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NEW PRODUCT!! FOLLIDRONE FAQ

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With the 3mg a cap boron would it make a difference taking all 3 at once or spacing them out? Like morning preworkout and bed?
 
Follidrone arrived for me today as well. Ready to rumble
 
mavado said:
Is there an ETA on the restock? NP still on soldout status :(
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Its gonna be a bit before NP has more.

We are shipping to the UK next and then hopefully within 7-10 days we will start shipping to all of our US retailers.
So not long. A week or so it will be available. Probably not NP first though as our other retailers want a crack at it.

Strong supps
TGB supps
Orbit nutrition

7-10 days
 
It was so weird, I been randomly checking Nutraplant for it to be on stock as I missed the presale....so a few times at work for sh!ts and giggles i'll hit refresh on the product page....did it yesterday afternoon and all of a sudden there was "1 left"....I ordered it and choose expedited shipping, and it was shipped last night.....I'm assuming I'm actually getting follidrone and it wasn't an error.....but so weird it would randomly have 1 left. Not that I'm complaining haha.

Going to start this, Formeron and cistamax on a cut. Codense as my pre and also have AAV2 on hand.
 
WHEN NP get follidrone back in stock, will they also get formeron in stock at the same time? I'd like to order them together
 
funkd0c said:
WHEN NP get follidrone back in stock, will they also get formeron in stock at the same time? I'd like to order them together
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Orbit will be getting of in stock sooner and also has stock of Formeron

Invalid Link Removed

Just sayin ;)
 
cubs1987 said:
not to be a smartass... but it says Out of Stock when I go to the orbit link you posted.
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Not being a smart ass, thats me being a dumb ass lol it was in stock this morning.

I would assume Formeron would be restocked with the Follidrone shipment

Sorry for that
 
Orbit will be in stock shortly. They just ordered yesterday and it generally takes a few days for us to fill orders under the best circumstances.
Orbit will have stock of Formeron and Follidrone at the same time. They will likely have Formeron first though.
 
Sorry to throw the conversation 'into Orbit' lol.


Back on track: day 3 of Folli for me now, didn't notice much difference until my finishing "destroyer" set of rows supersetted with wide-grip pull ups.

No rest between, continued until the sets drop below 3 reps. Took a LOT longer today. I tend not to keep a count in my finishers but out of interest while taking Folli I now will
 
Alright guys.... Get ready for the claim of the year!
Week 2 1/2 on follidrone. BEFORE folli my squat max was (x) for 6 reps, then 4, then 4. Due to being new to squats and under 145lbs for most of my weight lifting life I prefer to not state the number because it is EMBARRASSING. (Pm me if you really want to know). Well... I tried my max today, hit it TEN times. Put twenty more pounds on, hit it TEN times, then put 40 more pounds on then previous max and hit it SEVEN times. Holy crap. Long story short, before folli my max I could hit 6 times. 2 1/2 weeks in and I'm +40 pounds for 7 reps!!!
 
Looks like someone got the lucky bottle with the tren added in!

Haha. That is amazing, man. Good for you. Now the test is to log that and see if you can hit it the next time to make sure it is sustainable.
 
I always end up taking it on an empty stomach but I don't need if it really makes a difference.
 
Sounds like you're getting better at squats.

htghunterray said:
Alright guys.... Get ready for the claim of the year!
Week 2 1/2 on follidrone. BEFORE folli my squat max was (x) for 6 reps, then 4, then 4. Due to being new to squats and under 145lbs for most of my weight lifting life I prefer to not state the number because it is EMBARRASSING. (Pm me if you really want to know). Well... I tried my max today, hit it TEN times. Put twenty more pounds on, hit it TEN times, then put 40 more pounds on then previous max and hit it SEVEN times. Holy crap. Long story short, before folli my max I could hit 6 times. 2 1/2 weeks in and I'm +40 pounds for 7 reps!!!
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uubiduu said:
can folli be used in a otc pct after osta?or better to be used later?
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It can be used during PCT but it wont do anything to help you recover your HPTA so youll need to use Formeron or another PCT supp.
 
