Glucometric analysis of R-ALA/ALA/CLA/GLA/AlCar  

  RSS

Fonz
 Fonz
(@fonz)
Eminent Member
Joined: 11 months ago
Posts: 42
10/01/2019 12:53 pm  

Glucometric analysis of various OTC glucose utilization and insulin enhancing supplements. By Fonz.

In this study, that will be divided into part I and II, I will measure the Blood Glucose and temperature response to a meal with different supplements(5). In Part I, they will be used and tested independently. In Part II, I will explain how they can be used synergistically with one another and the numerous benefits the stack offers.

The supplements used:

1. None(Placebo)
2. CLA(Vitamin Shoppe)
3. GLA(Vitamin Shoppe)
4. R-ALA(Anabolic Fitness and 1fast400)
5. ALA (Kilosports)
6. Acetyl-L-Carnitine(Vitamin Shoppe)

Blood Glucose monitors used:

Principal: CVS Prestige Smart system. Serial Number: 6429796
Back-up: Glucotrend 2. Serial Number: GH022114809

Every original 1st reading by the principal Blood Glucose monitor(CVS) was checked by the back-up Glucometer(Glucotrend 2) to eliminate inconsistencies. I set the bar at + or – 10% of the original reading. If more or less than 10%, I repeated the specific dosaging for the supplement or combination of supplements being tested. I also measured my bodytemp to see if some of the supplements possessed thermogenic qualities.

Thermometer: Philips SensorTouch. Accurate to +-0.1C Type: HF 37C CE 0344

Specific Food = 500kcal, 6g Fat, 14.3g protein, 98g Carbs (Sugars = 47.5g)

Nutrient breakdown = 11% Fat/ 11% Protein / 78% carbs (Fibre = 1.5g) (Low Fat, high carb)

All measurements were done in the AM and/or anytime I hadn’t eaten for 12hrs, as there is NO FOOD present in the stomach after 12hrs, liver glycogen is empty, and BG levels are lowest. This is the BEST time to measure blood glucose fluctuations.

In fact, the GTT test is best performed in the AM on an empty stomach(Ask your doctor, he will verify this) (GTT=Glucose Tolerance test). Values for the blood glucose will be given according to the American system: i.e. mg/dl . This is the structure of each daily measurement.

1. Take initial BG(Blood glucose) measurement and BodyTemp.
2. Consume the SPECIFIC food and take the supplement in question at the specified dosage level.
3,4,5 and 6: Measure BG(Blood Glucose) levels at the 1 hr, 2hr, 3hr, and 4hr mark..
(Also taking bodytemp at each 1hr interval)

Supplement #1: Placebo

Intitial BG Measurement: 48mg/dl Temp: 37.3C (99.1F)
(Eat Food as described above)

T+1hr Measurement: 90mg/dl Temp: 37.2C (99F)

T+2hrs Measurement: 40mg/dl Temp: 36.8C (98.2F)

T+3hrs measurement: 74mg/dl Temp: 37.1C (98.8F)

T+4hrs Measurement: 72mg/dl Temp: 37.2F (99F)

Note: This clearly shows reactive hipoglycaemia(From T+1hr to T+3hrs), caused by the insulin surge of the High GI carb meal. Definately made me hungry and lethargic.

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

21 + 17.64 + 11.47 + 24 + 1 = 75.11 units squared

Area under initial BG measurement(negative):0.64 + 0.47 = 1. 11 units squared

Note2: Total Area: 75.11 + 1.11 = 76.22 units squared.

Note3: Time in Negative BG(Less than initial)(Approx): 14.7min(5.83% Total time)

Measurement #2 of Placebo:

Intitial BG Measurement: 50mg/dl Temp: 36.8C(98.2F)
(Eat Food as described above)

T+1hr Measurement: 96mg/dl Temp: 36.9C(98.4)

T+2hrs Measurement: 42mg/dl Temp: 36.9C(98.4F)

T+3hrs measurement: 78mg/dl Temp: 36.7C(98.2F)

T+4hrs Measurement: 70mg/dl Temp: 36.7C (98.2F)

Note: Again this clearly shows reactive hipoglycaemia(From T+1hr to T+3hrs), caused by the insulin surge of the High GI carb meal.

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

23 + 19.59 + 10.89 + 20 + 4 = 77.48 units squared

Area under initial BG measurement horizontal line:-0.59 – 0.89 = -1. 43 units squared

Note2: Total Area: 77.48 + 1.43 = 78.91 units squared.

Note3: Time in Negative BG(Less than initial)(Approx): 14.3min(5.97% Total time)

Measurement #3 of Placebo:

Intitial BG Measurement: 61mg/dl Temp: 36.8C(98.2F)
(Eat Food as described above)

T+1hr Measurement: 112mg/dl Temp: 36.8C(98.2F)

T+2hrs Measurement: 51mg/dl Temp: 37.0C(98.6F)

T+3hrs measurement: 80mg/dl Temp: 36.7C(98.1F)

T+4hrs Measurement: 78mg/dl Temp: 36.7C(98.1F)

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

25.5 + 21.32 + 6.22 + 18 + 1 = 72.04 units squared

Area under initial BG measurement horizontal line(negative):

0.82 + 1.72 = 2.54 units squared

Note: Total Area: 77.48 + 1.43 = 74.58 units squared.

Note2: Again this clearly shows reactive hipoglycaemia(From T+1hr to T+3hrs), caused by the insulin surge of the High GI carb meal.

