this is some good socialist **** right here

[Keith Wilson]

And again, Ted, that has little to do with the initial subject of the thread. The ratio between the production cost and the sale price of insulin has almost nothing to do with the affect of behavior on type II diabetes.

[George Jung]

plus we have to deal with all those folks who believe Google makes them experts, even moreso than the doctors.

[Keith Wilson]

Ted's a good guy, but sometimes he's sooooooooo Californian.

[David G]

plus we have to deal with all those folks who believe Google makes them experts, even moreso than the doctors.

Yes, I'm seeing this sort of thing on several threads. Not just limited to RWW conspiracy theorists. "My reading that magazine article, but otherwise ignorance, is just as legitimate as your years of formal study and practical experience." And they're very stubborn about it.

[George Jung]

Enabled, the lot of 'em.

I've pt's like that - I smile, make my recommendations, and move on.

Life is too short to do otherwise.

[Ted Hoppe]

Ted's a good guy, but sometimes he's sooooooooo Californian.

It takes Californians to think outside the box and change the way we approach what others say is impossible.

A81ACBFB-9206-4924-AB63-9B4217082CA6.jpg

[Keith Wilson]

It takes Californians to think outside the box and change the way we approach what others say is impossible.

True. And there's sometimes a very fine line between that and total blithering flakiness; sometimes no line at all. As I've said before, I have a real love-hate relationship with California, but I can certainly appreciate the virtues.

[L.W. Baxter]

Some people in this thread have gone as far as to call this virture signaling. Is the CDC virtue signaling?

name them. let me at um!

it's not virtue signalling to note the proven facts that better diet and more exercise can reduce symptoms or even fend off entirely some diabetes. i've never heard anyone claim otherwise. mcmike above goes so far to confess an addiction to the foods that hurt him.

the virtue signalling is an attitude of certitude in one's own agency (virtue), and the corresponding implicit critique for the failure of will (virtue) they see in others.

[WI-Tom]

That decrease [in insulin sensitivity] is caused by over-consumption of carbohydrates, which cause a spike in insulin production. Eat that way consistently, and--like a junkie chasing a high--the body has to produce more and more insulin to get the same effect (lowered blood sugar). Eventually the body can no longer make enough insulin on its own.

Tom

Perhaps you can link to your literature - I'm unfamiliar with that scenario .

George,

I'm surprised--really surprised--that this seems questionable to you. As I understand it, this is the prevailing view of how the process of decreasing insulin sensitivity to insulin resistance to pre-diabetes to type II diabetes works (with the caveat that excess body fat and sedentary lifestyle are also contributing factors). Here's a couple of sources from a quick google:

Of all the food components, carbohydrates affect your insulin levels the most. That’s not to say that you can have a free-for-all of other components. Dietary fat, for example, doesn’t have an impact on raising insulin after a meal

Source

What causes insulin resistance?

Obesity (being significantly overweight and belly fat), an inactive lifestyle, and a diet high in carbohydrates are the primary causes of insulin resistance.

Source

Diet: A diet of highly processed, high-carbohydrate foods and saturated fats has been linked to insulin resistance. Your body digests highly processed, high-carbohydrate foods very quickly, which causes your blood sugar to spike. This puts extra stress on your pancreas to produce a lot of insulin, which, over time, can lead to insulin resistance.

Source

As for your comments about people believing that Google makes them experts, a little background:

1. I've been around type II diabetics for much of my life. My father. One sister. Numerous uncles and aunts and cousins. So I do have some direct experience. I've seen the amputations and the blindness and the neuropathy firsthand.

2. I've lowered my fasting glucose level significantly (over 100 generally means insulin resistance; I was usually 70 or under when I used to check, after making changes in the way I eat. Again, I haven't been to medical school, but I have my own experience to draw on, not just Google. I've changed from pre-diabetic when I was consuming lots of carbs, to NOT pre-diabetic. I know it can be done for the simple reason that I have done it.

3. My sister was diagnosed as a type II diabetic, and was taking medicine to control her condition (not insulin--I never made any claim that people go directly from non-diabetic to insulin, which I think was one of the objections you raised about my posts). Then she made changes to the way she eats, and is no longer diabetic. That's per her MD, not a Google search.

I think you're being defensive, and are mischaracterizing my posts, and my level of knowledge, when you say I have "passion without correct information."