Mystere3 said:
Sounds like you're getting better at squats.
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I'd have to agree with you man! haha
alright screw it i'll spill the weights (dont make fun of me.) My bodyweight hovers from 145-150. My previous max before follidrone was 160. embarrassing as that is I could only get it up 6 times, then 4, then 4. 1st week into folli i got it 8,8,8.. I was happy with that. Today I hit 10 reps, put a ten on each side then hit it for ten more reps. Shocked at myself, I put two 45lb plates on each side and hit 7 reps. I honestly felt like I had 1-2 more in me. I am only taking follidrone along with protein and a pre-workout. I have never touched a pro hormone or steroid. I am only 19 and have been lifting for about 13 months. However, 13 months ago i was around 125.
 
The Follidrone may be helping but I think the bigger factor is simply progressing in your training.

htghunterray said:
I'd have to agree with you man! haha
alright screw it i'll spill the weights (dont make fun of me.) My bodyweight hovers from 145-150. My previous max before follidrone was 160. embarrassing as that is I could only get it up 6 times, then 4, then 4. 1st week into folli i got it 8,8,8.. I was happy with that. Today I hit 10 reps, put a ten on each side then hit it for ten more reps. Shocked at myself, I put two 45lb plates on each side and hit 7 reps. I honestly felt like I had 1-2 more in me. I am only taking follidrone along with protein and a pre-workout. I have never touched a pro hormone or steroid. I am only 19 and have been lifting for about 13 months. However, 13 months ago i was around 125.
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Mystere3 said:
The Follidrone may be helping but I think the bigger factor is simply progressing in your training.
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You may be right, but the thing is my bench has been stuck for almost 2 months. I thought it was crazy for my squats to spike up like that.
 
htghunterray said:
You may be right, but the thing is my bench has been stuck for almost 2 months. I thought it was crazy for my squats to spike up like that.
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It can happen. That's just how training works. In an inexperienced lifter that's the most likely explanation.

I've noticed modest improvements in strength on stable doses of dmz/trest.
 
htghunterray said:
I'd have to agree with you man! haha
alright screw it i'll spill the weights (dont make fun of me.) My bodyweight hovers from 145-150. My previous max before follidrone was 160. embarrassing as that is I could only get it up 6 times, then 4, then 4. 1st week into folli i got it 8,8,8.. I was happy with that. Today I hit 10 reps, put a ten on each side then hit it for ten more reps. Shocked at myself, I put two 45lb plates on each side and hit 7 reps. I honestly felt like I had 1-2 more in me. I am only taking follidrone along with protein and a pre-workout. I have never touched a pro hormone or steroid. I am only 19 and have been lifting for about 13 months. However, 13 months ago i was around 125.
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This sort of increase was seen in 2 of our trial testers.
Im not sure why it hits some harder than others.
Thats a big increase. More than anyone would expect just from weekly improvements in a novice trainer.
This indicates that the follidrone is having an impact.
 
this stuff available yet?
 
I've been kinda quiet about it, because I'm just kinda waiting for the punch line. Deads up 30 lbs, bench up 20 lbs, pull-ups added 3 reps, barbell curls another 10 lbs... I just don't get it. My shoulders look bigger, dips I've added 5 reps to a set and my triceps feel godly after the set. I'm going on vacation in a few days, most likely won't be working out, should I maintain dosing, drop to one pill a day, or save it for when I get back?
 
Brundel I saw this study quoted on another forum, can you explain what it means in relation to follidrone, I might be a bit thick but does it say there was heart growth or not?