Note3: Time in Negative BG(Less than initial)(Approx): 21.03min(8.76% Total time)

Placebo Analysis:Positive Area Negative Area Total Area
(Units Squared)

Measurement 1: 75.11 1.11 76.22

Measurement 2: 77.48 1.43 78.91

Measurement 3: 72.04 2.54 74.58

Mean Area: 74.88 1.69 76.57

Time in Negative BG(Approx):

Measurement 1 : 14.7min(5.83%)
Measurement 2 : 14.3min(5.97%)
Measurement 3 : 21.03min(8.76%)

Supplement #2: CLA (Tonalin) Vitamin Shoppe Brand.

Dosages: 8g, 10g, 12g. (But Tonalin is 74-82% CLA by content)

So, taking an average of 78% CLA, we get;

Dose 1: 12g Tonalin CLA) = 9.36g CLA
Dose 2: 10g Tonalin CLA)= 7.8g CLA
Dose 3: 8g Tonalin CLA) = 6.24g CLA

Food = 500kcal, 6g Fat, 14.3g protein, 98g Carbs (Sugars = 47.5g)

Nutrient breakdown = 11% Fat/ 11% Protein / 78% carbs (Fibre = 1.5g)

Dose 1: 12g Tonalin CLA: 9.36g CLA by content

Intitial BG Measurement: 48mg/dl Temp: 37.1C(98.8F)
(Eat Food as described above)

T+1hr Measurement: 61mg/dl Temp: 37.1C(98.8F)

T+2hrs Measurement: 83mg/dl Temp: 36.8C(98.2F)

T+3hrs measurement: 64mg/dl Temp: 36.9C(98.4F)

T+4hrs Measurement: 70mg/dl Temp: 36.6C(97.9F)

Note: CLA stabilized BG levels for the 4hrs.

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

6.5 + 13 + 11 + 16 + 9.5 + 16 + 3 = 75units squared.

Note: No reactive hypoglycaemia occurred like the placebo. CLA modulated the insulin surge from the pancreas, causing BG levels to not drop sharply...but instead they stabilized. This is how CLA works in diets and will be talked about later.

Dose 2: 10g Tonalin CLA: 7.8g CLA by content

Intitial BG Measurement: 72mg/dl Temp: 36.7C(98.1 F)
(Eat Food as described above)

T+1hr Measurement: 96mg/dl Temp: 37.0C(98.6 F)

T+2hrs Measurement: 117mg/dl Temp: 36.7C(98.1 F)

T+3hrs measurement: 78mg/dl Temp: 36.7C(98.1 F)

T+4hrs Measurement: 66mg/dl Temp: 36.7C(98.1 F)

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

12 + 24 + 10.5 +19.5 + 6 + 1.5 = 73.5 units squared

Area under initial BG measurement(negative)(Approx):

(0.5)(6)(0.5) = 1.5 units squared

Note: Total Area: 73.5 + 1.5 = 75 units squared.

Note2: CLA stabilized BG readings after the high GI carb meal. But BG readings still dipped below initial BG reading after less than 4 hours.

Note3: Time in Negative BG(Less than initial)(Approx): 30 min(12.5% of time)

Dose 3: 8g Tonalin CLA: 6.24g CLA by content

Intitial BG Measurement: 76mg/dl Temp: 37.0C(98.6F)
(Eat Food as described above)

T+1hr Measurement: 104mg/dl Temp: 37.1C(98.8F)

T+2hrs Measurement: 120mg/dl Temp: 37.0C(98.6F)

T+3hrs measurement: 70mg/dl Temp: 37.0C(98.6F)

T+4hrs Measurement: 60mg/dl Temp: 36.9C(98.6F)

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

14 + 28 + 8 +19.36 = 69.36 units squared

Area under initial BG measurement(negative)(Approx):

3 + 5 + 0.36 = 8.36 units squared

Note: Total Area: 69.36 + 8.36 = 77.72 units squared.

Note2: CLA stabilized BG readings after the high GI carb meal. But BG readings still dipped below initial BG reading after less than 3 hours.

Note3: Time in Negative BG(Less than initial): 67.2min(28% of time)

CLA Analysis:
(Units Squared)

Positive Area Negative Area Total Area Negative BG Time

Dose 1(12g)75.0 0 75.0 0.0

Dose 2(10g)73.5 1.5 75.0 30min(12.5%)

Dose 3(8g) 69.36 8.36 77.72 67.2min(28%)

As can be clearly seen, there exists a definite correlation between the amount of CLA needed per amount of carbs ingested. The 12g CLA completely stabilized BG levels after the initial spike(CLA is a fat, so it takes time to be digested and work), and they remained stable for 4 hours. The length of my BG analysis. The 10g and 8g doses stabilized BG levels for the first 3 hours. After that, BG levels dropped to below initial levels.

Supplement #3: GLA

Dosages: 1560mg GLA, 1300mg GLA, 1040mg GLA

(These dosages come from 1300mg Borage Oil Gel Caps containing 260mg GLA per gel cap). They are from the VitaminShoppe.

Food = 500kcal, 6g Fat, 14.3g protein, 98g Carbs (Sugars = 47.5g)

Nutrient breakdown = 11% Fat/ 11% Protein / 78% carbs (Fibre = 1.5g)

Dose 1: 1560mg GLA(From 7800mg Borage Oil)

Initial BG measurement: 59mg/dl Temp: 36.5C(97.7F)
(Eat food as described above)

T+1hr Measurement: 83mg/dl Temp: 36.8C(98.2F)

T+2hrs Measurement: 72mg/dl Temp: 37.1C(98.8F)

T+3hrs Measurement: 79mg/dl Temp: 36.4C(97.5F)

T+4hrs Measurement: 73mg/dl Temp: 36.5C(97.7F)

Note: No hypoglycaemic effect seen with this dosage of GLA included w/ high GI carb meal. BG levels spiked initially during the first hour then leveled off, and remained stable for the next 3 hours. Temperature did increase 0.6F from initial measurement to T=2hrs. This is statistically significant, and will be talked about later because GLA seems to have a slight thermogenic effect. Also, total area under blood glucose curve was smaller than placebo.

