79 replies to this topic

[nameless]

Have you tried 50g of tomato paste a day (or equivalent amount of tomato products) plus 25-50g of unsweetened cocoa powder per day?

I haven't tried those yet, but they are on my list of future possibilties. I want to see if krill does anything first. I have a bad habit of trying multiple things at once, and if anything does help, I don't know which particular item did. One at a time will take longer, but at least I'll know what is beneficial or not.

As for carbs, I wouldn't say I'm on a high carb sort of diet, but it's probably not low carb either. It's sort of the low processed foods/low sugar/low corn syrup sort of diet. My carbohydrates probably consist of wheat, oats, plus sugars from fruit. I once tried dropping fruit and fruit juices for several months, and my HDL didn't rise... but my triglycerides oddly went up.

[health_nutty]

Imho, I would try the tomato or cocoa powder first, because they have much more research behind them than krill oil.

[krillin]

Niacin and niacinamide have very different effects. Niacin is good with respect to cholesterol and SIRT1, and lowers cAMP. Niacinamide doesn't help cholesterol, raises cAMP, stimulates GABA receptors, and is bad with respect to SIRT1.

Yes, they have different effects at first, but one of former's metabolites may be the latter (albeit indirectly):

http://www.pdrhealth.../nia_0184.shtml

Nicotinic and nicotinamide are metabolized through different pathways. Nicotinic acid is not directly metabolized to nicotinamide. It undergoes a number of metabolic steps to yield NAD+ which in turn can be converted to nicotinamide. Nicotinamide can be directly converted to nicotinic acid. Nicotinic acid is metabolized to nicotinic acid mononucleotide (NicMN, nicotinic acid ribonucleotide). NicMN is also the first niacin metabolite to which dietary L-tryptophan is converted. NicMN is converted to nicotinic acid adenine dinucleotide (NicAD, desamido-NAD+). NicAD is converted in turn to NAD+. NAD+ has a number of metabolic opportunities. These include, the formation of nicotinamide, NADP+, nicotinamide 5'-mononucleotide (NMN), cyclic ADP-ribose and nicotinic acid dinucleotide phosphate (NAADP). NAD+ also serves as the substrate for mono- (ADP-ribosyl)ation and poly(ADP-ribosyl)ation reactions. Nicotinamide is converted to nicotinic acid via the enzyme nicotinamidase. Nicotinamide is also metabolized to NMN which in turn is converted to NAD+.

You're forgetting that SIRT1 provides good effects in a process that converts NAD+ to nicotinamide, so nicotinic acid -> NAD+ -> nicotinamide is beneficial.

[tintinet]

Low carb to the benefit of what? Fat or protein? If the former, it would be consistent with the notion that low-fat diets tend to lower HDL.

Both- but likely fat predominant by caloric count.

[shadowrun]

Nameless -

The tomato data is also interesting, but I can't see myself eating half a can of tomato paste/sauce a day. Unless maybe V8 would work instead. Hmm... a glass of V8 + chocolate = big raise in HDL. That'd certainly be nice.

Watch out for V8!
I just found out the other day that it contains a version of MSG -
Bi or di sodium something or other, sorry I can't recall the substance exactly. I did look it up when I had the can in my hand and it was a version of Mono-sodium Glutamate (MSG)

Also most store bought stuffings...MSG laden!

[health_nutty]

Nameless -



Watch out for V8!
I just found out the other day that it contains a version of MSG -
Bi or di sodium something or other, sorry I can't recall the substance exactly. I did look it up when I had the can in my hand and it was a version of Mono-sodium Glutamate (MSG)

Also most store bought stuffings...MSG laden!

Which v8 is this? My spicy v8 in the US does not have MSG.

[lauritta]

What is your LDL/HDL and cholesterol/HDL ratio?

[nameless]

What is your LDL/HDL and cholesterol/HDL ratio?

I'll assume this question is for me, and not ilanso or someone else here.