Of course you can't control your patients' actions and lifestyles. And if they are not willing or able to take effective action through diet and lifestyle, then of course you have an obligation to treat them however you can.

But honestly, the fact that the ideas I'm talking about seem controversial to you is quite shocking to me.

I'm guessing you might also be skeptical about ketogenic diets (in my experience, much of the medical establishment is). But diabetes organizations are not:

Ketogenic diets are very effective at achieving two common aims of diabetes control, lowering blood glucose levels and reducing weight.

Source

If I have "passion" it's because I know (from firsthand experience, not from Google) how serious diabetes is, and how it can be prevented for some, probably many, people.

Tom

[George Jung]

George,

I'm surprised--really surprised--that this seems questionable to you. As I understand it, this is the prevailing view of how the process of decreasing insulin sensitivity to insulin resistance to pre-diabetes to type II diabetes works (with the caveat that excess body fat and sedentary lifestyle are also contributing factors). Here's a couple of sources from a quick google:



Source



Source



Source

As for your comments about people believing that Google makes them experts, a little background:

1. I've been around type II diabetics for much of my life. My father. One sister. Numerous uncles and aunts and cousins. So I do have some direct experience. I've seen the amputations and the blindness and the neuropathy firsthand.

2. I've lowered my fasting glucose level significantly (over 100 generally means insulin resistance; I was usually 70 or under when I used to check, after making changes in the way I eat. Again, I haven't been to medical school, but I have my own experience to draw on, not just Google. I've changed from pre-diabetic when I was consuming lots of carbs, to NOT pre-diabetic. I know it can be done for the simple reason that I have done it.

3. My sister was diagnosed as a type II diabetic, and was taking medicine to control her condition (not insulin--I never made any claim that people go directly from non-diabetic to insulin, which I think was one of the objections you raised about my posts). Then she made changes to the way she eats, and is no longer diabetic. That's per her MD, not a Google search.

I think you're being defensive, and are mischaracterizing my posts, and my level of knowledge, when you say I have "passion without correct information."

Of course you can't control your patients' actions and lifestyles. And if they are not willing or able to take effective action through diet and lifestyle, then of course you have an obligation to treat them however you can.

But honestly, the fact that the ideas I'm talking about seem controversial to you is quite shocking to me.

I'm guessing you might also be skeptical about ketogenic diets (in my experience, much of the medical establishment is). But diabetes organizations are not:



Source

If I have "passion" it's because I know (from firsthand experience, not from Google) how serious diabetes is, and how it can be prevented for some, probably many, people.

Tom

You have good second -hand knowledge, via your family. And for much, I'd agree - except:

That decrease [in insulin sensitivity] is caused by over-consumption of carbohydrates, which cause a spike in insulin production. Eat that way consistently, and--like a junkie chasing a high--the body has to produce more and more insulin to get the same effect (lowered blood sugar). Eventually the body can no longer make enough insulin on its own.

Maybe not so much. Lots of factors go into DMII, well beyond that scenario. You imply a direct correlation between carbs and insulin drop. It's not directly. From UpToDate:

• 
  
  • Impaired insulin secretion and insulin resistance
  • Impaired insulin processing
  • Role of islet amyloid polypeptide
  
  
• GENETIC SUSCEPTIBILITY
  
  • Genetic risk prediction for type 2 diabetes
  • Genetic insights into pathophysiology
  
  
• SUBTYPES OF DIABETES BASED ON PATHOGENESIS
• ROLE OF DIET, OBESITY, AND INFLAMMATION
  
  • Obesity and insulin resistance
  • Inflammation
  • Factors released from adipose tissue

[George Jung]

• 
  
  
• Obesity and insulin resistance — The prevalence of impaired glucose tolerance and type 2 diabetes has increased dramatically in the United States population in the past two decades [45]. The most striking features in these groups and of most patients who develop type 2 diabetes are increased weight gain (figure 1) and decreased physical activity, each of which increases the risk of diabetes (figure 6) [4]. Upper-body obesity, so-called "central adiposity," has a much greater association with insulin resistance and impaired glucose tolerance than lower-body obesity (figure 7). (See "Type 2 diabetes mellitus: Prevalence and risk factors", section on 'Fat distribution' and "Overweight and obesity in adults: Health consequences", section on 'Diabetes mellitus'.)
  