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

12 + 13 + 5.5 + 13 + 3.5 + 14 + 3 = 64 units squared

Dose 2: 1300mg GLA(From 6500mg Borage Oil)

Initial BG measurement: 81mg/dl Temp: 36.5C(97.7F)
(Eat food as described above)

T+1hr Measurement: 117mg/dl Temp: 36.7C(98.1F)

T+2hrs Measurement: 101mg/dl Temp: 37.0C(98.6F)

T+3hrs Measurement: 94mg/dl Temp: 36.9C(98.4F)

T+4hrs Measurement: 90mg/dl Temp: 36.8C(98.2F)

Area under positive BG Curve = 18 + 20 + 8 + 13 + 3.5 + 9 + 2 = 73.5 units squared

Note: No hypoglycaemic effect seen with GLA included w/ high GI carb meal.
Ending BG level > Initial BG level after T+4 hours. T+1hr BG Spike seen again like in GLA Dose #1.(1560mg GLA). Again, mean Temp. rose 0.5F from Initial BG temp to T=2hrs temp.

Dose 3: 1040mg GLA(From 5200mg Borage Oil)

Initial BG measurement: 83mg/dl Temp: 36.9C(98.4F)
(Eat food as described above)

T+1hr Measurement: 129mg/dl Temp: 37.4C(99.5F)

T+2hrs Measurement: 90mg/dl Temp: 37.0C(98.6F)

T+3hrs Measuremen 104mg/dl Temp: 36.9C(98.4F)

T+4hrs Measuremen 81mg/dl Temp: 36.9C(98.4F)

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

23 + 7 + 19.5 + 7 + 7 + 2 + 11.5 = 77 units squared.

Note: No hypoglycaemic effect seen with GLA included w/ high GI carb meal.
Ending BG level = Initial BG level after T+4 hours. T+1hr BG Spike seen again like in GLA Dose #1.(1560mg GLA) and dose #2(1300mg GLA). BG fluctuations were more erratic in dose#3 than in dose #1 and #2. Seems that this is the smallest amount of GLA for the dosage of carbs ingested for BG levels not to go below initial. Again, mean Temp. rose 0.5F from Initial BG temp to T=1hr temp.

GLA Analysis:
(Units squared)

Positive Area Max Temp increase(F) Total Area

Dose 1(1560mg): 64 0.6F 64

Dose 2(1300mg): 73.5 0.5F 73.5

Dose 3(1040mg): 77 0.5F 77

Comparison to Placebo:

Placebo: 76.57 units squared(mean total Area)

(Units Squared)

64/76.57 = 83.58% = - 17.42% reduction in BG Area
73.5/76.57 = 95.99% = - 4.01% reduction in BG Area
77/76.57 = No Net Change Seen.

Supplement #4: R-ALA

Dosages: 200mg R-ALA, 400mg R-ALA , 600mg R-ALA.
(From AF www.anabolicfitness.net and www.1fast400.com)

Food = 500kcal, 6g Fat, 14.3g protein, 98g Carbs (Sugars = 47.5g)

Nutrient breakdown = 11% Fat/ 11% Protein / 78% carbs (Fibre = 1.5g)

Dose 1: 200mg R-ALA

Initial BG measurement: 70mg/dl Temp: 36.9C(98.4F)
(Eat food as described above)

T+1hr Measurement: 110mg/dl Temp: 36.8C(98.2F)

T+2hrs Measurement: 80mg/dl Temp: 37.0C(98.6F)

T+3hrs Measurement: 75mg/dl Temp: 36.9C(98.4F)

T+4hrs Measurement: 70mg/dl Temp: 37.1C(98.8F)

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

20 + 10 + 15 + 5 + 2.5 + 2.5 = 55 Units Squared

Dose 2: 400mg R-ALA

Initial BG measurement: 70mg/dl Temp: 36.8C(98.2F)
(Eat food as described above)

T+1hr Measurement: 95mg/dl Temp: 36.8C(98.2F)

T+2hrs Measurement: 80mg/dl Temp: 37.0C(98.6F)

T+3hrs Measurement: 70mg/dl Temp: 37.0C(98.6F)

T+4hrs Measurement: 60mg/dl Temp: 36.9C(98.4F)

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

12.5 + 10 + 7.5 + 5 = 35 Units squared

Area under negative BG Curve(Taking initial BG measurement as the horizontal) =

0.5(10) = 5 Units squared

Dose 3: 600mg R-ALA

Initial BG measurement: 80mg/dl Temp: 36.9C(98.4F)
(Eat food as described above)

T+1hr Measurement: 100mg/dl Temp: 36.9C(98.4F)

T+2hrs Measurement: 90mg/dl Temp: 36.9C(98.4F)

T+3hrs Measurement: 75mg/dl Temp: 36.9C(98.4F)

T+4hrs Measurement: 70mg/dl Temp: 37.0C(98.6F)

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

10 + 10 + 5 + 3.33 = 28.33 Units squared

Area under negative BG Curve(Taking initial BG measurement as the horizontal) =

5 + 2.5 + 0.83 = 8.33 Units squared

R-ALA Analysis:
(Units squared)
Positive Area Negative Area Total Area

Dose 1(200mg): 55.0 0.0 55.00

Dose 2(400mg): 35.0 5.0 40.00

Dose 3(600mg): 28.33 8.33 36.67

Comparison to Placebo:

Placebo: 76.57 units squared(mean total Area)

(600mg R-ALA)(36.67 Units Squared) 36.67/76.57 = (1-47.89%) = 52.11% reduction

(400mg R-ALA)(40.00 Units Squared) 40.0/76.57 = (1-52.24%) = 47.76% reduction

(200mg R-ALA)(55.00 Units Squared) 55.0/76.57 = (1-71.83%) = 28.17% reduction

Supplement #5: ALA

Dosages: 600mg ALA, 1200mg ALA , 1800mg ALA.

