serious mass made me gain 1.5 kg in 5 days lmao
i thought this was a scam, id. if its fat or abs (my abs look the same anyway) my chest got bigger in circunference tho, cant tell about arms or forearms
this shit seems good, why the fuck didnt i buy this before,i could never broke the 180 lbs mark
i wanna reach 230 lbs and go or the strongfat look
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This is a one way ticket to Diabetes. The main ingredient is actually WORSE than sugar. I used a few bottles before wisening up. It fucked my shit up BIG time.
>It fucked my shit up BIG time.
what do you mean ? im not plaining on taking this forever, honestly im happy with anything from 200-225 lbs whatever its muscle or fat
also i was thinking on going for creatine but if my body responds well to serious mass, wont
made my face and gut fat as fuck, gave me acne etc. Its fucking dogshit. Make your own mass gainer shake using peanut butter, blended oats and fruit, you can easily mix those ingredients with protein powder and get 600-750 cals a shake.
Sugar isn't bad for you lol
why cant you just eat more? lmao
how much weight did you gain in how much time ?
did your lifting numbers improve
also did you reverse its effects ?
i have very good lactose tolerance btw
im doing both
have you seen strength gains from this yet?
yes on deadlifts,3 pl8 felt harder a week ago, now feels lighter
the rest, didnt feel that much difference still
Natties can only gain 1.5 lbs actual muscle per month.
>1.5 kg in 5 days lmao
You're just getting fat, you fat fuck
i said that i didnt care if it was fat or lean muscle since my abs are still visible
This. Find a gainer without a lot of sugar in it.
Disease pathology of diabetes is the chronic elevation of blood sugar, whereby chronic insulin release causes a loss of insulin sensitivity by the cells in the body. Alzheimers is said to be type 3 diabetes.
The mass release of insulin as caused by sugar which triggers a human physiological mechanism for fat storage. They use this mechanism purposefully on farm animals to fatten them faster. It also destroys their bodies and requires they be pumped full of antibiotics to treat numerous metabolic degenerations of their body. Excessive glucose also glycates cells in your body making them far more likely to oxidize due to inflammatory factors, or chronic infammatory factors, ie constantly snacking throughout the day.
In terms of your body requirement for sugar(table sugar, carbohydrate) there is no such requirement. You body at any given period is utilizing 50% of its energy from body fat. Vastly more so when you're "fat adapted". In terms of athletics, its starting to show in data and with specific outliers.
Best thing about fat, it almost doesn't even create a spike. Because fat is extremely easy for out enzymatic stomachs to uptake, its extremely soluble at room temperature and the natural stuff is described as "melting in ones mouth". Grain and corn feed animals have a noticeably different fat composition which is harder to chew.
*slowly sips on my whey isolate protein shake*
NOOOOOOO
It's over
so what are you trying to say
u sure its the mass gainer and not u getting used to the weight?
Listen, dipshit, you're not gaining more than .25 of muscle a week EVEN IF you're gaining more weight than that. Stop turning into a fat fuck for no reason.
Based
>Stop turning into a fat fuck for no reason.
what if being a bloatlord is my path ?
We can see the poster count staying the same while they replies fly in asshole
I own this shit too
based and redpilled
is it good? thinking about joining the club
Ur an idiot if u believe this
Its very good! Look at my guns!
Provide a counter point
WHAT!?
Yeah good job writing that little essay user but it doesn't mean you're right. FAT causes type 2 diabetes. By your retarded logic EVERYONE should be diabetic by age 30 because every time you eat something there's going to be more glucose in your blood stream thus releasing more insulin and making you some how diabetic. You're just another keto/carnitard parroting bullshit.
Samefag.
Studies dating back nearly a century noted a striking finding: If you take young, healthy people and split them up into two groups—half on a fat-rich diet and half on a carbohydrate-rich diet—we find that within just two days, glucose intolerance skyrockets in the fat group. The group that had been shoveling fat in ended up with twice the blood sugar. As the amount of fat in the diet goes up, so does one’s blood sugar. Why would eating fat lead to higher blood sugar levels? It would take scientists nearly seven decades to unravel this mystery, but it would end up holding the key to our current understanding of the cause of type 2 diabetes.
The reason athletes carb-load before a race is to build up the fuel supply within their muscles. We break down the starch into glucose in our digestive tract; it circulates as blood glucose (blood sugar) and is taken up by our muscles to be stored and burnt for energy.
Blood sugar, though, is like a vampire. It needs an invitation to come into our cells. That invitation is insulin. Insulin is the key that unlocks the door that lets glucose in the blood enter muscle cells. When insulin attaches to the insulin receptor on the cell, it activates an enzyme, which activates another enzyme, which activates two more enzymes, which finally activates glucose transport (as diagrammed in my video What Causes Insulin Resistance?).
Part 2 coming.