I don't recall my exact numbers off-hand, but my ldl was around 125 or so (I think), and as I stated earlier in this thread, my hdl was 27, (from my last test). I don't recall my ratio, but it wasn't very good. Overall cholesterol was around 180ish.

My LDLs aren't perfect, but they've always been in the normal range, or thereabouts (under 130). Over the past 2 years they were usually in the 105-115 range. They recently shot up into the 120s, because I increased my dosage of omega 3s. This resulted in a reduction of my triglycerides and vldl, putting them into normal range (just barely). This ldl rise could be temporary (I'll find out), as I think when omega 3s lower vldl and intermediate ldl, it also converts some to normal ldl.

And I tried several other things at the same time, so I can't be 100% certain the omega 3s are what reduced my triglycerides. I was just happy to finally get them down. From a scientific standpoint, my triglyceride and HDL problems would indicate a pre-diabetic state or metabolic X syndrome. Only problem is, I have none of the other symptoms of metabolic X -- my fasting glucose levels are always normal, my body weight is fine, and I don't have hypertension. Sugar or reduction in carbohydrates doesn't seem to affect my HDL levels much either.

[ilanso]

You're forgetting that SIRT1 provides good effects in a process that converts NAD+ to nicotinamide, so nicotinic acid -> NAD+ -> nicotinamide is beneficial.

You mean, because the nicotinamidase longevity gene PNC1 (or human PBEF) reconverts niacinamide back to niacin under adverse conditions (such as CR or taking resveratrol, or even metformin)?
In that case, one wonders if supplementing with Niacin has not been rendered redundant by taking enough res / stress.
I see a related link by Lucid a few months ago (http://www.imminst.o...=0). Was there any follow-up?

[ilanso]

Have you tried 50g of tomato paste a day (or equivalent amount of tomato products) plus 25-50g of unsweetened cocoa powder per day?

I am using tomato powder (I bought a few kg), but am not sure how to convert into paste dosage. To compound the conversion dilemma, the study below uses whole tomatoes:

PMID: 17144439

CONCLUSION: We found that tomatoes'-rich diet (300g daily for one month) increased HDL-cholesterol level significantly by 15.2%.

There is a whole 'nother thread on cocoa - seems you need a special, hard to find kind (undutched).

Still, the most promising avenue may be:

While niacin's LDL-C lowering is linear, its effect on triglycerides and HDL-C is curvilinear. Modest doses of niacin can significantly alter these two lipid levels. For example, 1 g/d of immediate-release niacin can increase HDL-C by 25-30% and reduce triglycerides by a similar margin. Niacin is the most effective drug available for raising HDL-C. It also lowers lipoprotein(a) by about 30%.

I am going back on it, but @ 1g/d (immediate) before bed rather than 3g/d.

[health_nutty]

There is a whole 'nother thread on cocoa - seems you need a special, hard to find kind (undutched).

Undutched is incredibly easy to find in any supermarket. Most cocoa powder is undutched unless it specifically says dutched.

[tintinet]

Undutched cocoa (that be the non-alkali processed type) ain't hard to find. Harder to find the dutched type, IME.

[krillin]

You're forgetting that SIRT1 provides good effects in a process that converts NAD+ to nicotinamide, so nicotinic acid -> NAD+ -> nicotinamide is beneficial.

You mean, because the nicotinamidase longevity gene PNC1 (or human PBEF) reconverts niacinamide back to niacin under adverse conditions (such as CR or taking resveratrol, or even metformin)?

I haven't given much thought to that. My reasoning was that if you want SIRT1 to do something nice for you, you have to feed it NAD+ and it gives you niacinamide. This niacinamide product thus is something you can live with. Ingested niacinamide would be a negative because it would give you inhibition of the process without having received the beneficial effect of the process.

This paper says that niacin is better than niacinamide at increasing NAD+.

