To be fair, he did qualify the statement.
Best of luck on your own frontline!
To be fair, he did qualify the statement.
To be fair, he did qualify the statement.
If he is drawing SJWs he’s a traitor to the ‘pit.ConcentratedH2O, OM wrote: ↑ I won't say where, but I stumbled upon another forum recently, and my eye was drawn by a very familiar style of photoshopped image. Yes, Pitizen Ape+Lust is doing his thing elsewhere. He goes by a different name, but his work is drawing amazed gasps over there just as it used to do here...and who knows where else before the Pit.
God bless you, Ape, you're a wonderful person.
"Harry Miller was visited by Humberside Police at work in January last year after a complaint about his tweets.
He was told he had not committed a crime, but it would be recorded as a non-crime "hate incident".
The court found the force's actions were a "disproportionate interference" with his right to freedom of expression.
Officers visited Mr Miller's workplace and then spoke with him on the phone, and he was left with the impression "that he might be prosecuted if he continued to tweet", according to a judge.
Speaking after the ruling, Mr Miller, from Lincolnshire, said: "This is a watershed moment for liberty - the police were wrong to visit my workplace, wrong to 'check my thinking'."
His solicitor Paul Conrathe added: "It is a strong warning to local police forces not to interfere with people's free speech rights on matters of significant controversy.
Naw, the burkini is back. https://swimsuit.si.com/swim-daily/2020 ... del-revealMatt Cavanaugh wrote: ↑ no burkinis
Will do.
Blip. You know it. Poor devil will be on the hit list for his local police for decades. If he tries to drive under the speed limit they will get him for "failure to make normal progress" (yes, it really exists!)
Be careful what you ask for: we will all have to look at it and then we will come after you.Matt Cavanaugh wrote: ↑ Sports Illustrated's "most diverse evah" swimsuit issue:
Also includes one morbidly obese model, a baldy, and a fairly hawt 57-year-old. Still, no vitiligo this year, no burkinis, and when will SI truly diversify with achondroplasia and downs syndrome models?!!!
You get to call all the bullshit you want down on anyone today. We make allowances.Phil_Giordana_FCD wrote: ↑ We cremated my brother today. One of the longest mornings of my life. I think I've lost enough weight to call bullshit on Brive's diet.
Yes "we" do. You need the right (aka wrong) genes, and then excess calories and inadequate exercise. There is no confusion about this in the medical world, although I can see why there might be amongst the amateur dietitians and all the rest of the fat fucks who don't pay attention. A small difference in glucose control allows hyperglycemia to occur. Hyperglycemia kills beta cells in the pancreas. Remaining beta cells compensate by secreting extra insulin, masking the problem for several years, but also accelerating it as extra insulin increases appetite for carbs. When you finally run out of beta cells you get diagnosed, as blood sugars rise beyond normal limits. At this point you may be able to 'cure' yourself with dramatic weight loss and lots of exercise, but you will have to keep up with that regime forever. Otherwise, we have drugs to flog the few remaining beta cells to squeeze out more insulin, drugs to slow glucose absorption, and exogenous insulin. Pick your parents well, because you can't change the genes they give you.
My son has come home for a month. I've spent the day introducing him to the external ballistics of the .17 HMR cartridge. Miracles do happen.
screwtape wrote: ↑Sat Feb 15, 2020 1:11 pmThis may be a long one, but one has to shoot when one has the ammo:
Yes "we" do. You need the right (aka wrong) genes, and then excess calories and inadequate exercise. There is no confusion about this in the medical world, although I can see why there might be amongst the amateur dietitians and all the rest of the fat fucks who don't pay attention. A small difference in glucose control allows hyperglycemia to occur. Hyperglycemia kills beta cells in the pancreas. Remaining beta cells compensate by secreting extra insulin, masking the problem for several years, but also accelerating it as extra insulin increases appetite for carbs. When you finally run out of beta cells you get diagnosed, as blood sugars rise beyond normal limits. At this point you may be able to 'cure' yourself with dramatic weight loss and lots of exercise, but you will have to keep up with that regime forever. Otherwise, we have drugs to flog the few remaining beta cells to squeeze out more insulin, drugs to slow glucose absorption, and exogenous insulin. Pick your parents well, because you can't change the genes they give you.
free thoughtpolice wrote: ↑A day in the life of a Vancouver Island arborist. He's a limey that apparently was inspired by the Python's Lumberjack Song to move to BC and chop down mighty trees.