Effects of myostatin deletion in aging mice.
Morissette MR1, Stricker JC, Rosenberg MA, Buranasombati C, Levitan EB, Mittleman MA, Rosenzweig A.
Author information
Abstract
Inhibitors of myostatin, a negative regulator of skeletal muscle mass, are being developed to mitigate aging-related muscle loss. Knock-out (KO) mouse studies suggest myostatin also affects adiposity, glucose handling and cardiac growth. However, the cardiac consequences of inhibiting myostatin remain unclear. Myostatin inhibition can potentiate cardiac growth in specific settings (Morissette et al., 2006), a concern because of cardiac hypertrophy is associated with adverse clinical outcomes. Therefore, we examined the systemic and cardiac effects of myostatin deletion in aged mice (27-30 months old). Heart mass increased comparably in both wild-type (WT) and KO mice. Aged KO mice maintained twice as much quadriceps mass as aged WT; however, both groups lost the same percentage (36%) of adult muscle mass. Dual-energy X-ray absorptiometry revealed increased bone density, mineral content, and area in aged KO vs. aged WT mice. Serum insulin and glucose levels were lower in KO mice. Echocardiography showed preserved cardiac function with better fractional shortening (58.1% vs. 49.4%, P = 0.002) and smaller left ventricular diastolic diameters (3.41 vs. 2.71, P = 0.012) in KO vs. WT mice. Phospholamban phosphorylation was increased 3.3-fold in KO hearts (P < 0.05), without changes in total phospholamban, sarco(endo)plasmic reticulum calcium ATPase 2a or calsequestrin. Aged KO hearts showed less fibrosis by Masson's Trichrome staining. Thus, myostatin deletion does not affect aging-related increases in cardiac mass and appears beneficial for bone density, insulin sensitivity and heart function in senescent mice. These results suggest that clinical interventions designed to inhibit skeletal muscle mass loss with aging could have beneficial effects on other organ systems as well.
 
heavyweight83 said:
Brundel I saw this study quoted on another forum, can you explain what it means in relation to follidrone, I might be a bit thick but does it say there was heart growth or not?

Effects of myostatin deletion in aging mice.
Morissette MR1, Stricker JC, Rosenberg MA, Buranasombati C, Levitan EB, Mittleman MA, Rosenzweig A.
Author information
Abstract
Inhibitors of myostatin, a negative regulator of skeletal muscle mass, are being developed to mitigate aging-related muscle loss. Knock-out (KO) mouse studies suggest myostatin also affects adiposity, glucose handling and cardiac growth. However, the cardiac consequences of inhibiting myostatin remain unclear. Myostatin inhibition can potentiate cardiac growth in specific settings (Morissette et al., 2006), a concern because of cardiac hypertrophy is associated with adverse clinical outcomes. Therefore, we examined the systemic and cardiac effects of myostatin deletion in aged mice (27-30 months old). Heart mass increased comparably in both wild-type (WT) and KO mice. Aged KO mice maintained twice as much quadriceps mass as aged WT; however, both groups lost the same percentage (36%) of adult muscle mass. Dual-energy X-ray absorptiometry revealed increased bone density, mineral content, and area in aged KO vs. aged WT mice. Serum insulin and glucose levels were lower in KO mice. Echocardiography showed preserved cardiac function with better fractional shortening (58.1% vs. 49.4%, P = 0.002) and smaller left ventricular diastolic diameters (3.41 vs. 2.71, P = 0.012) in KO vs. WT mice. Phospholamban phosphorylation was increased 3.3-fold in KO hearts (P < 0.05), without changes in total phospholamban, sarco(endo)plasmic reticulum calcium ATPase 2a or calsequestrin. Aged KO hearts showed less fibrosis by Masson's Trichrome staining. Thus, myostatin deletion does not affect aging-related increases in cardiac mass and appears beneficial for bone density, insulin sensitivity and heart function in senescent mice. These results suggest that clinical interventions designed to inhibit skeletal muscle mass loss with aging could have beneficial effects on other organ systems as well.
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In many cases, cardiac hypertrophy is an indicator of another pathological condition such as high blood pressure, hence the association. Hypertrophy in response to exercise is fine.
 
Alright you guys, I'm back. lol. This is NOT placebo... i've lost ten pounds from being bed ridden a week or so ago. So psychically i'm just getting back into the swing of things. The week before i got sick (and before folli) I hit 60lbs on seated arnold press for 8,7,5.. this week, still getting back to my normal self and down ten pounds from the virus I hit 60lbs 8 times, then 9, then 8. Folli is LEGIT guys. For reps to go up like that after being bed-ridden for a week is insane to me.
 
digitalducki said:
I've been kinda quiet about it, because I'm just kinda waiting for the punch line. Deads up 30 lbs, bench up 20 lbs, pull-ups added 3 reps, barbell curls another 10 lbs... I just don't get it. My shoulders look bigger, dips I've added 5 reps to a set and my triceps feel godly after the set. I'm going on vacation in a few days, most likely won't be working out, should I maintain dosing, drop to one pill a day, or save it for when I get back?
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I didnt believe it at first either.....It was just too hard to believe that something thats been sitting in front of us forever hasnt been utilized.
Especially when its this good.
These days there are not many supplements that are new to the industry. They are all repackaging of old stuff or combos of old stuff.
Nothing really making waves as a new ingredient.

