9 replies to this topic

[ta5]

There's a supplement called Provinal that LEF, Swanson, and others are selling.

 

This is LEF's description for their product:

 

Provinal® contains purified palmitoleic acid, an omega-7 monounsaturated fatty acid (MUFA). Palmitoleic acid is formed in the body from the conversion of glucose to fatty acids, or can be obtained in the diet from plant and marine sources. This fatty acid has been shown to support healthy cholesterol and C-reactive protein levels1 for those already within a normal range, and has a beneficial effect on other metabolic parameters.2

 

Palmitoleic acid acts as a direct regulator of metabolism, with actions including:

 

• suppression of adipocyte cytokine expression
• promotion of pancreatic B cell proliferation and secretory function to support insulin production and glucose management
• enhancement of skeletal muscle glucose uptake
• stimulation of adipocyte peroxisome proliferator–activated receptor (PPAR)-gamma transcriptional activity, a nuclear receptor involved in fatty acid metabolism as well as modulation of cell proliferation and differentiation

 

Provinal® contains no GMO ingredients.  Each softgel contains less than 1% palmitic acid, which is less than the amount of palmitic acid contained in half a macadamia nut.

 

References
1. Tersus Pharmaceuticals. Unpublished study 2013.
2. Yang ZH et al. Lipids in Health and Disease. 2011;10:120.

 

 

But, I see some troubling studies on palmitoleic acid, so I'm confused if it's good or bad. Can someone make sense of this? Do the negative studies not apply to this supplement?

 

 

Biochem Biophys Res Commun. 2015 Jul 17-24;463(1-2):29-36.
Palmitoleic acid induces the cardiac mitochondrial membrane permeability transition despite the presence of L-carnitine.
Oyanagi E1, Uchida M2, Miyakawa T2, Miyachi M3, et al.
Although palmitoleic acid (C16:1) is associated with arrhythmias, and increases in an age-dependent matter, the effects of L-carnitine, which is essential for the transport of long-chain fatty acids into the mitochondria, are unclear. It has been postulated that L-carnitine may attenuate palmitate (C16:0)-induced mitochondrial dysfunction and the apoptosis of cardiomyocytes. The aim of this study was to elucidate the activity of L-carnitine in the prevention of the palmitoleic acid-induced mitochondrial membrane permeability transition and cytochrome c release using isolated cardiac mitochondria from rats. Palmitoleoyl-CoA-induced mitochondrial respiration was not accelerated by L-carnitine treatment, and this respiration was slightly inhibited by oligomycin, which is an inhibitor of ATP synthase. Despite pretreatment with L-carnitine, the mitochondrial membrane potential decreased and mitochondrial swelling was induced by palmitoleoyl-CoA. In the presence of a combination of L-carnitine and tiron, a free radical scavenger, there was attenuated mitochondrial swelling and cytochrome c release following palmitoleoyl-CoA treatment. We concluded that palmitoleic acid, but not palmitate, induces the cardiac mitochondrial membrane permeability transition despite the presence of L-carnitine.
PMID: 25983324

 

Am J Clin Nutr. 2014 Mar;99(3):551-8.
Cancer death is related to high palmitoleic acid in serum and to polymorphisms in the SCD-1 gene in healthy Swedish men.
Byberg L1, Kilander L, Warensjö Lemming E, Michaëlsson K, Vessby B.
BACKGROUND:
A high proportion of monounsaturated fatty acids (MUFAs) or a high ratio of MUFAs to saturated fatty acids in plasma, reflecting a high activity of the lipogenic enzyme stearoyl-CoA desaturase-1 (SCD-1), has been shown to be related to cancer death and incidence in some studies.
OBJECTIVES:
The objective was to study whether the serum cholesteryl ester proportion of palmitoleic acid [16:1n-7 (16:1ω-3)] and the ratio of palmitoleic to palmitic acid (16:1n-7/16:0), as an estimation of the activity of SCD-1, are related to cancer death and to investigate whether polymorphisms in the SCD-1 gene are related to cancer mortality.
DESIGN:
A community-based cohort of 50-y-old men was followed for a maximum of >40 y. Survival analysis was used to relate fatty acid composition in serum, analyzed at baseline by gas-liquid chromatography (n = 1981), and single nucleotide polymorphisms in the SCD-1 gene (n = 986) to cancer death. A 7-d dietary record was completed at age 70 y (n = 880).
RESULTS:
The proportions of 16:1n-7 and the ratio of 16:1n-7 to 16:0 were associated with cancer mortality during follow-up in a comparison of the highest with the lowest quartile of 16:1n-7 (adjusted HR: 1.37; 95% CI: 1.04, 1.82). Inherited variance of the SCD-1 gene seemed to be related to cancer death, especially among men with a low proportion of PUFA in the diet in a comparison of the highest with the lowest weighted genetic risk score (HR: 2.14; 95% CI: 1.13, 4.04).
CONCLUSION:
The findings are compatible with the hypothesis that there is an association between endogenously synthesized MUFAs and cancer death.
PMID: 24368438