  Obesity causes peripheral resistance to insulin-mediated glucose uptake [11,46,47] and may also decrease the sensitivity of the beta cells to glucose [47]. The causal nature of these defects is demonstrable as they are largely reversed by weight loss, leading to a fall in blood glucose concentrations toward normal with remission of diabetes [48] (see "Nutritional considerations in type 2 diabetes mellitus"). Although not as effective as weight loss, an exercise regimen also may improve glucose tolerance and prevent the development of overt diabetes. (See "Prevention of type 2 diabetes mellitus", section on 'Exercise'.)
  
  The mechanism by which obesity induces insulin resistance is poorly understood. The pattern of fat distribution and perhaps a genetic abnormality in the beta-3-adrenergic receptor, as described above, appear to contribute. The c-Jun amino-terminal kinase (JNK) pathway may be an important mediator of the relationship between obesity and insulin resistance as JNK activity is increased in obesity, an effect that can interfere with insulin action. In animal models of obesity, absence of JNK1 results in decreased adiposity and enhanced insulin sensitivity [49]. (See "Obesity: Genetic contribution and pathophysiology".)
  
  Inflammation — Many studies have focused on the role of inflammation as a common mediator linking obesity to both the pathogenesis of diabetes and atherosclerosis [50,51]. The incidence of type 2 diabetes has been correlated with increased levels of markers of inflammation, including C-reactive protein, interleukin (IL) 6, plasminogen activator inhibitor 1 (PAI-1) [52], tumor necrosis factor (TNF)-alpha [53,54], chemokines (chemotactic proinflammatory cytokines) [55], and white cell count [56-59]. Adipokines (factors released from adipose tissue) stimulate inflammatory activity, which correlates with insulin resistance [60]. Intensive lifestyle interventions have been shown to decrease markers of inflammation [61].
  
  Anti-inflammatory properties of medications including thiazolidinediones and statins [62] may contribute therapeutic benefit beyond their activity to lower glucose and cholesterol levels, respectively. Among patients with rheumatoid arthritis or psoriasis, use of anti-inflammatory, disease-modifying antirheumatic drugs (such as TNF inhibitors and hydroxychloroquine) is associated with a lower incidence of diabetes than other agents [63]. However, no trials of anti-inflammatory agents have shown a convincing reduction in the development of diabetes or amelioration of hyperglycemia [64].
  

[George Jung]

