Jump to content
tasbin

Impaired glucose tolerance now

Recommended Posts

All,

 

This new post discussing PMID 27534842 is quite relevant to the problem of CR-induced impaired glucose tolerance. In a nutshell, it found in rhesus monkeys that the combination of low-testosterone + CR is associated with insulin insensitivity and impaired glucose tolerance, likely as a result of reduced skeletal muscle mass.

 

--Dean

Share this post


Link to post
Share on other sites

All:

I think things have gotten a bit confused ...

Impaired Glucose Tolerance (IGT) and Impaired Fasting Glucose (IFT) are two quite different conditions, diagnostically and metabolically. Neither is diabetes, but either of them are classed as prediabetic (meaning that they are associated with higher risk of becoming diabetic), and their metabolic origins are distinct to the extent that they are known and any unknown factors almost tautologically must be largely distinct as well.
 

Quote

Impaired Glucose Tolerance (IGT)
People with IGT have blood glucose levels that are higher than normal but not high enough to say they have diabetes. This condition is diagnosed using the oral glucose tolerance test (OGTT). After a fast of 8 to12 hours, a person's blood glucose is measured before and 2 hours after drinking a [75 g] glucose-containing solution.

  • In normal glucose tolerance, blood glucose rises no higher than 140 mg/dl 2 hours after the drink.
  • In impaired glucose tolerance (IGT), the 2-hour blood glucose is between 140 and 199 mg/dl.
  • If the 2-hour blood glucose rises to 200 mg/dl or above, a person has diabetes.
How does the fasting blood glucose test differ from the oral glucose tolerance test?
In the fasting blood glucose test, a person's blood glucose is measured after a fast of 8 to 12 hours:
  • A person with normal blood glucose has a blood glucose level below 100.
  • A person with impaired fasting glucose has a blood glucose level between 100 and 125 mg/dl.
  • If the fasting blood glucose level rises to126 mg/dl or above, a person has diabetes.
For a person with IGT, what is the risk of developing type 2 diabetes?

As few as 1 to as many as 10 of every 100 persons with IGT will develop diabetes per year. The risk of getting diabetes rises as people become more overweight and more sedentary, have a stronger family history of diabetes, and belong to an "at-risk" racial or ethnic minority group.

 

 

Now:
 

 

On 7/6/2016 at 1:21 AM, tasbin said:

Has anyone ever had to deal with a sudden impaired glucose tolerance ?
I am doing some intermittent dry fast(18h per day) during 1 month & maybe it is related .

I am used to control my blood sugar since 6 months so I know that it was not present many months ago.

My BMI is 20.5 & I have lost 10kg (22 lbs) around slowly (a year) so It is not related to any obesity. But my overweight mother is diabetic type 2 (and grand-father too). ...

My fasting blood sugar (FBS) is good (82-83mg/dl). But after a meal breaking the fast with also a home-made smoothie with only fruits, it raises above 140mg and <180mg after 2 hours. I have tested again with a simple fruit & oats, milk some honey and again same values. ... I have confirmed those abrnormal values 4 times in 2-3 days. ...

My last hba1C last year was 5.2%(maybe different now) so I am not diabetic at least on two definitions (FBS<1g & HBA1C<6%).

So, at that point (one month ago), you (Tasbin) clearly at minimum had IGT — but not IFT, and not diabetes absent a sufficiently high OGTT. But note that Tasbin had not undergone a formal OGTT at that point, and while his postprandial 2 h glucose was sufficiently high to obviously be at minimum a sign of IGT, it's still quite possible that an OGTT proper (100% glucose solution, no food matrix, no protein, no low-glycemic carb) would have diagnosed him as frankly diabetic.

On 7/6/2016 at 1:21 AM, tasbin said:

I am used to control my blood sugar since 6 months so I know that it was not present many months ago.

What exactly did you mean by this, Tasbin? In what sense had you been "controlling" your blood sugar for that 6 month period? Did you simply mean measuring it, or were you actually taking steps to lower some aspect of glucoregulation? And in either case, why were you "controlling" it?

Relatedly, what was your BMI before you lost the weight? And would I be right to assume that this lost weight was mostly excess fat? If not, why were you losing weight?

And when you say that you "know that it [postprandial hyperglycemia] was not present many months ago", had you been doing your postprandial glucose previously? You only report fasting data prior to your recent post-smoothie problems.

On 8/17/2016 at 11:59 PM, tasbin said:

My fasting blood sugar (FBS) was around good 83mg/dl 2 months ago, max 92mg.
Not [sic — I take it that tasbin intends "now" -MR] it is around 100mg or just above on average even after eating ad libitum for 1 month (BMI:21) & not more on CR.
I have tested with another glucometer with the same results.