What if there was no insulin? Blood sugar would be stuck in the bloodstream banging on the door to our muscles, unable to get inside. With nowhere to go, sugar levels in the blood would rise and rise. That’s what happens in type 1 diabetes: the cells in the pancreas that make insulin get destroyed, and without insulin, sugar in the blood can’t get out of the blood into the muscles, and so blood sugar rises. But there’s a second way we could end up with high blood sugar.
What if there’s enough insulin, but the insulin doesn’t work? The key is there, but something’s gummed up the lock. This is insulin resistance. Our muscle cells become resistant to the effect of insulin. What’s gumming up the locks on our muscle cells? What’s preventing insulin from letting glucose in? Tiny droplets of fat inside our muscle cells, so-called intramyocellular lipid.
Fat in the bloodstream can build up inside the muscle cells, creating toxic fatty breakdown products and free radicals that block the insulin signaling process. No matter how much insulin we have in our blood, it’s not able to sufficiently open the glucose gates, and blood sugar levels build up in the blood. And this can happen within three hours. One hit of fat can start causing insulin resistance, inhibiting blood sugar uptake after just 160 minutes.
This mechanism by which fat induces insulin resistance wasn’t known until fancy MRI techniques were developed to see what was happening inside people’s muscles as fat was infused into their bloodstream. That’s how we found that elevation of fat levels in the blood causes insulin resistance by inhibition of glucose transport into the muscles.
Part 3
We can also do the opposite experiment. Lower the level of fat in people’s blood and the insulin resistance comes right down. If we clear the fat out of the blood, we also clear the sugar out. That explains the finding that on the high fat, ketogenic diet, insulin doesn’t work very well. Our bodies become insulin resistant. But as the amount of fat in our diet gets lower and lower, insulin works better and better—a clear demonstration that the sugar tolerance of even healthy individuals can be impaired by administering a low-carb, high-fat diet. We can decrease insulin resistance, however, by decreasing fat intake.
The effect is really dramatic–check out at least the end of my video What Causes Insulin Resistance? to see what happens as dietary fat intake drops.
The most concerning downside of low-carb diets, though, is heart health: Low Carb Diets and Coronary Blood Flow.
Got plenty more studies to back up these claims, just let me know if you want to be BTFO even harder than you have already.
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Osteoporosis:
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Low Carbohydrate Diets and mortality:
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Eat shit, keto-tard.
>Diabetes Mellitus
>Diabetes mellitus (DM) is a group of diseases characterized by a disrupted carbohydrate metabolism leading to elevated blood glucose levels (= hyperglycemia) and secretion of glucose in the urine (= glycosuria) as a result of insufficient production or functioning of the pancreatic hormone insulin, combined with a number of yet undefined predisposing factors.
>DM is not a pathogenic entity but a group of etiologically different metabolic defects. Chronic hyperglycemia causes long-term damage, dysfunction and failures of various cells, tissues and organs.
Sauce: diagnostics.eu.tosohbioscience.com
Fat causes almost no insulin response, and that it does is severely short, any diabetic with a blood sugar tester and any glycemic load index will tell you the obvious. Fat alone cannot create a diabetic, its almost impossible, save one particular context where it works well.
If you mashed in carbohydrates into that mix, as per the human physiological mechanism of the Randle Cycle. Mashing these macros fat+carbs would increase insuligenic response in the body, because these are two different competing energy systems. Thus the toxic effect of carbohydrates is significantly increased and the body launches a lot of insulin to store these energy sources.
>The reason athletes carb-load before a race is to build up the fuel supply within their muscles. We break down the starch into glucose in our digestive tract; it circulates as blood glucose (blood sugar) and is taken up by our muscles to be stored and burnt for energy.
Human energy systems are not linear, you're simply embarrassing yourself with these illiterate statements. If we had a linear energy system we would simply die out from fasting for 24-72hrs. Refer to gluconeogenesis in human physiology. Simplified after a meal once the insulin response dies off, your body starts to always defaults to fat burning.
P2 coming
I'm currently eating
>ignores all the links to studies posted
>post more ketotard babbel.
Yeah nah you're wrong and have been proven wrong already. You didn't even read what I posted because you said
>Fat causes almost no insulin response
That's not the point at all, you brainlet. The point is that fat stops your cells from responding to insulin. Look I don't really care, if you wanna kill yourself slowly on your high fat, high meat diet then go ahead but keep that Ivor cummins shilling to yourself.
Look, they even made a simplistic little graphic so brainlets can understand it.
Imagine being such a fucking moron you think glucose and insulin cause diabetes lmao.
Every single time you eat something there's gonna be a rise in blood sugar and a release of insulin, it's as simple as that. By your braindead keto-tard, clogged artery logic, all humans should be diabetic by their 30s.
Part 1 Part 2
>That explains the finding that on the high fat, ketogenic diet, insulin doesn’t work very well.
People on those diets unsurprisingly become highly insulin sensitive, because of the lacking insulin spike or duration of it. People on those diets also are far less likely to chronically elevate blood sugar, thus insulin. Thus achieving insulin sensitivity. Without insulin sensitivity you basically slide towards diabetes. This is not a difficult concept as to the original diabetes Diabetes Mellitus link.