GENETIC SUSCEPTIBILITYType 2 diabetes is a polygenic disease, with likely thousands of genetic factors contributing to disease risk together with complex interaction with environmental factors.
Observations that demonstrate a genetic influence on the development of type 2 diabetes include:
●Thirty-nine percent of patients with type 2 diabetes have at least one parent with the disease [27].
●Among monozygotic twin pairs with one affected twin, approximately 90 percent of unaffected twins eventually develop the disease [28].
●The lifetime risk for a first-degree relative of a patient with type 2 diabetes is 5 to 10 times higher than that of age- and weight-matched subjects without a family history of diabetes [29].
More than 500 distinct genetic signals have been robustly associated with type 2 diabetes from large-scale genome-wide association studies, including over 300 newly discovered in one of the largest multi-ancestral meta-analyses involving 1.4 million human participants (figure 5) [30]. There have been advances using genetics for prediction of risk of developing diabetes as well as for gaining insights into disease pathophysiology.
Genetic risk prediction for type 2 diabetes — In contrast to monogenic causes of diabetes, where inheriting a given causative mutation imparts a substantial risk of developing disease (typically odds ratios [ORs] >10), the genetic variants associated with type 2 diabetes each have small impact on risk (typically ORs <1.2) [31]. Common genetic variants can be combined together to generate polygenic risk scores that allow greater prediction of disease risk than individual common variants.
Polygenic risk scores for type 2 diabetes have incorporated thousands of genetic markers, including those not reaching the stringent "genome-wide" statistical significance required to indicate a genetic variant as robustly associated with disease. One type 2 diabetes polygenic risk score captured approximately 20 percent of the variance in individual predisposition to type 2 diabetes (approximately one-half the total estimated heritability) [32]. Using such a type 2 diabetes polygenic risk score, individuals with the top 2.5 to 5 percent scores can be identified as having approximately threefold increased risk compared with the population mean [32,33]. The risk of diabetes conferred to individuals with type 2 diabetes polygenic risk scores in the top 1 percent remains significantly lower than that conferred by the rare variants causing monogenic diabetes [31]. (See "Classification of diabetes mellitus and genetic diabetic syndromes", section on 'Monogenic diabetes (formerly called maturity onset diabetes of the young)'.)
Another way to consider information conferred by a test is to calculate the area under the receiver operator characteristic curve (the AUROC, or C-statistic), which provides a measure of the proportion of times such a test will correctly assign disease state between a pair of individuals, one who has the disease of interest and another who does not. The AUROC for type 2 diabetes polygenic risk scores are 0.73 when adjusting for age and sex [32,33], indicating some utility, but not reaching levels >0.80 typically required for clinical implementation.
Among groups with increased genetic risk for diabetes, environmental factors still play a major role in the development of diabetes. The Diabetes Prevention Program (DPP) demonstrated that in a population at high risk for diabetes (based on rising subdiabetic glucose levels and overweight or obesity), even those at very high genetic risk had substantial reductions in risk when "environmental" factors (including overweight, obesity, and a sedentary lifestyle) were ameliorated [34].
Genetic insights into pathophysiology — The wealth of genome-wide associations with type 2 diabetes offer an opportunity to improve understanding of the pathophysiology of type 2 diabetes; however, since the majority of these genetic signals reside in nonprotein-coding regions of the genome, determining the mechanisms underlying genetic signals has proved challenging. As a result, the disease mechanisms underlying the majority of association signals for type 2 diabetes remain unknown.
Insights from genome-wide association studies into disease mechanism have generally come from:
●Signals residing near genes with known relevance to diabetes
or
●Extensive laboratory-based investigation of the chromosomal regions containing type 2 diabetes association signals
Type 2 diabetes association signals that have been mapped to genes already implicated in diabetes pathophysiology include signals near PPARG, HNF1A, HNF4A, HNF1B, KCNJ11/ABCC8, WSF1, and GCKR. Such findings also demonstrate a genetic continuum that exists between monogenic and polygenic diabetes (see "Classification of diabetes mellitus and genetic diabetic syndromes", section on 'Monogenic diabetes (formerly called maturity onset diabetes of the young)'). For example, a protein-coding variant in the gene HNF1A (p.E508K) was identified in Latino populations conferring approximately fourfold increased risk of type 2 diabetes [35]. This variant is almost exclusively seen in Latino populations, where its population frequency is approximately 0.3 percent. HNF1A is a known cause of monogenic diabetes, where patients have defective beta cell insulin secretion. In experimental assays, the HNF1A protein encoding the p.E508K mutant demonstrated transactivation activity that was reduced compared with wild-type protein, but greater than HNF1A proteins encoding HNF1A mutations known to cause monogenic diabetes. Analysis of protein coding variants in over 40,000 individuals demonstrated that individuals with type 2 diabetes carry more rare variants in monogenic diabetes genes than would be expected by chance [36], further supporting a genetic continuum existing between type 2 diabetes and

[George Jung]

monogenic diabetes.
For several signals arising from type 2 diabetes genetic association studies, extensive laboratory-based investigation has elucidated shared disease mechanisms. For example, investigation of the CILP2/TM6SF2 locus [37] implicated two amino acid-altering variants in TM6SF2 as driving the association signal [38]. One of these genetic variants was also found to be associated with nonalcoholic fatty liver disease in an independent analysis, with the same allele associated with increased risk of type 2 diabetes and nonalcoholic fatty liver disease, as well as with higher circulating levels of alanine transaminase (a marker of liver injury) and with lower levels of triglycerides [39]. Functional experiments knocking down Tm6sf2 in mice [39] as well as TM6SF2 in human hepatoma cell lines [40] suggest that reduced gene expression increases liver triglyceride content and decreases secretion of triglyceride-rich lipoproteins from liver tissue, thus implicating TM6SF2 in liver fat metabolism. Defective liver triglyceride secretion results in increased hepatic fat content and hepatic insulin resistance [41]. These findings indicate a disease pathway of primary liver tissue origin leading to increased risk of type 2 diabetes.

You have good second-hand knowledge about DMII, dealing with family. But this is just a 'glimpse', many, many factors involved in this complex disease. New discoveries, new txments all the time.

As it happens, I have good first-hand knowledge of DMII - I've been type II for ten years or so. Low-normal BMI, excellent diet, daily exercise, and positive family history.

[Paul Pless]

have you researched this george? ​really??
or did you just google that??

[John Meachen]

have you researched this george? ​really??
or did you just google that??