In USA, a FBS of 1g is the definition of prediabetes. In france, it is 1.1g ... I will request for an hba1C soon and post it here.

... but you neither post new postprandial glucose nor (again) any postprandial glucose or OGTT prior to the smoothie incident.

It seems to me that one possibility is that you (Tasbin) have simply been prediabetic with IGT all along and slid into diabetes, or possibly even frankly diabetic all along but with decent fasting glucose and HbA1c. Do you have any strong reason to doubt that?

On 8/18/2016 at 12:56 AM, Dean Pomerleau said:

Tasbin, Sorry to hear your impaired glucose tolerance (IGT) appears to have returned. Is your post-meal glucose also elevated?

Careful. As is implicit in your question, Tasbin hadn't to this point said anything about what his post-meal glucose was like in the same period of his posts announcing his recent elevations in fasting glucose, after having ostensibly "cured" his IGT through his very slight muscle gain, and if he doesn't have that then by definition his IGT hasn't returned. Conversely, if one has IGT, that doesn't imply anything about whether one has IFT or fasting-diagnosed diabetes.

On 8/17/2016 at 11:59 PM, tasbin said:

Probably, my insulin resistance has inscrease or/and less working Pancreatic β-Cell :(xyz .

Your change in fasting glucose is highly unlikely to be related to your beta-cells: normally, that's all about hepatic insulin resistance until you become an advanced diabetic and have simply burned them out.

On 7/12/2016 at 8:03 AM, Dean Pomerleau said:

As [Tasbin] suggest, one potential mechanism by which CR might induce impaired glucose tolerance in some folks is because of very low muscle mass. ...

The only thing I questioned about your explanation in your own case was the apparent step-function you postulated between good and terrible glucose metabolism. If IGT really is a direct function of muscle mass as you suggest, then adding a tiny amount of muscle mass (as you did) should change your glucose metabolism by only a tiny bit. But this doesn't appear to have been the case. Instead you saw a huge improvement in glucose metabolism associated with just a very small amount of weight / muscle gain.

So it seems to me like low muscle mass can't be the only explanation for CR-induced IGT. It appears from his new IGT thread that Michael thinks along the same lines.

Indeed.

On 7/12/2016 at 8:03 AM, Dean Pomerleau said:

[Tasbin] wrote:

Quote

In this video Paul McGlothin mentions that : "We had some of our slimmest CR people, the past couple of years... this is kind of sad. They really limited calories a lot. Fasting glucose levels 200. Both died of pancreatic cancer"


Here is a link to the video cued up at the spot  ... at 25:00, he talks about "passing out glucometers at a recent CR workshop". He says "75% of CR folks had fasting glucose over 100". I'm not sure what workshop he's talking about, but I find that hard to believe. CR folks I know with IGT generally have normal fasting glucose.

Indeed. Remember, Paul has a very loosey-goosey definition of CR, which sometimes seems to amount to "anyone who eats a healthy diet and isn't overweight, especially if they do a bunch of non-CR stuff that I [Paul] hypothesize based on data of highly variable quality will modulate pathways that I [Paul] hypothesize based on data of highly variable quality to be critical to the anti-aging effects of CR." And long before these reported cases, he was stridently opposed to anyone reaching BMIs <18.5, on a far cruder basis than your (Dean's) generally quite reasoned arguments.
 
NB that prior to the Fontana study, “none of the CR volunteers reported a diagnosis of type 2 diabetes, impaired glucose tolerance, or impaired fasting glucose before or after starting CR,” and in study measurements “all CR subjects [CR-NGT and CR-IGT] were extremely lean and had very low fasting plasma concentrations of glucose and insulin, and an outstanding metabolic profile”. I'm not sure that I'd say they all had very low fasting glucose — the average was 83±8mg/dL — but it was IAC well below the diabetic threshold, and in monitoring the CR List and Forums for >15 years I don't believe that I have ever heard of a person on CR without preexisting disease convert to IFT, let alone frank diabetes that could be diagnosed fasting. Moreover, while CR rodents exhibit IGT, and and nonhuman primates on the pseudo-CR protocols at WUSTL and NIA exhibited low insulin levels in response to glucose (albeit without clear post-challenge hyperglycemia in either case), frank fasting hyperglycemia is nonexistent in rodents on CR proper (as opposed to acute starvation protocols), and much rarer in even the questionable and mild CR imposed on nonhuman primates at NIA than in the controls, and (again) AFAIK unheard-of in humans genuinely on CR.