 

Am J Clin Nutr. 2012 Nov;96(5):970-6.
Associations of erythrocyte palmitoleic acid with adipokines, inflammatory markers, and the metabolic syndrome in middle-aged and older Chinese.
Zong G1, Ye X, Sun L, Li H, Yu Z, Hu FB, Sun Q, Lin X.
BACKGROUND:
Palmitoleic acid has been shown to regulate adipokine expression and systemic metabolic homeostasis in animal studies. However, its association with human metabolic diseases remains controversial.
OBJECTIVE:
We aimed to investigate associations of erythrocyte palmitoleic acid with adipokines, inflammatory markers, and metabolic syndrome (MetS) in a Chinese population.
DESIGN:
Erythrocyte fatty acids were measured in a population-based sample of 3107 men and women aged 50-70 y, for whom plasma glucose, insulin, lipid profile, adiponectin, retinol binding protein 4 (RBP-4), plasminogen activator inhibitor type 1, and high-sensitivity C-reactive protein (hsCRP) were measured. MetS was defined according to the updated National Cholesterol Education Program Adult Treatment Panel III criteria for Asian Americans.
RESULTS:
The mean (±SD) erythrocyte palmitoleic acid value was 0.41 ± 0.20% of total fatty acids. Palmitoleic acid was positively correlated with RBP-4 (r = 0.14, P < 0.001) and inversely correlated with adiponectin (r = -0.15, P < 0.001). After multivariable adjustment, palmitoleic acid was strongly associated with MetS and its components. ORs (95% CIs) for comparisons of extreme quartiles of palmitoleic acid were 3.50 (2.66, 4.59) for MetS, 7.88 (5.90, 10.52) for hypertriglyceridemia, 2.13 (1.66, 2.72) for reduced HDL cholesterol, 1.99 (1.60, 2.48) for central obesity, and 1.86 (1.41, 2.44) for elevated blood pressure (all P < 0.001). Further control for adipokines and hsCRP abolished the association of palmitoleic acid with central obesity but not with other MetS components.
CONCLUSION:
Erythrocyte palmitoleic acid is associated with an adverse profile of adipokines and inflammatory markers and an increased risk of MetS in this Chinese population.
PMID: 23015321

[albedo]

Good finding Ta5. I am afraid I am now confused too !

 

I was considering supplementing with palmitoleic, with the intent to see if I can induce change in the palmitic free fatty acid (FFA) which, despite I try to have it under control, has tendency to rise. My log shows an increase over the years of both FFAs but, as the rise rate of palmitic is greater than palmitoleic, the ratio (serum, not RBC) of palmitoleic to palmitic (which the study you reports indicates as a marker of the activity of the desaturase SCD1 enzyme) is decreasing indicating a lower activity of the enzyme.

 

In general, as FFA are quite touchy, I tend first to test them (not expensive) and use diet first. Only after that I suggest you use supplementation. As an example (but off topic), I recently I had a deficiency with GLA which should IMHO be only supplemented after testing (see Barry Sears on the Zone Diet, potentially triggering inflammation)). I could improve my GLA with a very moderate supplementation.

 

 

[albedo]

On the positive side, I am sure you have seen this too:

 

Purified palmitoleic acid for the reduction of high-sensitivity C-reactive protein and serum lipids: A double-blinded, randomized, placebo controlled study

http://www.sciencedi...933287414002815

[Darryl]

Just ran across this today (while searching for something positive to sayabout macadamia nuts):

 

Nestel, P., Clifton, P., & Noakes, M. (1994). Effects of increasing dietary palmitoleic acid compared with palmitic and oleic acids on plasma lipids of hypercholesterolemic men. Journal of lipid research, 35(4), 656-662.

Because macadamia oil is at least one potentially large source of palmitoleic acid, we tested its effect on plasma lipid levels against two other dietary fatty acids, oleic acid and palmitic acid. The dietary adjustments, through the use of supplements, provided comparisons of the three test fatty acids in which palmitoleic could be judged as behaving either like a saturated or a monounsaturated acid. Thirty-four hypercholesterolemic men ate the three test diets in random order in 3-week periods. Plasma total cholesterol and low density lipoprotein (LDL) cholesterol concentrations were similar with palmitic and palmitoleic acids and significantly higher than with oleic acid. High density lipoprotein (HDL) cholesterol was significantly lower with palmitoleic than with palmitic acid. The study confirms that, at least in hypercholesterolemic men, a modest increase in palmitic acid (+4% en) raises LDL cholesterol relative to oleic acid (+3% en), even when dietary cholesterol is low (< 165 mg/day). Palmitoleic acid (+4% en) behaves like a saturated and not a monounsaturated fatty acid in its effect on LDL cholesterol.