It's quite hard to place although I'm not picking up any hints of scouser. Subtle hints of Yorkshire in the way he pronounces certain words but not enough to be sure. Maybe an English 'pitter will have a better idea?free thoughtpolice wrote: ↑Maybe some of the Brits here might place his accent. A Scouser maybe?
Well, I just finished watching November - absolutely loved it! The story, suitably nutty, was very enjoyable (and well acted) but for me, the real selling point was the cinematography! Almost every shot is like a work of art; I could easily see framed stills being used to decorate an artsy-fartsy home. I particularly liked the stark, almost bleached, black & white scenes that hyper-focus the eye center-screen.
I would place it as Manchester, modified by some years in North America. Turns out he also spent some time in the antipodean penal colony to further confound matters: http://www.rctree.ca/about/Bhurzum wrote: ↑
It's quite hard to place although I'm not picking up any hints of scouser. Subtle hints of Yorkshire in the way he pronounces certain words but not enough to be sure. Maybe an English 'pitter will have a better idea?free thoughtpolice wrote: ↑Maybe some of the Brits here might place his accent. A Scouser maybe?
I listened again, and I might say Lancashire rather than Manchester. But this guy has lived in multiple other countries which I think is making it difficult to easily tell. Perhaps Bhurzum is right wit Yorkshire, he certainly is with his toffe-chewing arsehole. What a way to make a living *shivers*ConcentratedH2O, OM wrote: ↑I would place it as Manchester, modified by some years in North America. Turns out he also spent some time in the antipodean penal colony to further confound matters: http://www.rctree.ca/about/Bhurzum wrote: ↑
It's quite hard to place although I'm not picking up any hints of scouser. Subtle hints of Yorkshire in the way he pronounces certain words but not enough to be sure. Maybe an English 'pitter will have a better idea?free thoughtpolice wrote: ↑Maybe some of the Brits here might place his accent. A Scouser maybe?
Yes, insulin is required to allow glucose in the blood enter cells. Resistance simply means you need more insulin to have the same effect. As resistance develops, more insulin is needed, while at the same time the higher glucose levels are slowly killing off the pancreatic cells that make insulin. We know insulin resistance is heritable, and that it is expressed when one becomes overweight; you can come from a family of Type 2 diabetics and avoid it by staying thin and exercising a lot. It's obvious from the mechanism above that type 2 DM is a condition that progresses (diet-control, then diet + metformin, then diet + metformin + sulfonylurea, then diet + insulin), but the important thing to understand is that good control slows the progression as you keep your beta cells alive for longer if they aren't exposed to high blood sugars. Making the effort to do it right when the disease is mild is therefore very important, as it will do you more good in the long run than being obsessional about it at a later stage.Brive1987 wrote: ↑ After reading up I tried to summarise IR and eventual T2D into Brive-speak. Less technical but is it accurate?
So insulin normally tells cells to ‘open’ and accept necessary energy/cell fuel from blood glucose.
But, the onset of insulin resistance makes the cells resistant to insulin’s efforts and they don’t accept enough glucose. This then requires higher insulin doses to achieve a partial brute-force outcome. This dynamic in turn raises insulin levels and keeps resting or fasting blood sugar high with more glucose getting stored as fat rather than expended as energy. The cells, however, think they are starving and demand more food - you eat and the cycle repeats.
Eventually the brute force secretion of excess insulin wears the pancreas out. Insulin production fails and you are fucked with T2D.