J Biol Chem. 2007 Aug 24;282(34):24574-82.
Elevation of cellular NAD levels by nicotinic acid and involvement of nicotinic acid phosphoribosyltransferase in human cells.
Hara N, Yamada K, Shibata T, Osago H, Hashimoto T, Tsuchiya M.
Department of Biochemistry, Shimane University Faculty of Medicine, 89-1, Izumo, Shimane 693-8501, Japan. nhara@shimane-u.ac.jp

NAD plays critical roles in various biological processes through the function of SIRT1. Although classical studies in mammals showed that nicotinic acid (NA) is a better precursor than nicotinamide (Nam) in elevating tissue NAD levels, molecular details of NAD synthesis from NA remain largely unknown. We here identified NA phosphoribosyltransferase (NAPRT) in humans and provided direct evidence of tight link between NAPRT and the increase in cellular NAD levels. The enzyme was abundantly expressed in the small intestine, liver, and kidney in mice and mediated [(14)C]NAD synthesis from [(14)C]NA in human cells. In cells expressing endogenous NAPRT, the addition of NA but not Nam almost doubled cellular NAD contents and decreased cytotoxicity by H(2)O(2). Both effects were reversed by knockdown of NAPRT expression. These results indicate that NAPRT is essential for NA to increase cellular NAD levels and, thus, to prevent oxidative stress of the cells. Kinetic analyses revealed that NAPRT, but not Nam phosphoribosyltransferase (NamPRT, also known as pre-B-cell colony-enhancing factor or visfatin), is insensitive to the physiological concentration of NAD. Together, we conclude that NA elevates cellular NAD levels through NAPRT function and, thus, protects the cells against stress, partly due to lack of feedback inhibition of NAPRT but not NamPRT by NAD. The ability of NA to increase cellular NAD contents may account for some of the clinically observed effects of the vitamin and further implies a novel application of the vitamin to treat diseases such as those associated with the depletion of cellular NAD pools.

PMID: 17604275

[pycnogenol]

I tried pantethine for about 2 months and it didnt seem to radically improve my #'s so I gave up and tried to get more disciplined with my experimentation.

Hi brainengineer,

What brand of pantethine were you taking? I've been taking Jarrow brand Pantethine 450 mg x 2 daily (900 mg) at breakfast and dinner for 3 months now and will have blood
work done at the end of October to see if it has helped me. I will post the results here.

[ilanso]

(tintinet)
Low carb diet raised my HDL from 65 mg/dl to 105 mg/dl....

(ilanso)
Low carb to the benefit of what? Fat or protein? If the former, it would be consistent with the notion that low-fat diets tend to lower HDL.

(tintinet)
Both- but likely fat predominant by caloric count.

September 14, 2007 — A low-carbohydrate, high-fat (LCHF) diet and a high-carbohydrate, low-fat (HCLF) diet both improve weight loss and mood, but speed of cognitive processing improves less with the LCHF than the HCLF diet, according to the results of a study published in the September issue of the American Journal of Clinical Nutrition.

Conclusions:

* Use of an LCHF or an HCLF calorie-restrictive diet is associated with significant weight loss during 8 weeks, with greater weight loss for the LCHF diet.
* Mood and cognitive function are both improved with an LCHF and an HCLF diet, but the HCLF diet is associated with greater improvement in speed of processing.

[ilanso]

Thinking used to be HDL doesn't much matter if your LDL is under the radar. Now it seems low HDL is always undesirable:

HDL cholesterol, very low levels of LDL cholesterol, and cardiovascular events.
Barter P, Gotto AM, LaRosa JC, Maroni J, Szarek M, Grundy SM, Kastelein JJ, Bittner V, Fruchart JC; Treating to New Targets Investigators.