[ta5]

Cell Signal. 2015 Oct 13. pii: S0898-6568(15)00283-1. 
Palmitic acid but not palmitoleic acid induces insulin resistance in a human endothelial cell line by decreasing SERCA pump expression.

Gustavo Vazquez-Jimenez J1, Chavez-Reyes J1, Romero-Garcia T1, et al.

PMID: 26475209

 

 

 

J Clin Lipidol. 2014 Nov-Dec;8(6):612-7. 
Purified palmitoleic acid for the reduction of high-sensitivity C-reactive protein and serum lipids: a double-blinded, randomized, placebo controlled study.

Bernstein AM1, Roizen MF2, Martinez L3.

Abstract

BACKGROUND:

Purified palmitoleic acid (16-1; omega-7) has shown lipid-lowering and anti-inflammatory benefits in open label, epidemiologic, and animal studies.

OBJECTIVE:

Our objective was to perform the first randomized controlled trial of purified palmitoleic acid supplementation in humans.

METHODS:

Adults with dyslipidemia and evidence of mild systemic inflammation (high-sensitivity C-reactive protein [hs-CRP] between 2 and 5 mg/L) were randomly allocated to receive either 220.5 mg of cis-palmitoleic acid (n = 30) or an identical capsule with placebo (1000 mg of medium chain triglycerides, n = 30) once per day for 30 days. Participants were asked to maintain their current diet. Serum lipids and hs-CRP were drawn at baseline and study completion.

RESULTS:

At 30 days, there were significant mean (95% confidence interval [CI]) reductions in CRP (-1.9 [-2.3 to -1.4] mg/L), triglyceride (-30.2 [-40.2 to -25.3] mg/dL), and low-density lipoprotein (LDL) (-8.9 [-12.0 to -5.8] mg/dL), and a significant increase in high-density lipoprotein (HDL) (2.4 [1.5, 3.3] mg/dL) in the intervention group compared with control. These changes equated to 44%, 15%, and 8% reductions in CRP, triglyceride, and LDL respectively, and a 5% increase in HDL compared with control.

CONCLUSIONS:

Purified palmitoleic acid may be useful in the treatment of hypertriglyceridemia with the beneficial added effects of decreasing LDL and hs-CRP and raising HDL. Further study is needed to elucidate mechanisms and establish appropriate human doses.

PMID: 25499944

 

 

 

 

[niner]

Very interesting.  Bernstein's 2014 result is the opposite of Nestel's 1994 report.  Both used dyslipidemic subjects, but the dose and specific form were quite different.  Bernstein used 220 mg/d of the purified fatty acid in the form of a modified anchovy oil (omega 3s removed), while Nestel used 4% en, which I take to mean 4 energy % of the diet.  Assuming a 2000 kcal/d diet, that would be about 9 grams of palmitoleic acid per day, which was given in the form of macadamia oil.  The fatty acid composition of the two oils was quite different, but I suspect the overriding factor is the dose.  This appears to be a case of low dose good, high dose bad.

 

ta5, I'm not too worried about the three papers in your first post,  The first of the is an in vitro experiment, and those are usually not very relevant to human use.  The second is really more about a problem with a gene than with consumption of palmitoleic acid, with the mutant gene raising the level of endogenous palmitoate.  The last one was an association, but it's likely that the higher level of palmitoate was a marker of the disease rather than a reflection of dietary consumption.

 

If someone is looking to improve their CRP and lipid profile, it looks like a low dose of palmitoleic acid isn't a terrible idea; just don't OD on it.

[albedo]

Maybe interesting would also be looking at SNP rs603424 of the gene SCD1. It looks strongly influencing the palmitic to palmitoleic ratio. See http://www.snpedia.c...ex.php/Rs603424 and studies therein. Also http://www.ncbi.nlm....les/PMC3832838/ and Table 1.

[airplanepeanuts]

If I'm not mistaken 5 grams of macadamia have more palmitoleic acid that a provinal capsule.

 

A couple of macadamias daily?

Edited by airplanepeanuts, 02 March 2016 - 07:26 PM.

[albedo]

Omega-7 An Overlooked Fatty Acid

http://www.lifeexten...ty-Acid/Page-01

[Castiel]

I eat a handful of macadamia a day, as I've heard a handful of nuts a day has been found to be a healthy practice.   They're also very low in protein which at least doesn't activate some of the nutrient sensors in the body allowing for a fasting or CR like state to continue, hypothetically.   At least in some other species even high calorie diet led to life extension with reduction of solely the protein nutrient component, suggesting that protein, and some amino acids in particular are critical to the activation of CR like mechanisms, and probably fasting mechanisms too.

 

So if one is to limit food, say for alternate day fasting, etc.  This looks like a snack that could hypothetically be eaten in moderation during the fasting period without affecting the fasting regenerative mechanisms, though I've not looked into it and don't know if it's been tested.