On 7/12/2016 at 8:03 AM, Dean Pomerleau said:

Having had really bad IGT in the past (see my terrible OGTT results from Luigi's study at the bottom of by blood tests - 252 mg/dL at 60min and 199 mg/dL at 2h!), all this discussion makes me nervous.

So I tested my blood glucose once again this morning. I ate my usual, huge (~3500kcal) meal over a 2h period from 5am to 7am. Ten minutes after I finished eating, and over 2 hours since I started eating my meal (which BTW is front-loaded with most of the carbs and fruit) my glucose was 106 mg/dL. I then went on a brisk 30min walk. When I got back I tested it again, 45min after finishing my meal. It was 94 mg/dL. Given my history of IGT, It looks like I'm doing something right.

 

On 7/13/2016 at 2:13 AM, Dean Pomerleau said:

 

Tasbin said:

But you are cheating :Dxyz . What would be your PP BS without exercice before & after the meal? Do you still have a IGT and only manage it with exercice?


Cheating!? Did you actually read the text ... During the 10 minutes between the end of my meal and my extremely respectable postprandial blood glucose reading of 106 mg/dL, I was engaging in my rather obsessive oral hygiene routine. While I readily acknowledge that routine is quite rigorous, I seriously doubt flossing and interdental picking my teeth is the kind of rigorous activity that might bring down my glucose dramatically ☺.

While I assume that your outrage at being accused of "cheating" is largely for comedic effect, you clearly do think it's a mischaracterization. I actually have to agree with Tasbin's overall point here, Dean. An OGTT is performed first thing in the morning, fasting, when counterregulatory hormones (glucagon and catecholamines) are elevated, is performed while quietly sitting or lying down, and uses a 75 g bolus of liquid glucose solution. By contrast, you were consuming much lower-glycemic carbs, along with protein and plenty of fat, and you took 2 hours to consume it, giving your tissues time to absorb the glucose slowly dripping into your bloodstream and your glucagon and catecholamines time to lay off.
 
Moreover, were you really inactive that whole time? You've certainly written in the past that you often make almost continuous use of your treadmill desk or under-desk pedaling machine. At the very least, you've got to shovel all that food into your maw and chew — and, yes, mess with your teeth ? . And then, for your later results, you exercised — and (as my half-completed post reviews) there is now good evidence that the bulk of the benefit of post-meal exercise comes starting about half an hour after finishing a regular meal (tho' CR meals may vary), and that you're actually better off resting a bit immediately after finishing and only engaging in moderate (rather than intense) exercise.
 
Your glucose levels clearly reflect good glucose management, albeit not your complete glucose management protocol: they don't tell us much about your response to an OGTT, when all of those management strategies are denied to you.

On 7/13/2016 at 4:59 AM, Dean Pomerleau said:

 

Tasbin said:

In the LC circle, it is well-know that you need to "carb" up 2-3days before doing a OGTT to avoid IGT result. Their usual explanation is that LC increase insulin resistance in the muscle, an utterly normal physiological response to carbohydrate restriction.


Yeah. I believe that's what the low carbers say - along with "ignore LDL, it's X that matters" where X might be "LDL particle size", "HDL", "APoB" or a host of other, less relevant biomarkers of CVD risk. Oh yeah - and butter is a health food. If it's grass fed you should put it in your coffee ...

In my book, when CR folks start to exhibit the metabolic profile of low carbers and start to use their same excuses for what is clearly impaired metabolic health (i.e. "benign starvation diabetes"), I say that's the time to start worrying.

Well, first, while low-carbers and Paleo people who eat a lot of SaFA often fall into a caricature of the underlying science by just ignoring a high LDL-C (or not even bothering to get it measured) on the assumption that no matter what their LDL-C measurement may be, their apoB or NMR-measured particle count must be low and that SaFA intake is just utterly disconnected from the latter — a distortion promoted by the confusion between LDL-P and LDL particle size — it is true that low apoB or LDL-P on NMR puts you in a low-risk state even if your LDL-C is borderline high, and some low-carbers do exhibit this pattern.
 
And in this case I think there's strong biological plausibility to what they're saying about the OGTT. Acutely, in response to a meal with a non-trivial amount of carb, the body releases insulin and the peripheral tissues respond to suck the glucose up. But during normal daily overnight fasting — and more dramatically in extended fasting (so-called "starvation diabetes"(3,4) which Blagoskonny thinks is informative on the effects of rapamycin), counterregulatory hormones are up to facilitate release of stored glucagon, enable ketosis and gluconeogenesis, and the liver and muscles are in a state of metabolic insulin resistance as part of normal mitochondrial fuel-switching; all of this helps shield the brain's glucose supply. This situation is completely reversible after break-fast on a daily basis, and after a short period of refeeding in "starvation diabetes".
 