(These dosages come from www.kilosports.com ALA)

Kilosports: Lot# C07351

Food = 500kcal, 6g Fat, 14.3g protein, 98g Carbs (Sugars = 47.5g)

Nutrient breakdown = 11% Fat/ 11% Protein / 78% carbs (Fibre = 1.5g)

Dose 1: 600mg ALA

Initial BG measurement: 65mg/dl Temp: 36.7C(98.1F)
(Eat food as described above)

T+1hr Measurement: 100mg/dl Temp: 36.8C(98.2F)

T+2hrs Measurement: 75mg/dl Temp: 36.8C(98.2F)

T+3hrs Measurement: 75mg/dl Temp: 36.8C(98.2F)

T+4hrs Measurement: 70mg/dl Temp: 37.0C(98.6F)

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

17.5 + 22.5 + 17.5 = 57.5 Units Squared

Dose 2: 1200mg ALA

Initial BG measurement: 60mg/dl Temp: 37.0C(98.6F)
(Eat food as described above)

T+1hr Measurement: 90mg/dl Temp: 36.9C(98.4F)

T+2hrs Measurement: 70mg/dl Temp: 36.8C(98.2F)

T+3hrs Measurement: 65mg/dl Temp: 37.0C(98.6F)

T+4hrs Measurement: 60mg/dl Temp: 36.8C(98.2F)

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

15 + 10 + 10 + 5 + 2.5 + 2.5 = 45 Units Squared

Dose 3: 1800mg ALA

Initial BG measurement: 70mg/dl Temp: 37.0C(98.6F)
(Eat food as described above)

T+1hr Measurement: 95mg/dl Temp: 36.8C (98.2F)

T+2hrs Measurement: 80mg/dl Temp: 36.8C(98.2F)

T+3hrs Measurement: 70mg/dl Temp: 37.0C(98.6F)

T+4hrs Measurement: 60mg/dl Temp: 36.9C(98.4F)

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

12.5 + 10 + 7.5 + 5 = 35 Units Squared

Area under negative BG Curve(Taking initial BG measurement as the horizontal) =

(0.5)(10) = 5.0 Units Squared

ALA Analysis:
(Units squared)
Positive Area Negative Area Total Area

Dose 1(600mg): 57.5 0.0 55.00

Dose 2(1200mg) 45.0 0.0 45.00

Dose 3(1800mg): 35.0 5.0 40.00

Comparison to Placebo:

Placebo: 76.57 units squared(mean total Area)

(1800mg ALA)(40.00 Units Squared) 40.00/76.57 = (1-52.24%) = 47.76% reduction

(1200mg ALA)(45.00 Units Squared) 45.00/76.57 = (1- 58.77%) = 41.23% reduction

(600mg ALA)(57.50 Units Squared) 57.50/76.57 = (1- 75.09%) = 24.91% reduction

Supplement #6: Acety-L-Carnitine

Dosages: 1000mg AlCar, 2000mg ALCar , 3000mg ALCar

Food = 500kcal, 6g Fat, 14.3g protein, 98g Carbs (Sugars = 47.5g)

Nutrient breakdown = 11% Fat/ 11% Protein / 78% carbs (Fibre = 1.5g)

Dose 1: 1000mg Acetyl-L-Carnitine

Initial BG measurement: 60mg/dl Temp: 37.0C(98.6F)
(Eat food as described above)

T+1hr Measurement: 90mg/dl Temp: 37.0C(98.6F)

T+2hrs Measurement: 80mg/dl Temp: 36.9C(98.4F)

T+3hrs Measurement: 80mg/dl Temp: 36.8C(98.2F)

T+4hrs Measurement: 70mg/dl Temp: 37.0C(98.6F)

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

15 + 20 + 25 + 15 = 75.0 Units Squared

Dose 2: 2000mg Acetyl-L-Carnitine

Initial BG measurement: 70mg/dl Temp: 36.7C(98.1F)
(Eat food as described above)

T+1hr Measurement: 100mg/dl Temp: 36.7C(98.1F)

T+2hrs Measurement: 90mg/dl Temp: 36.8C(98.2F)

T+3hrs Measurement: 85mg/dl Temp: 37.0C(98.6F)

T+4hrs Measurement: 75mg/dl Temp: 36.9C(98.4F)

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

15 + 25 + 17.5 + 10 = 67.5 Units Squared

Dose 3: 3000mg Acetyl-L-Carnitine

Initial BG measurement: 65mg/dl Temp: 37.1C(98.8F)
(Eat food as described above)

T+1hr Measurement: 95mg/dl Temp: 37.1C(98.8F)

T+2hrs Measurement: 90mg/dl Temp: 37.2C(99.0F)

T+3hrs Measurement: 75mg/dl Temp: 37.1C(98.8F)