Heart Research Institute, Sydney, Australia. barterp@hri.org.au

BACKGROUND: High-density lipoprotein (HDL) cholesterol levels are a strong inverse predictor of cardiovascular events. However, it is not clear whether this association is maintained at very low levels of low-density lipoprotein (LDL) cholesterol. METHODS: A post hoc analysis of the recently completed Treating to New Targets (TNT) study assessed the predictive value of HDL cholesterol levels in 9770 patients. The primary outcome measure was the time to a first major cardiovascular event, defined as death from coronary heart disease, nonfatal non-procedure-related myocardial infarction, resuscitation after cardiac arrest, or fatal or nonfatal stroke. The predictive relationship between HDL cholesterol levels at the third month of treatment with statins and the time to the first major cardiovascular event was assessed in univariate and multivariate analyses and was also assessed for specific LDL cholesterol strata, including subjects with LDL cholesterol levels below 70 mg per deciliter (1.8 mmol per liter). RESULTS: The HDL cholesterol level in patients receiving statins was predictive of major cardiovascular events across the TNT study cohort, both when HDL cholesterol was considered as a continuous variable and when subjects were stratified according to quintiles of HDL cholesterol level. When the analysis was stratified according to LDL cholesterol level in patients receiving statins, the relationship between HDL cholesterol level and major cardiovascular events was of borderline significance (P=0.05). Even among study subjects with LDL cholesterol levels below 70 mg per deciliter, those in the highest quintile of HDL cholesterol level were at less risk for major cardiovascular events than those in the lowest quintile (P=0.03). CONCLUSIONS: In this post hoc analysis, HDL cholesterol levels were predictive of major cardiovascular events in patients treated with statins. This relationship was also observed among patients with LDL cholesterol levels below 70 mg per deciliter. (ClinicalTrials.gov number, NCT00327691 [ClinicalTrials.gov].). Copyright 2007 Massachusetts Medical Society.

PMID: 17898099 [PubMed - in process]

[brainengineer]

I tried pantethine for about 2 months and it didnt seem to radically improve my #'s so I gave up and tried to get more disciplined with my experimentation.

Hi brainengineer,

What brand of pantethine were you taking? I've been taking Jarrow brand Pantethine 450 mg x 2 daily (900 mg) at breakfast and dinner for 3 months now and will have blood
work done at the end of October to see if it has helped me. I will post the results here.

I was taking Jarrow 300mg 3x daily. I must admit I was taking several other things at the same time so I couldnt attribute anything specific to pantethine since it was an uncontrolled experiment so to say.

I will however comment that I just got my lipids checked and while taking Niacin I was able to increase my HDL from 32 to 43. So Im pretty happy about that.

Right now Im taking Krill Oil for 2 months to see if that helps increase it even more.

--
BrainEngineer

[nameless]

I will however comment that I just got my lipids checked and while taking Niacin I was able to increase my HDL from 32 to 43. So Im pretty happy about that.

That's good news regarding the niacin helping your HDL. What type of niacin are you using, immediate-release or timed release?

I'm trying the krill thing too, but if doesn't work out, I'm thinking of re-visiting niacin. I can't take immediate release, but perhaps Niaspan or Slo-Niacin wouldn't be so bad.

There is one thing that I'm not sure about in relation to high dose niacin -- are you supposed to take a B complex along with it, or no? I thought I read somewhere that it was advisable, as otherwise niacin would sort of throw things out of balance B-wise... hence why homocysteine sometimes rises on high-dose niacin.

I'm not sure where I read that though, so I have no clue if it's fact or just something a vitamin company stated somewhere.

[krillin]

Found out about a cool enzyme called paraoxonase 1 today.

http://www.pubmedcen...bmedid=17592556

Paraoxonase 1 (PON1) is an esterase closely associated to HDL containing both apolipoprotein A-I and apolipoprotein J (apoA-I and apoJ) and is believed to confer antioxidant properties to HDL (7). In this sense, PON1 has been shown to effectively hydrolyze the oxidized phospholipids present in LDL, thus retarding the oxidation of these lipoproteins and attenuating their pro-inflammatory effects (8–10). LDL oxidation is known to be influenced by diet, altering both LDL susceptibility to oxidation and serum PON1 activity (6,11). Thus, and as far as PON1 response to dietary fat is concerned, the consumption of high-fat (HF), as well as hypercholesterolemic diets, has been associated with a reduction of PON1 activity in both mice and rabbits (9,12). However, and in agreement with the improvement of the antioxidant and anti-inflammatory protection reported to be exerted by oleic acid (13), supplementation and in vitro studies have reported a higher MUFA-related PON1 stability and activity in comparison with PUFA (14–16).