Midlands for sure. Not Mancunian or Brummie, and certainly not a scouser. Northants, Leics, Staffs or even Cheshire.free thoughtpolice wrote: ↑ A day in the life of a Vancouver Island arborist. He's a limey that apparently was inspired by the Python's Lumberjack Song to move to BC and chop down mighty trees. Maybe some of the Brits here might place his accent. A Scouser maybe?
Strongly disagree. There's stuff at 6:54 which is very Manc IMHO.screwtape wrote: ↑Midlands for sure. Not Mancunian or Brummie, and certainly not a scouser. Northants, Leics, Staffs or even Cheshire.free thoughtpolice wrote: ↑ A day in the life of a Vancouver Island arborist. He's a limey that apparently was inspired by the Python's Lumberjack Song to move to BC and chop down mighty trees. Maybe some of the Brits here might place his accent. A Scouser maybe?
Metformin is big with the life extension set. I don't know why.screwtape wrote: ↑Yes, insulin is required to allow glucose in the blood enter cells. Resistance simply means you need more insulin to have the same effect. As resistance develops, more insulin is needed, while at the same time the higher glucose levels are slowly killing off the pancreatic cells that make insulin. We know insulin resistance is heritable, and that it is expressed when one becomes overweight; you can come from a family of Type 2 diabetics and avoid it by staying thin and exercising a lot. It's obvious from the mechanism above that type 2 DM is a condition that progresses (diet-control, then diet + metformin, then diet + metformin + sulfonylurea, then diet + insulin), but the important thing to understand is that good control slows the progression as you keep your beta cells alive for longer if they aren't exposed to high blood sugars. Making the effort to do it right when the disease is mild is therefore very important, as it will do you more good in the long run than being obsessional about it at a later stage.Brive1987 wrote: ↑ After reading up I tried to summarise IR and eventual T2D into Brive-speak. Less technical but is it accurate?
So insulin normally tells cells to ‘open’ and accept necessary energy/cell fuel from blood glucose.
But, the onset of insulin resistance makes the cells resistant to insulin’s efforts and they don’t accept enough glucose. This then requires higher insulin doses to achieve a partial brute-force outcome. This dynamic in turn raises insulin levels and keeps resting or fasting blood sugar high with more glucose getting stored as fat rather than expended as energy. The cells, however, think they are starving and demand more food - you eat and the cycle repeats.
Eventually the brute force secretion of excess insulin wears the pancreas out. Insulin production fails and you are fucked with T2D.
Metformin is interesting, as it has several mechanisms of action, and they aren't well understood. It does not squeeze out extra insulin from the pancreas (like sulfonylureas and their descendants) so it rarely causes hypoglycemia when used alone. The main effect seems to be on the liver's control of the short term storage and dispensation of glucose. Glucose is stored as glycogen in the liver, as a ready-use locker - a few molecules can be snipped off the chain and secreted into the blood when needed to keep the blood sugar at adequate levels when exercising or between meals. This is called gluconeogenesis. Metformin was felt to increase uptake of sugar into the liver, and to slow it's release later on. If, through insulin resistance, you have higher blood sugars the flip side of the coin is that sugar is stuff that ought to be intracellular. So the cells are short on glucose for energy and they don't like it. They signal the liver to release more glucose, raising the blood sugar but not doing them much good because that sugar still can't enter the cells. Type 2 diabetics have a lot more gluconeogenesis going on than non-diabetics as a result, and metformin interferes with this. It is also felt to interfere with the signalling by inhibiting production of glucagon, a hormone that raises blood glucose, and to reverse the insulin-insensitivity of some tissues to a small degree. An old, cheap, safe drug (more so than phenformin, which I'm old enough to remember). Should be in the water supply of fat western countries.