Ive been looking hard for years. Finally I found something.


Its a game changer.
 
To be honest, I was stronger when I was sick too (with less endurance) so you might want to wait a little bit longer before you give FD all the credit. Then again, Follidrone endurance seemed to kick in fast regardless.
 
heavyweight83 said:
Brundel I saw this study quoted on another forum, can you explain what it means in relation to follidrone, I might be a bit thick but does it say there was heart growth or not?

Effects of myostatin deletion in aging mice.
Morissette MR1, Stricker JC, Rosenberg MA, Buranasombati C, Levitan EB, Mittleman MA, Rosenzweig A.
Author information
Abstract
Inhibitors of myostatin, a negative regulator of skeletal muscle mass, are being developed to mitigate aging-related muscle loss. Knock-out (KO) mouse studies suggest myostatin also affects adiposity, glucose handling and cardiac growth. However, the cardiac consequences of inhibiting myostatin remain unclear. Myostatin inhibition can potentiate cardiac growth in specific settings (Morissette et al., 2006), a concern because of cardiac hypertrophy is associated with adverse clinical outcomes. Therefore, we examined the systemic and cardiac effects of myostatin deletion in aged mice (27-30 months old). Heart mass increased comparably in both wild-type (WT) and KO mice. Aged KO mice maintained twice as much quadriceps mass as aged WT; however, both groups lost the same percentage (36%) of adult muscle mass. Dual-energy X-ray absorptiometry revealed increased bone density, mineral content, and area in aged KO vs. aged WT mice. Serum insulin and glucose levels were lower in KO mice. Echocardiography showed preserved cardiac function with better fractional shortening (58.1% vs. 49.4%, P = 0.002) and smaller left ventricular diastolic diameters (3.41 vs. 2.71, P = 0.012) in KO vs. WT mice. Phospholamban phosphorylation was increased 3.3-fold in KO hearts (P < 0.05), without changes in total phospholamban, sarco(endo)plasmic reticulum calcium ATPase 2a or calsequestrin. Aged KO hearts showed less fibrosis by Masson's Trichrome staining. Thus, myostatin deletion does not affect aging-related increases in cardiac mass and appears beneficial for bone density, insulin sensitivity and heart function in senescent mice. These results suggest that clinical interventions designed to inhibit skeletal muscle mass loss with aging could have beneficial effects on other organ systems as well.
Click to expand...

Some drugs under development currently for sarcopenia, muscular dystrophy, cancer, aids wasting etc are myostatin inhibitors.
(-)-epicatechin is actually one of them.

Lots of them appear to potentially cause harm to the heart.
It doesnt appear (-)-epicatechin does this though.

In addition I dont think whoever posted this study read it.
This study shows it actually improved health.


Look at the same text now.