Does he lose points for the C&P links?They might pollute the purity of the research.....

Seriously,thanks George for sharing your in depth knowledge.

[George Jung]

UpToDate - current info gleaned from dozens of journals.

[Nicholas Carey]

Now my head hurts

[Canoeyawl]

From my nephew the Family doc in Vt. w/type I, to whom I sent this "news":

with a minor edit...

"I was asleep when you sent this and forgot to respond. But this is huge news. Kudos to your state for fighting against big pharma. In response, all of those f*ckers dropped their prices 75% in the last two weeks"

[George Jung]

Really big news. And they dropped their prices in spite of the Republicans blocking Biden's attempt at doing so. Public pressure can work.

[WI-Tom]

Really big news. And they dropped their prices in spite of the Republicans blocking Biden's attempt at doing so. Public pressure can work.

Yes, that is great. An all-too-infrequent triumph of the public good over profit. Well done!

Tom

[WI-Tom]

You have good second-hand knowledge about DMII, dealing with family. But this is just a 'glimpse', many, many factors involved in this complex disease. New discoveries, new txments all the time.

As it happens, I have good first-hand knowledge of DMII - I've been type II for ten years or so. Low-normal BMI, excellent diet, daily exercise, and positive family history.

George,

thanks for taking time to post those summaries of recent research. I think I knew (but had forgotten) that you are diabetic yourself. Obviously I can't compete with your level of medical knowledge on the scientific front, or the personal front for that matter. And I can understand that it must be annoying to have people without your knowledge and expertise posting thoughts that are not consistent with what you know. Thanks for being gracious about pointing out that I've drastically oversimplified a very complicated thing.

One quibble with the bolded bit: I have a little direct first-hand knowledge myself--a while back (10+ years?) my fasting glucose levels had brought me to the category of "insulin resistance," which is a first step in the progression to type II diabetes as I understand things. After significant changes to the way I eat, they're typically around 70 now. So I know, firsthand, that insulin sensitivity can be restored without medicine for at least some people.

I think that the kind of research you posted--the efforts to really understand things at a cellular (or sub-cellular?) level, is a very different kind of knowledge than the stuff that is most useful in people's day-to-day lives, which is the perspective from which I'm coming to the topic.

I'll pose an analogy:

I know even less about the science of gravity than I do about the science of diabetes. I don't pretend to understand gravity waves, and I can't detect the curving of space-time. I trust that what science tells us about all of these things represents our best real understanding of gravity, in detail.

But I don't really need to know any of that in my day-to-day life. What I need to know is how to avoid falling. When I fall off a cliff, it doesn't matter whether I'm falling because space-time has become curved, or because of the exchange of some quantum particles that we haven't yet managed to discover yet--or whether there's some entirely different, more complicated reason that gravity works. It's helpful to know the Newtonian stuff, maybe; 9.8 meters per second, per second, rate of acceleration tells me I won't drift to the foot of the cliff slowly, but will speed up to end my fall in a crumpled heap. But I don't need much beyond that.

So I think we need to acknowledge the difference between the types of knowledge and experience we're using, and the relevance (or not) of each.

It's a little too easy to be dismissive of the real practical understanding accessible to thoughtful, reflective people who just happen to have no clue what things like TM6SF2 is, and who have never seen a triglyceride-rich lipoprotein in the flesh. I don't see that in your response--and thanks again for that--but I sure see it in the gleeful, smug, "George-sure-showed-him!" kinds of comments that followed after.

More later--I appreciate the discussion! This is a topic of great interest to me, given my genetic ties to diabetes, and my personal aversion to having my fingers and toes chopped off.

Tom

[George Jung]

Thoughtful response, much appreciated, as well. And FWIW - I'm not interested in establishing as 'the expert' on this, or anything else. I'm not doing the research - I'm following everyone else who's doing it, and trying to stay current on 'best practices'. Esp in primary care, it's difficult - too much to know, and most fields are exploding with new findings.

My only quibble, when I jump into these threads, is a concern over what could be mis-information. You are exactly right with ' insulin sensitivity can be restored without medicine for at least some people.'
Although, recognize - this tends to be a temporary reprieve. Over time, most type II's progress, require more intervention. And there's no doubt, our lifestyle enters into that. It's really tough to live pure, esp in the USA. My wife reads labels - damn sugar is added to almost everything.