It's also what we use to detox organophosphates.

http://www.pubmedcen...bmedid=15169886

[brainengineer]

That's good news regarding the niacin helping your HDL. What type of niacin are you using, immediate-release or timed release?

Keep in mind, Im taking a lot of Niacin in order to control *both* TC & HDL. Enduracin is slow release, and EP Niacin is intermediate release. Check out http://www.endur.com

Morning: 500mg Enduracin
Lunch: 1000mg EP Niacin
Dinner: 1000mg EP Niacin
Bedtime: 500mg Enduracin

But I dropped my #s bigtime after about 6 weeks *and* all my liver enzyme tests were normal which means the Niacin isnt causing any problems with my liver.

TC was 145 (a drop of nearly 100 pts from my high of 239)
LDL was 82 (a drop of nearly 50% from my last visit of 158)
HDL was 43 (an increase of 25% from my last visit of 34)
TG was 101 (a drop of about 50% from my last visit of 190)

--
BrainEngineer

[maxwatt]

No one has mentioned that lecithin also raises HDL, more so in subjects where it is at the low end of the range to begin with.

[ilanso]

Keep in mind, Im taking a lot of Niacin in order to control *both* TC & HDL

You don't need that much. On 9/19, I quoted from some lipidsonline slides:

While niacin's LDL-C lowering is linear, its effect on triglycerides and HDL-C is curvilinear. Modest doses of niacin can significantly alter these two lipid levels. For example, 1 g/d of immediate-release niacin can increase HDL-C by 25-30% and reduce triglycerides by a similar margin. Niacin is the most effective drug available for raising HDL-C. It also lowers lipoprotein(a) by about 30%.

Another source (Medscape) ups it slightly:

The changes in serum triglyceride and HDL-C concentrations that are induced by niacin are curvilinear, whereas the changes in serum LDL-C concentrations are linear. Thus, a daily dose of 1500 to 2000 mg of niacin will substantially change the serum triglyceride and HDL-C concentrations without causing many of the mucocutaneous and hepatic adverse effects seen with higher doses.

Immediate release is better:

Hepatotoxicity has been reported in patients receiving niacin; it may be dose related (>2000 mg/d) and associated with the use of extended-release preparations. The symptoms and time course of niacin-induced hepatitis are similar to those associated with statins. Timed-release formulations of nicotinic acid are designed to minimize cutaneous flushing. However, the absence of flushing may indicate poor gastrointestinal absorption. Additional drawbacks of such formulations are lesser decreases in serum triglyceride concentrations and lesser increases in serum HDL-C concentrations than are induced with plain nicotinic acid. Healthcare professionals can suggest the timed-release formulations for patients who cannot tolerate plain niacin and can be sure to follow up for evaluation of antilipemic effect and effect on aminotransferase levels.

I am now taking 1.5g IR in one dose before bed.

Alcohol is another source:

Alcohol use increases HDL-C in a dose-dependent manner (although one must consider the amount of calories added to the diet by alcohol consumption), whereas caloric restriction acutely lowers HDL-C concentrations

Regarding MCTs (medium chain triglycerides), it seems my positive post on 9/18 is contradicted by:

Compared with the intake of high-oleic sunflower oil, MCT intake resulted in 11% higher plasma total cholesterol (P = 0.0005), 12% higher LDL cholesterol (P = 0.0001), 32% higher VLDL cholesterol (P = 0.080), a 12% higher ratio of LDL to HDL cholesterol (P = 0.002), 22% higher plasma total triacylglycerol (P = 0.0361), and higher plasma glucose (P = 0.033). Plasma HDL-cholesterol and insulin concentrations and activities of cholesterol ester transfer protein and phospholipid transfer protein did not differ significantly between the diets. CONCLUSIONS: Compared with fat high in oleic acid, MCT fat unfavorably affected lipid profiles in healthy young men by increasing plasma LDL cholesterol and triacylglycerol. No changes in the activities of phospholipid transfer protein and cholesterol ester transfer protein were evident.