T+4hrs Measurement: 65mg/dl Temp: 37.0C(98.6F)

Area under positive BG Curve(Taking initial BG measurement as the horizontal) =

15 + 25 + 12.5 + 12.5 = 65.0 Units Squared

ALCar Analysis:
(Units squared)
Positive Area Negative Area Total Area

Dose 1(1000mg): 75.0 0.0 75.00

Dose 2(2000mg): 67.5 0.0 67.50

Dose 3(3000mg): 65.0 0.0 65.00

Comparison to Placebo:

Placebo: 76.57 units squared(mean total Area)

(3000mg ALCar)(65.00 Units Squared) 65.00/76.57 =(1-84.89%) = 15.11% reduction

(2000mg ALCar)(67.50 Units Squared) 67.50/76.57 =(1-88.15%) = 11.85% reduction

(1000mg ALCar)(75.00 Units Squared) 75.00/76.57 =(1-97.95%) = 2.05% reduction

Next post.


Quote
Fonz
 Fonz
(@fonz)
Eminent Member
Joined: 11 months ago
Posts: 42
10/01/2019 1:36 pm  

Conclusions:

Mechanisms via how you can manipulate nutrient partitioning....i.e. Insulin levels/Blood Glucose levels.

a)Non-insulin mediated glucose partitioning(Or if you prefer disposal). These types of supplements(For example R-ALA and Acetyl-L-Carnitine) work INDEPENDENT of insulin. They have little effect on its release or degradation in the bloodstream. What they do, is increase translocation of intra-cellular Glut-4’s(Glucose Transporters) to the outside of the cellular membrane albeit in the adipocytes(fat cells) and miocytes(muscle cells). The net result, is that more glucose is diverted to the miocytes, and less to the adipocytes. In hypocaloric diets, this means, more fat-loss, and better muscle preservation. In hypercaloric diets, this means more muscle gain, and less fat gain.
b) Insulin mediated glucose partitioning(or disposal). These types of supplements actually influence AA transport b/c they work through insulin signalling pathways. CLA is a good example. CLA works by increasing AA and glucose transport into the muscle cells via insulin stimulated pathways, and therefore in hypocaloric diets acts as an anti-catabolic. CLA
also keeps blood glucose levels more stable. In essence preventing preventing high blood glucose or hypoglycaemia after a carb meal.
c)Non-stimulating thermogenics. GLA. In order to explain a bit how GLA works, I will briefly explain what prostaglandins are.

Series 1 Prostaglandins = Good(PgF2A)( Anabolic) They are incredibly thermogenic and help build muscle.
Series 2 Prostaglandins = Bad(PgE2)(Catabolic) They break down protein.
Series 1 and 2 produced by your cells always at a 1:1 ratio.
Series 3 Prostaglandins block the production of series 2.
Series 1 and 2 Prostaglandins are made from the essential fatty acid Linoleic Acid.
Linoleic Acid = Omega-6 Fatty Acid .
Linolenic Acid(Alpha-linolenic acid) is an Omega-3 fatty Acid Series 3 Prostaglandins are derived from this acid.
GLA = Omega-6 Fatty Acid (Gamma-Linolenic Acid) This BLOCKS series 2 Prostaglandins.
By Blocking series 2 prostaglandins, GLA shifts the normal 1:1 Prostaglandin ratio to the PgF2A(Anabolic) side. In essence, promoting thermogenesis. As can be shown in my study of GLA. Its anabolic effects were not measured(As this is also a direct consequence of a positive PgF2A environment) .

These explanations for the different workings of each substance can be seen to be true when one compares each to the Placebo measurements.

Comparison to Placebo(GLA):

Placebo:

Mean Area(Average): 74.88 units squared
Negative Area: 1.69 units squared
Total Area: 76.57 units squared

GLA:

Dose 1(1040mg): Area: 77.00 Units squared
Dose 2(1300mg): Area: 73.50 Units squared
Dose 3(1560mg): Area: 64.00 Units squared

1560mg GLA = 64 Units squared.
Placebo total Area average: 76.57 Units squared

Reduction in Total Area: ((76.57 – 64)/ 76.57) = 16.42% reduction
Temp increase: +0.6F

GLA caused a reduction in the area under the blood glucose curve by diverting some of the calories ingested into heat energy i.e. increasing the meals thermogenic value.

Comparison to Placebo(CLA):

Placebo:

Mean Area(Average): 74.88 units squared
Negative Area: 1.69 units squared
Total Area: 76.57 units squared

CLA:

Dose 1(12g): Area: 75.00 Units squared
Dose 2(10g): Area: 75.00 Units squared(1.5 negative)
Dose 3(8g): Area: 77.72 Units squared(8.36 negative)

Comparison to Placebo(R-ALA):

Placebo:

Mean Area(Average): 74.88 units squared
Negative Area: 1.69 units squared
Total Area: 76.57 units squared

R-ALA

Dose 1(200mg): 55.00 Units Squared
Dose 2(400mg): 40.00 Units Squared(5.00 Negative)
Dose 3(600mg): 36.67 Units Squared(8.33 Negative)

Comparison to Placebo(ALA):

Placebo:

Mean Area(Average): 74.88 units squared
Negative Area: 1.69 units squared
Total Area: 76.57 units squared

ALA

Dose 1 (600mg): 57.50 Units Squared
Dose 2(1200mg): 45.00 Units Squared
Dose 3(1800mg): 40.00 Units Squared(5.00 Negative)

Both ALA and R-ALA decreased the area under the blood glucose curve significantly. This is due to an increase in both glucose uptake and glucose oxidation.