Metformin is big with the life extension set. I don't know why.katamari Damassi wrote: ↑
Thanks - as a hippo, my PCP has me on this, and in the last three months my glucose and A1c have gone down noticeably, so I've dropped out of pre-diabetes ranges for both.screwtape wrote: ↑Yes, insulin is required to allow glucose in the blood enter cells. Resistance simply means you need more insulin to have the same effect. As resistance develops, more insulin is needed, while at the same time the higher glucose levels are slowly killing off the pancreatic cells that make insulin. We know insulin resistance is heritable, and that it is expressed when one becomes overweight; you can come from a family of Type 2 diabetics and avoid it by staying thin and exercising a lot. It's obvious from the mechanism above that type 2 DM is a condition that progresses (diet-control, then diet + metformin, then diet + metformin + sulfonylurea, then diet + insulin), but the important thing to understand is that good control slows the progression as you keep your beta cells alive for longer if they aren't exposed to high blood sugars. Making the effort to do it right when the disease is mild is therefore very important, as it will do you more good in the long run than being obsessional about it at a later stage.Brive1987 wrote: ↑ After reading up I tried to summarise IR and eventual T2D into Brive-speak. Less technical but is it accurate?
So insulin normally tells cells to ‘open’ and accept necessary energy/cell fuel from blood glucose.
But, the onset of insulin resistance makes the cells resistant to insulin’s efforts and they don’t accept enough glucose. This then requires higher insulin doses to achieve a partial brute-force outcome. This dynamic in turn raises insulin levels and keeps resting or fasting blood sugar high with more glucose getting stored as fat rather than expended as energy. The cells, however, think they are starving and demand more food - you eat and the cycle repeats.
Eventually the brute force secretion of excess insulin wears the pancreas out. Insulin production fails and you are fucked with T2D.
Metformin is interesting, as it has several mechanisms of action, and they aren't well understood. It does not squeeze out extra insulin from the pancreas (like sulfonylureas and their descendants) so it rarely causes hypoglycemia when used alone. The main effect seems to be on the liver's control of the short term storage and dispensation of glucose. Glucose is stored as glycogen in the liver, as a ready-use locker - a few molecules can be snipped off the chain and secreted into the blood when needed to keep the blood sugar at adequate levels when exercising or between meals. This is called gluconeogenesis. Metformin was felt to increase uptake of sugar into the liver, and to slow it's release later on. If, through insulin resistance, you have higher blood sugars the flip side of the coin is that sugar is stuff that ought to be intracellular. So the cells are short on glucose for energy and they don't like it. They signal the liver to release more glucose, raising the blood sugar but not doing them much good because that sugar still can't enter the cells. Type 2 diabetics have a lot more gluconeogenesis going on than non-diabetics as a result, and metformin interferes with this. It is also felt to interfere with the signalling by inhibiting production of glucagon, a hormone that raises blood glucose, and to reverse the insulin-insensitivity of some tissues to a small degree. An old, cheap, safe drug (more so than phenformin, which I'm old enough to remember). Should be in the water supply of fat western countries.
I can't remember any at all. Obviously, one could make some up with other anti-diabetic agents (take metformin with glyburide and you might get hypoglycemia - duh! Rather obvious.) Really, I can't think of any at all other than synergising with other drugs for diabetes.
Here's another:
Thanks. Do you reckon you can develop T2D without the inherited ... whatever? Has the gene(?) been identified such it can be tested for?screwtape wrote: ↑Yes, insulin is required to allow glucose in the blood enter cells. Resistance simply means you need more insulin to have the same effect. As resistance develops, more insulin is needed, while at the same time the higher glucose levels are slowly killing off the pancreatic cells that make insulin. We know insulin resistance is heritable, and that it is expressed when one becomes overweight; you can come from a family of Type 2 diabetics and avoid it by staying thin and exercising a lot. It's obvious from the mechanism above that type 2 DM is a condition that progresses (diet-control, then diet + metformin, then diet + metformin + sulfonylurea, then diet + insulin), but the important thing to understand is that good control slows the progression as you keep your beta cells alive for longer if they aren't exposed to high blood sugars. Making the effort to do it right when the disease is mild is therefore very important, as it will do you more good in the long run than being obsessional about it at a later stage.Brive1987 wrote: ↑ After reading up I tried to summarise IR and eventual T2D into Brive-speak. Less technical but is it accurate?