PMID: 15051598 [PubMed - indexed for MEDLINE]

[stephen_b]

No one has mentioned that lecithin also raises HDL, more so in subjects where it is at the low end of the range to begin with.

Thanks for that -- I was unaware. I've been taking 2g/day transresveratrol for a few months now mixed in with soy lecithin, and a couple of days ago I got a full blood workup. I'll post the lipid info when the results come in.

Stephen

[health_nutty]

No one has mentioned that lecithin also raises HDL, more so in subjects where it is at the low end of the range to begin with.

Could you point me to more info on this?

[maxwatt]

No one has mentioned that lecithin also raises HDL, more so in subjects where it is at the low end of the range to begin with.

Could you point me to more info on this?

It takes a lot of lecithin....

: Nutr Metab Cardiovasc Dis. 2006 Sep;16(6):395-404. Epub 2005 Nov 4.
Effects of soybean D-LeciVita product on serum lipids and fatty acid composition in type 2 diabetic patients with hyperlipidemia.Ristić Medić D, Ristić V, Arsić A, Postić M, Ristić G, Blazencić Mladenović V, Tepsić J.
Institute for Medical Research, Laboratory for Nutrition and Metabolism, Dr Subotića 4a, Belgrade, PO Box 102, 11 129 Belgrade, Serbia and Montenegro. danijelar@imi.bg.ac.yu

BACKGROUND AND AIM: Hyperlipidemia is one of the major risk factors of cardiovascular complication in diabetes. High intake of soy product has been suggested to prevent cardiovascular disease. The purpose of this study was to evaluate if dietary supplement of soybean D-LeciVita product, rich in polyunsaturated phospholipids (with 12% lecithin, 35% soy protein) affects serum lipids and serum and erythrocyte phospholipid fatty acid composition in type 2 diabetic patients. METHODS AND RESULTS: Forty-seven patients (men and post-menopausal women) with isolated hypertriglyceridemia (IHTG) and combined hyperlipidemia (CHL), aged 43-70 years, were given 15g of D-LeciVita powder as a water suspension in a single evening dose during the follow-up period of 12 weeks. Patients kept their diabetic diet relatively constant. Treatment was associated with a significant (p < or = 0.001) decrease in serum total cholesterol and triglyceride levels by 12% and 22%, respectively. LDL-cholesterol decreased by 16% and HDL-cholesterol increased by 11% (p < or = 0.001). Our study shows a 27% decrease in LDL-cholesterol (p < or = 0.001) and a 12% increase in HDL-cholesterol (p < or = 0.01) in CHL type 2 diabetic patients. Triglyceride levels decreased in type 2 diabetic patients with IHTG and CHL by 29% and 13%, respectively (p < or = 0.01 and p < or = 0.05). Our results show decrease in SFA and increase in n-6 and n-3 PUFA in serum and erythrocyte phospholipids. SFA decreased and n-3 PUFA increased in serum and erythrocyte phospholipids in IHTG and CHL groups. CONCLUSION: The present study indicated that added to a regular diet, soybean D-LeciVita product (combination of soy protein and lecithin) is associated not only with lipid-lowering effects but also with more favorable serum phospholipids fatty acid profile in type 2 diabetic patients with hyperlipidemia.

PMID: 16935698

[stephen_b]

The study "Phosphatidylinositol increases HDL-C levels in humans" reported:

Subjects received either 2.8 or 5.6 g of PI, with or without food. PI was well tolerated by all subjects. PI significantly affected the levels of HDL-C and triglyceride in the plasma of subjects receiving PI with food. The lower dose showed a 13% increase in HDL-C, whereas the high dose showed an increase of 18% over the 2 week period. Both low- and high-dose groups showed significant increases in plasma apolipoprotein A-I. The high dose of PI also decreased plasma triglycerides by 36% in the fed subjects.

