Re: Re: Arthritis >>>> CHD ALA

[Guest guest]

I think neither.

This pain was not diagnosable by my doc. And I think it points up something we continually do - we evaluate our condition in common medical terms. We don't have a medical eval for CRONies. Even WUSTL takes data and compares it with common medical limits.

Combine a low fat lacto, low sodium diet with a weight loss regimen, and an exercise regimen, and a lowered calorie regimen and you maybe get conflicts.

When I do a test, I'm pretty disciplined, so I can SEE the effect on ME. A lot of conventional stuff just doesn't work for me. I've done that since 1990 when I first decided to find out what causes hypertension.

I didn't, but I found out how to control it.

So the precise diet I need has been developing since Mar 2000. I've tested all kinds of fats/oils and came quickly to the conclusion that the least fat was best. But a low fat diet is tricky. I settled on soy oil back then to get the essentials. My veggie intake was not enough.

So it's hard to describe where the pain is. Place your finger on the right inside thigh between the large muscles. Also, on the right side of the upper arm between the bicep and bone. Also, on the inside of the forearm muscles.

It's taken me a cupla years to figure out if diet was involved. The pain started in my right shoulder using Niaspan which removes arachidonic acid. The low fat diet means I don't get a lot of burn with niacin since then. But AA comes from LA, so maybe I've been short of delta 6 desaturase. But using sunf oil should not have altered the gen of AA.

Anyway, one night I got the idea there's a connection between niacin, prostate, LA and ALA and the pain. So I added back the soy ALA. If the ALA is connected to inflammation, perhaps the pain of athero can be felt in the artery? Does ALA remove athero or build it?

Low fat = lowered LA and ALA.

Low fat --> prostate inflammation.

Low fat --> pain.

Niacin --> less AA --> pain.

Altern Ther Health Med. 2005 May-Jun;11(3):24-30; quiz 31, 79.

Does alpha-linolenic acid intake reduce the risk of coronary heart disease? A

review of the evidence.

Alpha-linolenic acid (ALA) is an n-3 polyunsaturated fatty acid found mainly in plant sources, including flaxseed oil, canola oil, and walnuts. Although substantial evidence indicates that consumption of long-chain n-3 polyunsaturated fatty acids from seafood reduces the risk of coronary heart disease (CHD), the effect of ALA intake on CHD risk is less well-established.

ALA may reduce cardiovascular risk through a variety of biologic mechanisms, including platelet function, inflammation, endothelial cell function, arterial compliance, and arrhythmia. Although clinical benefits have not been seen consistently in all studies, most prospective observational studies suggest that ALA intake reduces the incidence of CHD, and two randomized trials have demonstrated that a dietary pattern that includes fruits, vegetables, whole grains, nuts or legumes, and ALA-rich foods substantially reduces the recurrence of CHD events.

Additional observational and clinical studies will help establish the effects of ALA on CHD risk and determine whether such effects vary based on gender, duration of intake, background dietary intake of seafood, or other factors. Presently, the weight of the evidence favors recommendations for modest dietary consumption of ALA (2 to 3 g per day) for the primary and secondary prevention of CHD. PMID: 15945135

Br J Nutr. 2004 Oct;92(4):649-55.

Background diet influences the anti-inflammatory effect of alpha-linolenic acid in dyslipidaemic subjects.

Long-chain n-3 PUFA from fish oils are known to have anti-inflammatory effects. We evaluated the effect of alpha-linolenic acid (ALA), precursor of n-3 fatty acids, on serum inflammatory markers and soluble cellular adhesion molecules (sCAM) of dyslipidaemic males, relative to their background diet. Participants were assigned to two groups, based upon food intake patterns: (a) twenty-one dyslipidaemic subjects who habitually ate a Mediterranean-Cretan-type diet; ( nineteen dyslipidaemic subjects who normally ate a Westernised Greek diet. All were supplemented with 8.1 g ALA/d for 12 weeks. We determined serum amyloid A (SAA), C-reactive protein (CRP), macrophage colony-stimulating factor (MCSF), IL-6, soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 and soluble E-selectin concentrations at the beginning and the end of the ALA supplementation period. Serum baseline concentrations of inflammatory markers and sCAM were similar across the diet groups. Type of diet had a significant impact on the response of inflammatory markers to ALA supplementation. The Westernised Greek diet group showed a reduction in SAA (P<0.001), CRP (P=0.002), MCSF (P=0.005) and IL-6 (P=0.04) concentrations. The Mediterranean-Cretan-type background diet group showed a significant reduction only in MCSF concentrations (P=0.003). The sVCAM-1 concentrations were significantly reduced in both the Westernised Greek diet group (P=0.001) and the Mediterranean-Cretan-type diet group (P<0.001). The present study demonstrated that ALA supplementation lowered the serum concentrations of inflammatory markers more profoundly when the background diet was rich in saturated fatty acids and poor in MUFA. PMID: 15522134