Comparison to Placebo(Acetyl-L-Carnitine):

Placebo:

Mean Area(Average): 74.88 units squared
Negative Area: 1.69 units squared
Total Area: 76.57 units squared

Acetyl-L-Carnitine

Dose 1 (1000mg): 75.00 Units Squared
Dose 2 (2000mg): 67.50 Units Squared
Dose 3 (3000mg): 65.00 Units Squared

Acetyl-L-Carnitine caused a moderate reduction in the area under the blood glucose curve.

Fonz


ReplyQuote
jboldman
(@jboldman)
Honorable Member
Joined: 11 months ago
Posts: 523
10/01/2019 2:09 pm  

Fonz, for the love of god, make some charts!

jb


ReplyQuote
Trevdog
(@trevdog)
Trusted Member
Joined: 11 months ago
Posts: 70
10/01/2019 2:58 pm  

Obviously you put a lot of time into performing and documenting this study. Thank you.

Clearly I'm going to have to find more time than I have now to digest the results.

In the meantime, I wonder if you might have any comments regarding the relative "bang for the buck" of the various supplements studied and/or any combinations of those supplements? This would be useful because, as an example, I don't see myself ever spending the money to take more than 1-1.5 grams of ALA (racemic) per day.

Thanks again.


ReplyQuote
Judah Bauer
(@judah-bauer)
Active Member
Joined: 5 months ago
Posts: 5
10/01/2019 3:58 pm  

excellent...wow. I'm gonna have to read over this a few times to fully appreciate it...but great job bro


ReplyQuote
virtualcyber
(@virtualcyber)
New Member
Joined: 5 months ago
Posts: 4
10/01/2019 4:55 pm  

Fonz:

Great work. Couple of questions.

If r-ALA causes GLUT-4 to be translocated on fat cells, wouldn't that cause lipogenesis as well? [See referenced abstract below]

What I am asking is basically: WHY should muscles be preferentially treated to glucose when both muscle and fat cells' GLUT4 are translocated?

==================================

Transgenic GLUT-4 overexpression in fat enhances glucose metabolism: preferential effect on fatty acid synthesis.

Tozzo E, Shepherd PR, Gnudi L, Kahn BB.

Harvard Thorndike Research Laboratory, Harvard Medical School, Boston, Massachusetts, USA.

GLUT-4 expression varies widely among normal humans and those with obesity and diabetes. Using the alpha P2 promoter/enhancer ligated to the human GLUT-4 gene, we created transgenic mice to study the impact of alterations in GLUT-4 expression selectively in adipocytes on glucose homeostasis and body composition. Here we investigated molecular mechanisms for enhanced glucose tolerance and obesity in these mice. [U-14C]glucose incorporation into triglycerides, glyceride-glycerol, glyceride-fatty acids, CO2, and lactate was measured in adipocytes incubated at 3, 0.5, and 3 microM glucose with or without maximally stimulating insulin. In nontransgenic and transgenic mice, the major pathway for glucose metabolism shifts from lipogenesis at tracer glucose concentration to glycolysis at physiological glucose concentration. In transgenic adipocytes incubated at 3 microM glucose, metabolism via all major pathways is enhanced by 8.6- to 38-fold in the absence of insulin and 3- to 13-fold in the presence of insulin. At physiological glucose concentration, constitutive metabolism to triglycerides, CO2, and lactate is two- to threefold greater in transgenic than in nontransgenic adipocytes. De novo fatty acid synthesis is preferentially increased: 31-fold for basal and 21-fold for insulin-stimulated compared with nontransgenic adipocytes. Thus overexpression of GLUT-4 in adipocytes of transgenic mice results in increased glucose metabolism in all major pathways, with differential regulation of the pathways involved in lipogenesis.


ReplyQuote
Judah Bauer
(@judah-bauer)
Active Member
Joined: 5 months ago
Posts: 5
10/01/2019 5:26 pm  

This deserves a bump.. I just read over it for the third time and I really appreciate the info and can't wait for part 2.


ReplyQuote
Spencer
(@spencer)
New Member
Joined: 4 months ago
Posts: 1
10/01/2019 6:11 pm  
Posted by: virtualcyber
Fonz:

Great work. Couple of questions.

If r-ALA causes GLUT-4 to be translocated on fat cells, wouldn't that cause lipogenesis as well? [See referenced abstract below]

What I am asking is basically: WHY should muscles be preferentially treated to glucose when both muscle and fat cells' GLUT4 are translocated?

==================================

Transgenic GLUT-4 overexpression in fat enhances glucose metabolism: preferential effect on fatty acid synthesis.

Tozzo E, Shepherd PR, Gnudi L, Kahn BB.

Harvard Thorndike Research Laboratory, Harvard Medical School, Boston, Massachusetts, USA.

GLUT-4 expression varies widely among normal humans and those with obesity and diabetes. Using the alpha P2 promoter/enhancer ligated to the human GLUT-4 gene, we created transgenic mice to study the impact of alterations in GLUT-4 expression selectively in adipocytes on glucose homeostasis and body composition. Here we investigated molecular mechanisms for enhanced glucose tolerance and obesity in these mice. [U-14C]glucose incorporation into triglycerides, glyceride-glycerol, glyceride-fatty acids, CO2, and lactate was measured in adipocytes incubated at 3, 0.5, and 3 microM glucose with or without maximally stimulating insulin. In nontransgenic and transgenic mice, the major pathway for glucose metabolism shifts from lipogenesis at tracer glucose concentration to glycolysis at physiological glucose concentration. In transgenic adipocytes incubated at 3 microM glucose, metabolism via all major pathways is enhanced by 8.6- to 38-fold in the absence of insulin and 3- to 13-fold in the presence of insulin. At physiological glucose concentration, constitutive metabolism to triglycerides, CO2, and lactate is two- to threefold greater in transgenic than in nontransgenic adipocytes. De novo fatty acid synthesis is preferentially increased: 31-fold for basal and 21-fold for insulin-stimulated compared with nontransgenic adipocytes. Thus overexpression of GLUT-4 in adipocytes of transgenic mice results in increased glucose metabolism in all major pathways, with differential regulation of the pathways involved in lipogenesis.