[Keith Wilson]

My goodness, an outbreak of amity and reasonableness! Well done, gentlemen! One way or another, nobody would argue that it's a good idea to spend all of one's time staring at a screen and living on a diet of Hershey bars and beer.

But that still has almost nothing to do with the selling price of insulin.

[elf]

The rough outline of the ex-Confederacy shows up on an astounding number of maps, graphing wildly different things. By county, it's even clearer:

Bernie is right. Look at Vermont.

[Keith Wilson]

Colorado's looking pretty good, too. Minnesota's not doing badly. Alabama and Mississippi OTOH . . .

[WI-Tom]

You are exactly right with ' insulin sensitivity can be restored without medicine for at least some people.'
Although, recognize - this tends to be a temporary reprieve. Over time, most type II's progress, require more intervention. And there's no doubt, our lifestyle enters into that. It's really tough to live pure, esp in the USA. My wife reads labels - damn sugar is added to almost everything.

My first reaction is to wonder whether the temporary nature of the reprieve isn't simply because people don't make permanent life changes and permanent eating habits, but that they aren't willing or able to sustain those changes. It appears to be pretty well accepted in the mainstream diabetes management organizations that restricting carbs really does work:

Americans get roughly half their daily calories from carbohydrates, with about 80% of those carb calories coming from added sugars and refined grains — think soda, candies, bagels, pastries and pizza crust.

To manage or prevent diabetes, the American Diabetes Association recommends the Mediterranean diet and other low-carb diets, as long as they minimize added sugars and refined grains and include non-starchy vegetables.


The ultra-low-carb ketogenic diet fulfills these criteria.

Source (Stanford Medicine)

Yes! You can prevent or delay type 2 diabetes with proven, achievable lifestyle changes—such as losing a small amount of weight and getting more physically active—even if you’re at high risk.

Source (CDC)

A study³ with 28 overweight participants with type 2 diabetes demonstrated that the keto diet could improve glycemic control to a point where diabetes drugs were discontinued or reduced.

Source

And this is probably worth a look for those who are interested:



Tom

[WI-Tom]

My goodness, an outbreak of amity and reasonableness! Well done, gentlemen! One way or another, nobody would argue that it's a good idea to spend all of one's time staring at a screen and living on a diet of Hershey bars and beer.

But that still has almost nothing to do with the selling price of insulin.

Reducing insulin prices is a big deal for those who need it. Preventing diabetes is potentially an even bigger deal, and would save lots of lives, and lots and lots of money. Saying one is not related to the other is a bit like saying:

"Hey, our kids want to play with dynamite, so let's make sure the price doesn't go too high!" instead of saying "Hey, maybe it's not a good idea for our kids to play with dynamite!"

Tom

[Nicholas Carey]

On a related note, Moderna's COVID-19 vaccine, which was created in partnership with the NIH using $1.7b in Federal grant money, costs $3/dose to manufacture.

Moderna has been selling the vaccine to the Federal government at a "modest" markup: the original vaccines were priced at $10-$15/dose, the updated boosters at $26/dose. When the Federal government's supplies run out later this year (due to Congress not appropriating funds for more purchases), COVID-19 vaccines will enter the commercial market.

Moderna is planning to raise the per-dose price from $26 to $130, a price increase of 500%.

Greed has no bounds.

https://arstechnica.com/science/2023...00-price-hike/

[George Jung]

Yep. Bastids. Pfizer is looking to do the same.

[WI-Tom]

Yep. Bastids. Pfizer is looking to do the same.

It's almost as if capitalism were an inherently flawed system.

Tom

[George Jung]

un-regulated capitalism is an inherently flawed system. Just ask KW.

[Paul Pless]

moderna is essentially arguing that the government should have a done a better job negotiating on behalf of taxpayers from the start

[Keith Wilson]

Right. it costs $3 to manufacture, most of their development costs were paid by the government, and they want to sell it for $130. Hooo boy. Sorry, but for all of my objections to communism, that almost justifies sending in the army, expropriating the production facilities, then taking the executives out back and shooting them. Bastards.

[David G]

moderna is essentially arguing that the government should have a done a better job negotiating on behalf of taxpayers from the start

Don't regulate us.

DON'T regulate us.

Oh... you should have done a better job of regulating us.

[Chip-skiff]

. . .that almost justifies sending in the army, expropriating the production facilities, then taking the executives out back and shooting them.

The MBAs should be tortured first.