I don't know if phosphatidylinositol is a component of soy lecithin though.

The same study however said "Prolonged oral administration of soy lecithin at doses ranging from 12 to 48 g per day have resulted in significant reductions in serum cholesterol and triglyceride levels and increased HDL-C levels", citing an earlier study, PMID 3778675, which reported:

Nine patients with type IIa hyperlipoproteinemia and nine patients with type IV hyperlipoproteinemia were given soya lecithin, 12 g/day, for 3 months. Plasma cholesterol and triglycerides were reduced by 15 and 23%, respectively, and HDL-cholesterol increased by 16% in the hypercholesterolemic patients.

12 g/day. About two tablespoons, maybe?

Stephen

Edit: Hey, cross-post with maxwatt.

[mike250]

No one has mentioned that lecithin also raises HDL, more so in subjects where it is at the low end of the range to begin with.

Could you point me to more info on this?

It takes a lot of lecithin....

: Nutr Metab Cardiovasc Dis. 2006 Sep;16(6):395-404. Epub 2005 Nov 4.
Effects of soybean D-LeciVita product on serum lipids and fatty acid composition in type 2 diabetic patients with hyperlipidemia.Ristić Medić D, Ristić V, Arsić A, Postić M, Ristić G, Blazencić Mladenović V, Tepsić J.
Institute for Medical Research, Laboratory for Nutrition and Metabolism, Dr Subotića 4a, Belgrade, PO Box 102, 11 129 Belgrade, Serbia and Montenegro. danijelar@imi.bg.ac.yu

BACKGROUND AND AIM: Hyperlipidemia is one of the major risk factors of cardiovascular complication in diabetes. High intake of soy product has been suggested to prevent cardiovascular disease. The purpose of this study was to evaluate if dietary supplement of soybean D-LeciVita product, rich in polyunsaturated phospholipids (with 12% lecithin, 35% soy protein) affects serum lipids and serum and erythrocyte phospholipid fatty acid composition in type 2 diabetic patients. METHODS AND RESULTS: Forty-seven patients (men and post-menopausal women) with isolated hypertriglyceridemia (IHTG) and combined hyperlipidemia (CHL), aged 43-70 years, were given 15g of D-LeciVita powder as a water suspension in a single evening dose during the follow-up period of 12 weeks. Patients kept their diabetic diet relatively constant. Treatment was associated with a significant (p < or = 0.001) decrease in serum total cholesterol and triglyceride levels by 12% and 22%, respectively. LDL-cholesterol decreased by 16% and HDL-cholesterol increased by 11% (p < or = 0.001). Our study shows a 27% decrease in LDL-cholesterol (p < or = 0.001) and a 12% increase in HDL-cholesterol (p < or = 0.01) in CHL type 2 diabetic patients. Triglyceride levels decreased in type 2 diabetic patients with IHTG and CHL by 29% and 13%, respectively (p < or = 0.01 and p < or = 0.05). Our results show decrease in SFA and increase in n-6 and n-3 PUFA in serum and erythrocyte phospholipids. SFA decreased and n-3 PUFA increased in serum and erythrocyte phospholipids in IHTG and CHL groups. CONCLUSION: The present study indicated that added to a regular diet, soybean D-LeciVita product (combination of soy protein and lecithin) is associated not only with lipid-lowering effects but also with more favorable serum phospholipids fatty acid profile in type 2 diabetic patients with hyperlipidemia.

PMID: 16935698

would it be logical to assume the same effect can occur in type 1 diabetics?

[health_nutty]

Interesting. Thanks for the info.

[malbecman]

Another good reason to take your resveratrol with lecithin if you ask me......

[health_nutty]

Another good reason to take your resveratrol with lecithin if you ask me......   

Absolutely, lecithin has health benefits on its own (is NOT laxative) and helps resveratrol absorption. win/win.