It would be surprising if a similar situation did not reign (on both fronts) for nutritional ketosis on a very-low-carb diet, and such a phenomenon is anecdotally reported (awful OGTTs that can be prevented by a few days' return to a non-ketogenic carb intake). However, I'm not aware of a formal study to document this.
 
Cf. the notion of type II diabetes secondary to chronic energy excess being the result of chronically overloading both systems at once, leading to loss of mitochondrial and metabolic capacity for fuel-switching,(5) and Denise Minger's similar notion of the "macronutrient swampland."
 
Finally, much of the metabolic profile of low carbers is really quite favorable, and resembles people on CR (super-low TG, high HDL, generally good fasting glycemia and HbA1c), etc. Of course, much of this is itself likely the result of energy restriction ...

On 7/12/2016 at 8:03 AM, Dean Pomerleau said:

But the pancreatic cancer deaths of two CR practitioners [reported by Paul] (if true), is really troubling. Pancreatic cancer strikes about 1 in 10,000 people. I can't imagine Paul has more than 100-200 people in his program. But let's be conservative and assume it's 500. That would give a 500/10,000 = 5% chance he'd see a single pancreatic cancer incident in his group. To see two such cases would be a 1 in 400 probability. And it would be more unlikely that than if he's following less than 500 people.

I'd actually go one step further than that. The increased relative risk of pancreatic ductal adenocarcinoma (which accounts for 95% of all pancreatic tumors, is what is normally actually meant when one says "pancreatic cancer," and is the most rapid and deadly) imparted by frank diabetes is 6.69 in the first year after diagnosis and rapidly declines to 1.36 at 10 years.(1) Even an RR of close to 7 in a cancer that has an absolute risk of 1 in 10,000 is still pretty rare. Having two people in his circle — most of whom are presumably not diabetic — develop some form of pancreatic cancer is unlikely, and the absolute increase in risk of the disease conferred by diabetes is sufficiently small that (combined with more biologically-based data, below), I'm inclined to say that this is a coincidence, not data.
 

 

On 7/12/2016 at 8:03 AM, Dean Pomerleau said:

Interestingly, these two reviews [1][2] found there is evidence to support both causal directions among diabetics - i.e. diabetes → β-cell dysfunction → pancreatic cancer and pancreatic cancer → β-cell dysfunction → diabetes, and that the two explanation for the link between diabetes and pancreatic cancer aren't mutually exclusive:
 

Quote

About 80% of pancreatic cancer patients have glucose intolerance or frank diabetes. This observation has led to the following two hypotheses: i. pancreatic cancer causes the associated diabetes and ii. the conditions associated with diabetes promote the development of pancreatic cancer. Evidence supporting both hypotheses has been accumulated in previous studies. This article reviews these studies, especially those that have been conducted recently...

Conclusion

Recent studies indicate that there is no simple answer to the question of which of the two hypotheses stated at the beginning of this review is right. However, it appears that these hypotheses are not mutually exclusive, since there is considerable experimental and epidemiological evidence in support of both of them. Clearly, the relationships between pancreatic cancer and alterations in glucose metabolism are very complex.

 

Note first that the review from which you're quoting ((2) below) was written in 2003. For epidemiological evidence, it relied on PMID 7745774, a 1995 meta-analysis of the available studies. Mixing its findings with the paper's own analysis of the underlying epidemiology available to that time, they write:

Quote

Everhart et al. examined 30 of the epidemiological studies that have looked at the association between diabetes and pancreatic cancer and used 20 of them in a meta-analysis. The pooled relative risk from these studies was 2.1 for diabetes with a duration of at least l year prior to cancer diagnosis or death and 2.0 for diabetes with a duration of at least 5 years. The authors concluded that pancreatic cancer could be added to the list of complications of diabetes. Several epidemiological studies have analyzed relative risks associated with the different periods of time after the diagnosis of diabetes and have found a relatively modest but persistent increased risk of death from pancreatic cancer even when the diagnosis of diabetes preceded death by many years. A population-based case-control study in the United States with 526 incident cases and 2,153 population controls showed a significant positive trend (P = 0.016) in risk with increasing years prior to diagnosis of cancer [Their (36) — was this your (Dean's) "(4)"?]. In other studies, the relative risk decreased with increasing follow-up time but remained significant. However, other epidemiological studies have concluded that diabetes is not a risk factor for pancreatic cancer or else that it is not a risk factor if recently-diagnosed cases are excluded.(2)