J Nutr. 2004 Nov;134(11):2991-7.

Dietary alpha-linolenic acid reduces inflammatory and lipid cardiovascular risk factors in hypercholesterolemic men and women.

Alpha-linolenic acid (ALA) reduces cardiovascular disease (CVD) risk, possibly by favorably changing vascular inflammation and endothelial dysfunction. Inflammatory markers and lipids and lipoproteins were assessed in hypercholesterolemic subjects (n = 23) fed 2 diets low in saturated fat and cholesterol, and high in PUFA varying in ALA (ALA Diet) and linoleic acid (LA Diet) compared with an average American diet (AAD). The ALA Diet provided 17% energy from PUFA (10.5% LA; 6.5% ALA); the LA Diet provided 16.4% energy from PUFA (12.6% LA; 3.6% ALA); and the AAD provided 8.7% energy from PUFA (7.7% LA; 0.8% ALA). The ALA Diet decreased C-reactive protein (CRP, P < 0.01), whereas the LA Diet tended to decrease CRP (P = 0.08). Although the 2 high-PUFA diets similarly decreased intercellular cell adhesion molecule-1 vs. AAD (-19.1% by the ALA Diet, P < 0.01; -11.0% by the LA Diet, P < 0.01), the ALA Diet decreased vascular cell adhesion molecule-1 (VCAM-1, -15.6% vs. -3.1%, P < 0.01) and E-selectin (-14.6% vs. -8.1%, P < 0.01) more than the LA Diet. Changes in CRP and VCAM-1 were inversely associated with changes in serum eicosapentaenoic acid (EPA) (r = -0.496, P = 0.016; r = -0.418, P = 0.047), or EPA plus docosapentaenoic acid (r = -0.409, P = 0.053; r = -0.357, P = 0.091) after subjects consumed the ALA Diet. The 2 high-PUFA diets decreased serum total cholesterol, LDL cholesterol and triglycerides similarly (P < 0.05); the ALA Diet decreased HDL cholesterol and apolipoprotein AI compared with the AAD (P < 0.05). ALA appears to decrease CVD risk by inhibiting vascular inflammation and endothelial activation beyond its lipid-lowering effects. PMID: 15514264

Regards.

----- Original Message -----

From: Rodney

Sent: Thursday, July 07, 2005 9:55 AM

Subject: [ ] Re: Arthritis >>>> CHD ALA

Hi JW:So the pain that the soybean oil fixed ........... do you think it was joint pain? Or muscle pain? .............. Rodney.> Hi Rodney,> I recall some years back the opposite effect. It was suggested because arthritis sufferers used a lot of aspirin, et al NSAIDS, the CAD was delayed.> It makes sense to me that inflammation effects arteries as well as joints.> > And I will note something else - I think ALA may be needed for inflammation.> Forgoing the prostate fear, I switched back to soybean oil from sunflower/safflower oil to relieve pains in leg, shoulder and arm. That pain started when I sampled 1 gm of Niaspan for a month several years ago. Really changed my lipids. > I think I was not getting enough ALA, maybe the right LA/ALA combination. No article search yet, But I'm not going back to saff/sunf oil. > > Regards. > ----- Original Message ----- > From: Rodney > > Sent: Wednesday, July 06, 2005 8:34 PM> Subject: [ ] Arthritis >>>> CHD> > > Hi folks:> > Inflammation link apparently:> > http://heart.healthcentersonline.com/newsstories/arthritispatientsatri> skcoronaryartery.cfm> > http://snipurl.com/g2x9> > Rodney.