So insulin normally tells cells to ‘open’ and accept necessary energy/cell fuel from blood glucose.
But, the onset of insulin resistance makes the cells resistant to insulin’s efforts and they don’t accept enough glucose. This then requires higher insulin doses to achieve a partial brute-force outcome. This dynamic in turn raises insulin levels and keeps resting or fasting blood sugar high with more glucose getting stored as fat rather than expended as energy. The cells, however, think they are starving and demand more food - you eat and the cycle repeats.
Eventually the brute force secretion of excess insulin wears the pancreas out. Insulin production fails and you are fucked with T2D.
It's probably polygenic, so it might be possible to have a milder or stronger tendency to insulin resistance, but there are enough fatties around with perfect blood sugars to show it's not inevitable. I think if you have the 'good' alleles of all the genes involved you won't get type 2 DM however hard you try. A few genes have been identified, and those can be tested for in a research setting if you want to do a full genotype. I'm not aware of any single gene tests available for clinical use, and given there are many genes not much point in testing for just one. But there are a few tricks - we know roughly where these genes live, given that they are often associated with genetic fellow travellers that ride just next door on the same chromosome. So we have some unrelated markers that if present mean you are much more likely to have the insulin-resistance genes. These include alcohol-related flushing (face goes red when you drink booze), acanthosis nigricans, necrobiosis lipoidica and excessive skin tag growth (may be part of acanthosis nigricans). If you have those you are very likely indeed to be carrying the genes for type 2 DM.
It’s been a death of thousand cuts. I think Holden went GM in the 1930s. Then the bottom fell out of the big car market in the 2000s with the take-up of SUVs. Local production stopped in 2017 after an announcement a few years prior. Now the foreign badged ring-ins are disappearing.
screwtape wrote: ↑It's probably polygenic, so it might be possible to have a milder or stronger tendency to insulin resistance, but there are enough fatties around with perfect blood sugars to show it's not inevitable. I think if you have the 'good' alleles of all the genes involved you won't get type 2 DM however hard you try. A few genes have been identified, and those can be tested for in a research setting if you want to do a full genotype. I'm not aware of any single gene tests available for clinical use, and given there are many genes not much point in testing for just one. But there are a few tricks - we know roughly where these genes live, given that they are often associated with genetic fellow travellers that ride just next door on the same chromosome. So we have some unrelated markers that if present mean you are much more likely to have the insulin-resistance genes. These include alcohol-related flushing (face goes red when you drink booze), acanthosis nigricans, necrobiosis lipoidica and excessive skin tag growth (may be part of acanthosis nigricans). If you have those you are very likely indeed to be carrying the genes for type 2 DM.
acanthosis nigricans.jpeg
necrobiosis lipoidica.jpeg
skin tags.jpeg
Ah. So the ‘narrative’ would be:
What’s your budget granddad? :)
Ah yeah, I did forget that for you it's steak and other artisanal proteins all the way these days, Croseus. That certainly seems like an expensive way to eat, but at least it will save your limbs from the ravages of diabetes as you say. However, you can have eight arms and fourteen legs, but they won't be of much use if all that fat dams up your brain, and one night your motor centers sit choking for oxygen for an hour or two.Brive1987 wrote: ↑What’s your budget granddad? :)
I reckon $7 lunch.
Say $8 for a reasonable steak at dinner.
$1 yogurt.
$5 for eggs, almond milk, cheese, lemon, butter, coffee, berries etc.
So maybe a bit off. And you could always go pork or mince, but I’d try and pack a punch with the beef. In any case, you get my drift. <8000kJ whole food need not cost the arm or the leg you’d otherwise lose to diabetes.