In a state of such relative uncertainty, the data are not inconsistent with the direction of causality running either way. But a more recent (2014) meta-analysis, after two decades of additional epidemiological evidence, was able to evaluate 88 studies, and the direction of causality became clearer: as already noted, they found that the increased relative risk of PDAC imparted by diabetes is 6.69 in the first year after diabetes diagnosis and rapidly drops for the first 7.5 years, reaching just 1.36 at 10 years.(1) Additionally, amongst those PDAC patents that do also have diabetes, “Chronological analyses show that for 40–74 % of PDAC patients, hyperglycemia was recent onset (less than 24–36 months). In addition, diabetes often improves after tumor resection." If diabetes — either hyperglycemia or hyperinsulinemia — caused PDAC, you would expect longer-term exposure to insulin (a mitogen) or glucose (a fuel) would progressively increase the risk of and aggressiveness of the cancer. Instead, you see the reverse.

When you look back at the mechanistic evidence put forward in (2), most of it is only consistent with diabetes driving PDAC rather than vice-versa under the more common situation of insulin resistance leading to compensatory overproduction of insulin by the beta-cells, which makes total sense mechanistically as insulin is a mitogen and is involved in many cancers (hence the risk of some cancers linked to diabetes and obesity) or is actually inconsistent either way, but is the exact opposite of CR-IGT:

Quote

In patients with Type II diabetes (non-insulin-dependent diabetes), the pancreas is generally exposed to substantial hyperinsulinemia for years [33], suggesting that insulin may be involved in the association between long-standing diabetes and pancreatic cancer. A number of experiments have tested the hypothesis that insulin may stimulate the growth of pancreatic cancers. Binding studies have shown the presence of insulin receptors on pancreatic cancer cells [42, 43, 44, 45]. In vitro studies have shown that insulin promotes growth of the hamster pancreatic cancer cell line H2T [42], the rat acinar pancreatic cancer cell line AR42J [45], and numerous human pancreatic cancer cells lines [44, 46, 47, 48, 49, 50, 51]. However, the human pancreatic cancer cell line SOJ-6 was not stimulated by insulin [46], and one of the studies using PANC-1 cells reported no response to exogenous insulin [49]. In addition to hyperinsulinemia, the increased blood glucose and free fatty acids in diabetes may also promote the growth of pancreatic cancer [52].

The genesis of the cancer is also influenced by the endocrine pancreas. In vivo studies concerning the effects of administration of exogenous insulin and/or induction of diabetes on pancreatic cancer have provided inconsistent data that reflect the complex interactions that may be involved in tumor growth [53, 54, 55, 56]. Exogenous insulin significantly reduced the induction of benign and malignant pancreatic lesions in hamsters when given 2 hours before BOP [an agent that causes ductular pancreatic tumors], but the reduction in incidence was not significant when insulin was given simultaneously with BOP or 2 hours after BOP [53]. Cancer incidence in hamsters receiving insulin twice daily starting before BOP administration and continuing through the experimental period did not differ significantly from that in controls that received BOP only [54]....

A study of pancreatic cancer in hamsters fed a high-fat diet that potentiated pancreatic cancer provided data suggesting that islet proliferation associated with insulin resistance enhances carcinogenesis [61]. In that study, high-fat-fed hamsters had elevated insulin levels but normal glucose levels, which was consistent with a state of insulin resistance [61]. The turn-over rate of cells in islets is significantly increased in the high-fat animals, suggesting a compensatory islet cell proliferation [61]. Administration of metformin, starting 2 weeks before the administration of BOP and continuing throughout the experiment, normalized insulin concentrations and the rate of islet cell turnover [61]. Malignant pancreatic lesions were found in 50% of the high-fat/BOP animals and none in the high-fat/BOP/metformin group (P < 0.05) [61].

 

By contrast, both it and even more so (1) give a range of mechanisms consistent with PDAC triggering diabetes by buggering up the beta-cells, leading to inadequate insulin secretion, and/or (surprisingly) by secondary impairment of peripheral insulin sensitivity:

Quote

Insulin sensitivity and overall diabetic state in pancreatic cancer patients who undergo tumor resection are markedly improved three months after the surgery. ... In their study of sera from patients with pancreatic cancer and culture media conditioned by human pancreatic cancer cells, Basso et al. found a 2030 MW peptide that they considered to be a putative pancreatic cancer associated diabetogenic factor [8].... [G]lycogen synthase activity was reduced in skeletal muscles of humans and rodents with pancreatic carcinoma [9, 11] and in isolated rat skeletal muscles exposed to human pancreatic tumor extracts in vitro [7]. ... When mice were treated with culture medium conditioned by the human pancreatic cancer cell line Mia PaCa2, blood glucose was elevated compared to the control value seen in mice treated with unconditioned medium [12]. In addition, isolated rat hepatocytes showed impaired glycolysis when incubated in culture media conditioned by four human pancreatic cancer cell lines ...