I would like to bump VC's questions as well.


ReplyQuote
Fonz
 Fonz
(@fonz)
Eminent Member
Joined: 11 months ago
Posts: 42
10/01/2019 7:03 pm  
Posted by: virtualcyber
Fonz:

Great work. Couple of questions.

If r-ALA causes GLUT-4 to be translocated on fat cells, wouldn't that cause lipogenesis as well? [See referenced abstract below]

What I am asking is basically: WHY should muscles be preferentially treated to glucose when both muscle and fat cells' GLUT4 are translocated?

==================================

Transgenic GLUT-4 overexpression in fat enhances glucose metabolism: preferential effect on fatty acid synthesis.

Tozzo E, Shepherd PR, Gnudi L, Kahn BB.

Harvard Thorndike Research Laboratory, Harvard Medical School, Boston, Massachusetts, USA.

GLUT-4 expression varies widely among normal humans and those with obesity and diabetes. Using the alpha P2 promoter/enhancer ligated to the human GLUT-4 gene, we created transgenic mice to study the impact of alterations in GLUT-4 expression selectively in adipocytes on glucose homeostasis and body composition. Here we investigated molecular mechanisms for enhanced glucose tolerance and obesity in these mice. [U-14C]glucose incorporation into triglycerides, glyceride-glycerol, glyceride-fatty acids, CO2, and lactate was measured in adipocytes incubated at 3, 0.5, and 3 microM glucose with or without maximally stimulating insulin. In nontransgenic and transgenic mice, the major pathway for glucose metabolism shifts from lipogenesis at tracer glucose concentration to glycolysis at physiological glucose concentration. In transgenic adipocytes incubated at 3 microM glucose, metabolism via all major pathways is enhanced by 8.6- to 38-fold in the absence of insulin and 3- to 13-fold in the presence of insulin. At physiological glucose concentration, constitutive metabolism to triglycerides, CO2, and lactate is two- to threefold greater in transgenic than in nontransgenic adipocytes. De novo fatty acid synthesis is preferentially increased: 31-fold for basal and 21-fold for insulin-stimulated compared with nontransgenic adipocytes. Thus overexpression of GLUT-4 in adipocytes of transgenic mice results in increased glucose metabolism in all major pathways, with differential regulation of the pathways involved in lipogenesis.

I'll give you a hypothetical situation.

R-ala both translocates both Glut-4's from the inside of the cell to the outside of the miocytes(muscle cells) and adipocytes(fat cells).

OK......that is the ghist of the study above.

One problem the study overlooks.

R-ALA reduces insulogenic output by roughly 17%.

By reducing insulogenic output you reduce the overral lipogenic environment in the blood(i.e. Blood glucose).

And here is where it all adds up.

1. you eat a meal...say milk(1.0L).

2. Blood Glucose rises and the glucose in the blood stream goes to either the fat cells or the muscle cells(Through their respective Glut-4 transporters) depending on THE INSULOGENIC LEVEL of the meal..basically its GI(Glycaemic index).
For a normal meal(not counting post-wo or AM) high insulin levels= lipogenesis(fat gain)

Now, lest try this is w/o R-ALA.

Now, with R-ALA:

1. You eat a meal..again milk(1.0L)

2. Blood glucose rises again, and the glucose in the blood stream goes to either the fat cells or muscle cells. But, in this case the r-ala has not only increased the Glut-4 content of both the fat cells and muscle cells, BUT(this is critical), it has reduced the INSULOGENIC OUTPUT of the meal by 17%.

What does this mean?

Less insulin present in the blood stream = less fat gain(lipogenesis) = More FFA's released(Lipolysis) energy

Glycogen storage by your eaten meal(milk) is not affected because the amount of insulin needed to store glucose as glycogen is MINISCULE and does not affect glycogen synthase activity (Unlike racemic ALA which does because of its S-ala content).

That about sums it up.

Fonz


ReplyQuote
duchaine
(@duchaine)
Eminent Member
Joined: 11 months ago
Posts: 24
10/01/2019 8:03 pm  
Posted by: Fonz
I'll give you a hypothetical situation.

R-ala both translocates both Glut-4's from the inside of the cell to the outside of the miocytes(muscle cells) and adipocytes(fat cells).

OK......that is the ghist of the study above.

One problem the study overlooks.

R-ALA reduces insulogenic output by roughly 17%.

By reducing insulogenic output you reduce the overral lipogenic environment in the blood(i.e. Blood glucose).

And here is where it all adds up.

1. you eat a meal...say milk(1.0L).

2. Blood Glucose rises and the glucose in the blood stream goes to either the fat cells or the muscle cells(Through their respective Glut-4 transporters) depending on THE INSULOGENIC LEVEL of the meal..basically its GI(Glycaemic index).
For a normal meal(not counting post-wo or AM) high insulin levels= lipogenesis(fat gain)

Now, lest try this is w/o R-ALA.