Inhibitors of myostatin, a negative regulator of skeletal muscle mass, are being developed to mitigate aging-related muscle loss. Knock-out (KO) mouse studies suggest myostatin also affects adiposity, glucose handling andcardiac growth. However, the cardiac consequences of inhibiting myostatin remain unclear. Myostatin inhibition can potentiate cardiac growth in specific settings (Morissette et al., 2006), a concern because of cardiac hypertrophy is associated with adverse clinical outcomes. Therefore, we examined the systemic and cardiac effects of myostatin deletion in aged mice (27-30 months old). Heart mass increased comparably in both wild-type (WT) and KO mice. Aged KO mice maintained twice as much quadriceps mass as aged WT; however, both groups lost the same percentage (36%) of adult muscle mass. Dual-energy X-ray absorptiometry revealed increased bone density, mineral content, and area in aged KO vs. aged WT mice. Serum insulin and glucose levels were lower in KO mice. Echocardiography showed preserved cardiac function with better fractional shortening (58.1% vs. 49.4%, P = 0.002) and smaller left ventricular diastolic diameters (3.41 vs. 2.71, P = 0.012) in KO vs. WT mice. Phospholamban phosphorylation was increased 3.3-fold in KO hearts (P < 0.05), without changes in total phospholamban, sarco(endo)plasmic reticulum calcium ATPase 2a or calsequestrin. Aged KO hearts showed less fibrosis by Masson's Trichrome staining. Thus, myostatin deletion does not affect aging-related increases in cardiac mass and appears beneficial for bone density, insulin sensitivity and heart function in senescent mice. These results suggest that clinical interventions designed to inhibit skeletal muscle mass loss with aging could have beneficial effects on other organ systems as well.


Please PM me a link to the thread this was in so I can tell people the truth.

Thanks
 
T-Bone said:
Your body will over-compensate naturally when recovering from a serious illness. Also how old are you?. Just would like to know, because in general younger guys, newer to training will recover faster. I'd put things in perspective before attributing all your gains to a supplement.
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Since every other user is seeing similar results it makes sense that Follidrone is working.
He lost 10lbs and retained his strength. THis is part of what (-)-epicatechin is being studied for. Strength and muscle retention during wasting.

Talking to the pilot of a study being done at UCdavis it appears that everything we are seeing in logs and by users is also happening in studies.
The new study will be out at the end of the year.

99% certain is the (-)-epi.
 
I don't really feel like I'm seeing gains on top of what I'd normally expect from the cycle I'm on. If anything Follidrone should greatly potentiate the effects of AAS.
 
Mystere3 said:
I don't really feel like I'm seeing gains on top of what I'd normally expect from the cycle I'm on. If anything Follidrone should greatly potentiate the effects of AAS.
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Its difficult to gauge when AAS are on board unless your at the end of a cycle. THis seems to be where it shines.
One of our trial runners was at the end of a super long cycle and he had stalled months before.
Follidrone seemed to restart the cycle as he started growing again.

This is likely because on cycle myostatin increases over time. Dropping it to normal or below normal will cause a growth spurt.

I would save it for the end.
 
wgere can i buy this stuff? does vitamin shoppe carry it?
 
Yeah I'm in the last week-week and a half. I'm def making gains I'm just not really sure it's secondary to the Follidrone. Also at this point strength isn't going to increase much for me. I have made modest gains though.

brundel said:
Its difficult to gauge when AAS are on board unless your at the end of a cycle. THis seems to be where it shines.
One of our trial runners was at the end of a super long cycle and he had stalled months before.
Follidrone seemed to restart the cycle as he started growing again.

This is likely because on cycle myostatin increases over time. Dropping it to normal or below normal will cause a growth spurt.

I would save it for the end.
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fightnews said:
wgere can i buy this stuff? does vitamin shoppe carry it?
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I just shipped to the UK.

Early next week Ill ship to TGB supps, strong supps and orbit nutrition.

There are only 60 units left so they will likely get 20/20/20

Reinforcements are en route though and I plan on paying extra to have them rush manufactured.
Should have stock for everyone within 2 weeks max.

NP will get a large shipment first on this one.

After this there should be no lapses although it sells extremely fast.

I shipped 70 to NP and it was gone in a couple hours lol.

Im working on vitamin shopp
GNC
BB.com
Europa
lonestar
Max muscle

The only thing holding us back currently is stock issues.
 
raz_kaz248 said:
Time to crack that whip and get the boys to put in the overtime!

I will be very sad if this stuff works out for me then have to wait months to get a descent supply
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I knew this stuff was amazing. For certain.
What I didnt expect was the sales response once logs went up. As soon as people saw it was working everyone jumped.
50 units in the first 30 min sold by NP.
This was not expected. We got slammed. now.....Im not complaining. Im stoked lots of guys got it because now there are tons of non sponsored logs and reviews up. There is just no denying it.

Im working with the manufacturer of the ingredient to make sure we dont hit any snags.
 
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