Reduced insulin release is seen in pancreatic cancer patients in response to classic stimuli. Insulin release was also reduced when isolated rat pancreatic islets were incubated in culture media conditioned by the human pancreatic cancer cell lines Panc-1 and HPAF or co-cultured with Panc-1 and HPAF cells [17, 18]. Studies of chemically-induced pancreatic cancer in hamsters found that glucose-stimulated insulin release was impaired in vivo [19] but not in isolated perfused pancreata [20]. Ishikawa et al. found an increase in proinsulin relative to insulin in pancreatic cancer patients [21], suggesting that the maturation of proinsulin may also be affected by the tumor.

Islet hormone profiles are changed in the circulation of pancreatic cancer patients, suggesting that secretion by different types of islet cells is disrupted by pancreatic cancer [22]. Changes in islet hormone concentrations in the circulation can also be seen in hamsters after induction of pancreatic cancer [23]. Human pancreatic islets adjacent to pancreatic carcinoma show morphological abnormalities characterized by abnormal co-localization of islet hormones in islet cells [24].

The diabetogenic potential of islet amyloid polypeptide (IAPP or amylin) has been investigated by several groups. IAPP is normally produced in islet beta cells and co-released with insulin at a constant ratio. [several groups] found elevated circulating levels of IAPP in patients with pancreatic cancer... The islets adjacent to human pancreatic carcinomas show reduced IAPP staining. In contrast, the expression of IAPP mRNA in these islets is unchanged, suggesting normal production but increased release of IAPP.

The molar ratio of IAPP/insulin was increased when rat pancreatic islets were co-cultured with Panc-1 and HPAF [pacreatic cancer] cells or cultured in media conditioned by these cell lines [17, 18]. The ratio was normalized after the co-cultured cancer cells were removed [18]. In a similar co-culture model, Ding et al. found that culture media conditioned by human pancreatic cancer cells contained a soluble molecule that selectively enhanced IAPP release from BRIN-BD11 beta cells [28]. Increased IAPP/insulin ratios were also seen in rats with azaserine-induced acinar pancreatic tumors and in hamsters with ductular pancreatic tumors induced by carcinogen N-nitrosobis(2-oxopropyl)amine (BOP) [29]. However, exposure of isolated rat pancreatic islets to hamster pancreatic cancer cells did not change the secretion of insulin and IAPP [17].

A physiological study of isolated rat pancreatic islets has shown that endogenous IAPP reduces arginine-stimulated insulin, glucagon, and somatostatin release [30]. Also, the improvement in glucose tolerance seen after tumor removal is associated with normalization of IAPP levels in the circulation [25]. Therefore, the increased IAPP release seen in pancreatic cancer patients may be responsible, at least in part, for the islet dysfunction seen in these individuals. (2)

 

On 7/12/2016 at 8:03 AM, Dean Pomerleau said:

The influence of poor glucose control on risk of pancreatic cancer hints that it may be the long-term glucose exposure and not (or perhaps in addition to) the insulin exposure that might do damage to the pancreas. Also a bit worrying is study [4], which found that those who had type 2 diabetes the longest were the ones most at risk (80% higher risk than the general population) for developing pancreatic cancer. ... So long-term, undiagnosed "latent pancreatic cancer" causing impaired glucose tolerance does not seem like a very plausible explanation for the association between pancreatic cancer and poor glucose control in diabetics (or Paul's clients), at least in the vast majority of cases of this rare disease.

 

You neglected to include a citation (4) in your post, so I can't know what that particular study found — but if that's a correct reading, it's an outlier: as noted, as the more recent meta-analysis found, the great majority of studies either find that there is a very high near-term association between diagnosis of diabetes and PDAC, followed by no or a small association at 5 years or more, or less commonly that there is only a small or moderate risk with no temporal variance. On meta-analysis, again, the RR of PDAC imparted by frank diabetes is 6.69 in the first year after diagnosis and slowly falls to 1.36 at 10 years.(1)

I agree that long-term, undiagnosed "latent pancreatic cancer" causing impaired glucose tolerance does not seem like a very plausible explanation, particularly since the more common and more rapid form is rapidly fatal, and appears in close temporal proximity to diabetes diagnosis — but that's therefore even more so of long-term, latent diabetes, which could easily occur as diabetes can be asymptomatic for decades. This makes a glucose exposure mechanism implausible, and also is part of the reason why it seems more plausible that PDAC rapidly causes diabetes than vice-versa.