Now, with R-ALA:

1. You eat a meal..again milk(1.0L)

2. Blood glucose rises again, and the glucose in the blood stream goes to either the fat cells or muscle cells. But, in this case the r-ala has not only increased the Glut-4 content of both the fat cells and muscle cells, BUT(this is critical), it has reduced the INSULOGENIC OUTPUT of the meal by 17%.

What does this mean?

Less insulin present in the blood stream = less fat gain(lipogenesis) = More FFA's released(Lipolysis) energy

Glycogen storage by your eaten meal(milk) is not affected because the amount of insulin needed to store glucose as glycogen is MINISCULE and does not affect glycogen synthase activity (Unlike racemic ALA which does because of its S-ala content).

That about sums it up.

Fonz

thanks fonz.
i'm an italo-canadian guy...so forgive my english!

i'm talking obout something like this in an italian-forum.
I was talking obout insulin lipneogenic and antilipolitic action over a long period(the forst-reaction:I hope it's the right term).

your post is going to help me to explain my thesis obout insulin-its receptorial and postreceptorial action.I think it's easier and more interesting if a person can axplain whit examples.so I 'll explain insulin also trought supplement that can span it.
thank you

underground


ReplyQuote
Miggy
(@miggy)
Eminent Member
Joined: 11 months ago
Posts: 21
10/01/2019 8:40 pm  
Posted by: Fonz
Less insulin present in the blood stream = less fat gain(lipogenesis) = More FFA's released(Lipolysis) energy

Glycogen storage by your eaten meal(milk) is not affected because the amount of insulin needed to store glucose as glycogen is MINISCULE and does not affect glycogen synthase activity (Unlike racemic ALA which does because of its S-ala content).

That about sums it up.

Fonz

So less insulin (from R-ala) in the bloodstream allows for less fat gain but glycogen storage in muscle and liver cells is unaffected even though insulogenic output is LESS?..

Is R-ala working at the receptor level?..How do muscle/liver cells acquire proper amounts of glycogen w/ less insulin output?

This is like the best of both worlds...Is this what your saying Fonz?...As an endurance athlete am I getting what I need for recovery through R-ala's moderating of insulin?....

Miggy


ReplyQuote
Fonz
 Fonz
(@fonz)
Eminent Member
Joined: 11 months ago
Posts: 42
10/01/2019 9:35 pm  
Posted by: Miggy
So less insulin (from R-ala) in the bloodstream allows for less fat gain but glycogen storage in muscle and liver cells is unaffected even though insulogenic output is LESS?..

Is R-ala working at the receptor level?..How do muscle/liver cells acquire proper amounts of glycogen w/ less insulin output?

This is like the best of both worlds...Is this what your saying Fonz?...As an endurance athlete am I getting what I need for recovery through R-ala's moderating of insulin?....

Miggy

Yer, but only R-ALA.

R-ALA will increase Glut-4 content in your muscle and fat cells(Leading to greater glycogen storage) BUT it will indirectly reduce insulin levels by 17% leading to a smaller lipogenic environment in the fat cells(Even though their glut-4 content has also been increased....but since insulin levels are lowered...they can't take in FFA's and store them as WAT).

The basic equation is:

1. You eat.

Take R-ALA. Glut-4's increase in fat and muscle cells(This means increased glycogen storage in muscle cells) + a insulin decrease oy 17% indirectly by the R-ALA(Decreases fat storage from a meal(lipogenesis), which = more FFA's released into the blood stream for burning.

What youbhave to know out of all this is that R-ALA increases glut-4's INDEPENDENTLY of insulin, while it decreases insulin release from the pancreas INDIRECTLY.

Racemic ALA does not posses even a fraction of these qualities except as an anti-oxidant.

Fonz


ReplyQuote
Judah Bauer
(@judah-bauer)
Active Member
Joined: 5 months ago
Posts: 5
10/01/2019 10:28 pm  

Just out of curiousity...is there anything that shouldn't be taken w/ r ALA that could affect its efficacy?


ReplyQuote
Fonz
 Fonz
(@fonz)
Eminent Member
Joined: 11 months ago
Posts: 42
10/01/2019 11:13 pm  
Posted by: Judah Bauer
Just out of curiousity...is there anything that shouldn't be taken w/ r ALA that could affect its efficacy?

Well...racemic ala.

Biotin should always be taken with r-ala. 1mg/100mg

GLA+r-ALA(+Biotin) will enhance R-ALA

And then CLA+GLA+R-ALA(+Biotin) will be the ultimate synergistic nutrient partitioning combo you can buy.

Cheap, but still the most effective. More so than metformin or phenformin.

Green tea I consider a thermogenic not a nutrient partitioning agent.

ALCar is more expensive and a more technical part of the stack. Beginners shouldn't really have to deal with it. They can do w/o it.

Fonz


ReplyQuote
iced
 iced
(@iced)
Active Member
Joined: 11 months ago
Posts: 19
11/01/2019 12:12 am  
Posted by: Fonz
Well...racemic ala.

Biotin should always be taken with r-ala. 1mg/100mg

GLA+r-ALA(+Biotin) will enhance R-ALA

And then CLA+GLA+R-ALA(+Biotin) will be the ultimate synergistic nutrient partitioning combo you can buy.

Cheap, but still the most effective. More so than metformin or phenformin.

Green tea I consider a thermogenic not a nutrient partitioning agent.

ALCar is more expensive and a more technical part of the stack. Beginners shouldn't really have to deal with it. They can do w/o it.

Fonz

What is the mess i hear about CLA and GLA comepting for the same enzyme or soemthing and shoudlnt be taken at the same time?


ReplyQuote
Share:
  
Working

Please Login or Register