth a
try to see if it does anything. Thank you so much, Taka.

I think acetyl coenzyme A that is supposed to help make cholesterol.
I looked for a supplement with that & but I've only found precursor
supplements. Anyone think this idea is worth pursuing?
Z

I don't know if this is of any help here but low cholesterol and
ulceration is common in cPLA2a deficiency (total cholesterol 110
mentioned in the enclosed paper). This can be "easily fixed" by
supplementing arachidonic acid (AA) (Mead acid is unfortunately not
available). AA is present in organ meats especially heart and also
grain-fed farmed salmon has been mentioned here. Sold as BB
supplement as well.

Taka

J Clin Invest. 2008 Jun 2;118(6):2121-2131.

Inherited human cPLA(2alpha) deficiency is associated with impaired
eicosanoid biosynthesis, small intestinal ulceration, and platelet
dysfunction.

Adler DH, Cogan JD, Phillips JA, Schnetz-Boutaud N, Milne GL, Iverson
T, Stein JA, Brenner DA, Morrow JD, Boutaud O, Oates JA.

Departments of Medicine and Pharmacology, Division of Clinical
Pharmacology, Vanderbilt University Medical Center, Nashville,
Tennessee, USA. Department of Pediatrics, Division of Medical
Genetics, Vanderbilt University Medical Center, Nashville, Tennessee,
USA. Center for Human Genetics Research, Vanderbilt University Medical
Center, Nashville, Tennessee, USA. Department of Pharmacology,
Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Department of Medicine, Division of Digestive and Liver Diseases,
Columbia University Medical Center, New York, New York, USA.

Cytosolic phospholipase A(2alpha )(cPLA(2alpha)) hydrolyzes
arachidonic acid from cellular membrane phospholipids, thereby
providing enzymatic substrates for the synthesis of eicosanoids, such
as prostaglandins and leukotrienes. Considerable understanding of
cPLA(2alpha )function has been derived from investigations of the
enzyme and from cPLA(2alpha)-null mice, but knowledge of discrete
roles for this enzyme in humans is limited. We investigated a patient
hypothesized to have an inherited prostanoid biosynthesis deficiency
due to his multiple, complicated small intestinal ulcers despite no
use of cyclooxygenase inhibitors. Levels of thromboxane B(2 )and 12-
hydroxyeicosatetraenoic acid produced by platelets and leukotriene
B(4 )released from calcium ionophore-activated blood were markedly
reduced, indicating defective enzymatic release of the arachidonic
acid substrate for the corresponding cyclooxygenase and lipoxygenases.
Platelet aggregation and degranulation induced by adenosine
diphosphate or collagen were diminished but were normal in response to
arachidonic acid. Two heterozygous single base pair mutations and a
known SNP were found in the coding regions of the patient's
cPLA(2alpha )genes (p.[Ser111Pro]+[Arg485His; Lys651Arg]). The total
PLA(2 )activity in sonicated platelets was diminished, and the urinary
metabolites of prostacyclin, prostaglandin E(2), prostaglandin D(2),
and thromboxane A(2 )were also reduced. These findings characterize
what we believe is a novel inherited deficiency of cPLA(2).
PMID: 18451993