Clarifying one related point:

On 7/12/2016 at 8:03 AM, Dean Pomerleau said:

While Steve Jobs had a slow growing form of pancreatic cancer, generally it grows very quickly - 80% of pancreatic cancer patients die within one year of diagnosis.

Not sure where you got this, but it doesn't seem to be true (all emphasis mine):
 

Quote

Jobs had a rare form of the cancer, known as neuroendocrine cancer, which grows more slowly and is easier to treat, explains Leonard Saltz, acting chief of the gastrointestinal oncology service at Memorial Sloan-Kettering Cancer Center. "Survival for many years or even decades with endocrine cancer is not surprising." For that type, the sort that Jobs had, "survival is measured in years, as opposed to pancreatic cancer, which is measured in months."

"When you have a pancreatic neuroendocrine tumor, that is substantially different from pancreatic cancer," Saltz says.

 

Quote

Jobs learned in 2003 that he had an extremely rare form of this cancer, an islet-cell neuroendocrine tumor. As the name implies, it arises from islet cells, the specialized factories within the pancreas that produce and secrete insulin ... Unlike pancreatic cancer, with neuroendocrine cancer “if you catch it early, there is a real potential for cure,” says cancer surgeon Joseph Kim of City of Hope, a comprehensive cancer center in Duarte, Calif. ...

patients with neuroendocrine cancer who were eligible for surgery (the cancer has not spread beyond the pancreas) “can have outstanding outcomes,” living for many more years. In part, that is because neuroendocrine cancers tend to be quite slow growing, or indolent. Even those that have been present for years, and in some cases decades, often stay safely confined to the pancreas. This kind of cancer can be so indolent that patients often die with it than from it. Although an estimated 2,000 to 3,000 people in the U.S. are diagnosed every year with neuroendocrine tumors of the pancreas, autopsies find the disease in hundreds more—people who were apparently not harmed by this very slow-growing cancer. Despite the expert consensus on the value of surgery, Jobs did not elect it right away.

 

Quote

Jobs revealed in 2004 that he had a pancreatic neuroendocrine tumor, kind of pancreatic cancer that tends to grow slowly. [Jobs died in 2011, so he survived 7 y despite delaying surgery for so long -MR]. It's relatively uncommon, representing only 5% of all pancreatic tumors. Diagnosis usually happens when the cancer has advanced; tumors are often detected after the cancer has spread to the liver, said Dr. Craig Devoe, pancreatic cancer specialist at the North Shore-LIJ Health System in New Hyde Park, New York, who did not treat Jobs.

 

Looking at the available data (11-20), it is very well-established that CR retards pancreatic cancer in multiple rodent models (with the exception of one study in the carcinogen-administered Syrian hamster (19)), and there is significant tho' not stellar evidence that lower energy intake —particularly from carbs, and possibly particularly from sugar — reduces risk of pancreatic cancer in humans.(13-15,22,24,25)  (Recalling again that 95% of pancreatic cancers arise in the exocrine pancreas, not the beta-cells, and that the association of diabetes with pancreatic cancer seems more likely to result from PDAC causing diabetes than vice-versa, this is unlikely to be mediated via overstimulation of the beta-cells; it seems a bit of a stretch to suggest it being mediated by effects on pancreatic amylase).
 
Of note, CR worked in rodents using the most physiologically-relevant models, including spontaneous precancerous lesions(18,20) and cancers driven by induced mutations in genes most commonly driving human PDAC.(12,14) The effect is dose-responsive(18,20). Also of note rapamycin also retards model prostate cancer, somewhat less effectively than CR(16), despite rapamycin unambiguously causing diabetes in rodents and humans (Glucoregulation was not monitored in most of these studies; surprisingly, in (16), CR improved glucose responsiveness on glucose tolerance test). Even very mild CR (10%, which I suspect in this case was actually obesity-avoidance rather than CR from a proper "healthy-AL" control group) has an effect, which even so was stronger than that for exercise.(23)
 
References
1: Batabyal P, Vander Hoorn S, Christophi C, Nikfarjam M. Association of diabetes mellitus and pancreatic adenocarcinoma: a meta-analysis of 88 studies. Ann Surg Oncol. 2014 Jul;21(7):2453-62. doi: 10.1245/s10434-014-3625-6. Epub 2014 Mar 9. PubMed PMID: 24609291.
 