>Lower the level of fat in people’s blood and the insulin resistance comes right down. If we clear the fat out of the blood, we also clear the sugar out.
You blood is loaded with lipo-proteins, google Cholesterol metabolism. You're clearly illiterate of human physiology, if you removed cholesterol from your blood stream you would drop dead, no questions asked
I'm not reading any of this unless you can annotate and reference the links in your own words, as in displaying you have actual comprehension of the materials, thus far you have proven otherwise. Secondly these are all (((correlations))), you don't actually have anything from human physiology, with known biological mechanisms to them. Like actual provable, repeatable research. Not some tin foil cheap shit they mass produce for clicks, which correlative studies are notorious for.
Again Diabetes Mellitus is known in human pathophysiology as being caused by chronic elevation of blood sugar, and thus insulin. This also causes a known inflammatory effect which causes numerous metabolic disorders in human physiology.
>Long-term complications of diabetes are:
>Macro-angiopathy: Ischemic heart disease (IHD), stroke, peripheral vascular disease (PVD)
>Micro-angiopathy: Retinopathy, nephropathy
>Neuropathy: Peripheral neuropathy, autonomic neuropathy
>Diabetic Heart
Sauce: diagnostics.eu.tosohbioscience.com
Yes, when you fat adapt you do not molest your metabolic rate as if you would on CICO(calories in, calories out). If you're on the snake juice fast, you will become a fat burning machine. Same thing if you were keto or carnivore diets. Especially more effective if you're body building, you can do OMAD(one meal a day) and eat a huge protein meal to retain muscle mass.
How do we know CICO suppresses the human metabolic rate? Recall the show biggest loser, a popular MSM torture of the obese? They did labs on these people after to follow up. They all had a suppressed metabolic rate after the show by doing CICO, unsurprisingly they almost all became fat shits again.
So drop the CICO annon, that shit is not effective. However keep up your fasts, you'll get better results on it alone then sabotaging it with CICO.
Part 3
>The point is that fat stops your cells from responding to insulin
>There are no GI values given for meat, poultry, fish,avocados, salad vegetables, cheese, or eggs because these foods contain little or no carbohydrate and it would be exceedingly difficult for people to consume a portion of the foods containing 50 gor even 25 g of available carbohydrate. Even in large amounts,these foods when eaten alone are not likely to induce a significant rise in blood glucose.
Sauce: International table of glycemic index and glycemic load values: 20021, 2 -Kaye Foster-Powell, Susanna HA Holt, and Janette C Brand-Miller
>The liver is an essential metabolic organ, and its metabolic activity is tightly controlled by insulin and other metabolic hormones. Glucose is metabolized into pyruvate through glycolysis in the cytoplasm, and pyruvate is completely oxidized to generate ATP through the TCA cycle and oxidative phosphorylation in the mitochondria. In the fed state, glycolytic products are used to synthesize fatty acids through de novo lipogenesis. Long-chain fatty acids are incorporated into triacylglycerol, phospholipids, and cholesterol esters in hepatocytes, and these complex lipids are stored in lipid droplets and membrane structures, or secreted into the circulation as VLDL particles. In the fasted state, the liver secretes glucose through both breakdown of glycogen (glycogenolysis) and de novo glucose synthesis (gluconeogenesis).
Energy Metabolism in the Liver
ncbi.nlm.nih.gov
Part 4
Energy Metabolism in the Liver
ncbi.nlm.nih.gov
>The point is that fat stops your cells from responding to insulin
Your body runs on cholesterol/fatty acids you retard. Secondly the thing "Dr.Gregor" that vegan runs his mouth on is his (((correlations))) of fatty liver and insulin resistance. Tell me what happens when you constantly pump glucose into blood stream for it to convert to adipose fat tissue? A fat liver you stupid retard, its seen in farm animals who're pumped full of starches(grains, corn).
Why does fat barely need insulin for storage? Because it comes in as usable form that the human body is naturally adapted too. Because guess what you stupid motherfucker, human energy systems run on fat and we're incredibly proficient fat burners for ATP energy production.
Guess what Glycation from excessive sugar consumption does?
>Glycation (sometimes called non-enzymatic glycosylation) is the result of the covalent bonding of a sugar molecule, such as glucose or fructose, to a protein or lipid molecule, without the controlling action of an enzyme. Glycation may occur either inside the body (endogenous glycation) or outside the body (exogenous glycation). It is a haphazard process that impairs the functioning of biomolecules, and does not require the expenditure of ATP (the energy carrying molecule).
>Glycosylation, in contrast, is the enzyme-mediated ATP-dependent attachment of sugars to protein or lipid molecules at defined sites on the target molecule. It is an important form of post-translational modification of proteins and is required for the functioning of the mature molecule.
>Much of the early laboratory research work on fructose glycations used inaccurate assay techniques that led to drastic underestimation of the importance of fructose in glycation.[1]
Its just extra calories dude probably mostly from dextrose which is carbs.