2: Mol Cancer. 2003; 2: 4.
Published online 2003 Jan 6. doi:  10.1186/1476-4598-2-4
The relationship between diabetes and pancreatic cancer
Feng Wang,1 Margery Herrington,1,2 Jörgen Larsson,1 and Johan Permert
Free full text: http://molecular-can...6/1476-4598-2-4
PMID 12556242
 
3: Soeters MR, Soeters PB, Schooneman MG, Houten SM, Romijn JA. Adaptive reciprocity of lipid and glucose metabolism in human short-term starvation. Am J Physiol Endocrinol Metab. 2012 Dec 15;303(12):E1397-407. doi: 10.1152/ajpendo.00397.2012. Epub 2012 Oct 16. Review. PubMed PMID: 23074240.

4: Fery F, d'Attellis NP, Balasse EO. Mechanisms of starvation diabetes: a study with double tracer and indirect calorimetry. Am J Physiol. 1990 Dec;259(6 Pt 1):E770-7. PubMed PMID: 2260646.
 
5: Muoio DM. Metabolic inflexibility: when mitochondrial indecision leads to metabolic gridlock. Cell. 2014 Dec 4;159(6):1253-62. doi: 10.1016/j.cell.2014.11.034. PubMed PMID: 25480291; PubMed Central PMCID: PMC4765362.

11: Harvey AE, Lashinger LM, Hays D, Harrison LM, Lewis K, Fischer SM, Hursting SD. Calorie restriction decreases murine and human pancreatic tumor cell growth, nuclear factor-κB activation, and inflammation-related gene expression in an insulin-like growth factor-1-dependent manner. PLoS One. 2014 May 7;9(5):e94151. doi: 10.1371/journal.pone.0094151. eCollection 2014. PubMed PMID: 24804677; PubMed Central PMCID: PMC4013119.

12: Lashinger LM, Harrison LM, Rasmussen AJ, Logsdon CD, Fischer SM, McArthur MJ, Hursting SD. Dietary energy balance modulation of Kras- and Ink[4a/Arf+/-]-driven pancreatic cancer: the role of insulin-like growth factor-I. Cancer Prev Res (Phila). 2013 Oct;6(10):1046-55. doi: 10.1158/1940-6207.CAPR-13-0185. Epub 2013 Aug 26. PubMed PMID: 23980075; PubMed Central PMCID: PMC3874288.

13: Wang J, Zhang W, Sun L, Yu H, Ni QX, Risch HA, Gao YT. Dietary energy density is positively associated with risk of pancreatic cancer in urban Shanghai Chinese. J Nutr. 2013 Oct;143(10):1626-9. doi: 10.3945/jn.113.178129. Epub 2013 Jul 31. PubMed PMID: 23902959; PubMed Central PMCID: PMC3771813.

14: Lanza-Jacoby S, Yan G, Radice G, LePhong C, Baliff J, Hess R. Calorie restriction delays the progression of lesions to pancreatic cancer in the LSL-KrasG12D; Pdx-1/Cre mouse model of pancreatic cancer. Exp Biol Med (Maywood). 2013 Jul;238(7):787-97. doi: 10.1177/1535370213493727. Epub 2013 Jul 4. PubMed PMID: 23828595.

15: Heinen MM, Verhage BA, Goldbohm RA, Lumey LH, van den Brandt PA. Physical activity, energy restriction, and the risk of pancreatic cancer: a prospective study in the Netherlands. Am J Clin Nutr. 2011 Nov;94(5):1314-23. doi: 10.3945/ajcn.110.007542. Epub 2011 Sep 28. PubMed PMID: 21955648.

16: Lashinger LM, Malone LM, Brown GW, Daniels EA, Goldberg JA, Otto G, Fischer SM, Hursting SD. Rapamycin partially mimics the anticancer effects of calorie restriction in a murine model of pancreatic cancer. Cancer Prev Res (Phila). 2011 Jul;4(7):1041-51. doi: 10.1158/1940-6207.CAPR-11-0023. Epub 2011 May 18. PubMed PMID: 21593197; PubMed Central PMCID: PMC3131470.

17: Lashinger LM, Malone LM, McArthur MJ, Goldberg JA, Daniels EA, Pavone A, Colby JK, Smith NC, Perkins SN, Fischer SM, Hursting SD. Genetic reduction of insulin-like growth factor-1 mimics the anticancer effects of calorie restriction on cyclooxygenase-2-driven pancreatic neoplasia. Cancer Prev Res (Phila). 2011 Jul;4(7):1030-40. doi: 10.1158/1940-6207.CAPR-11-0027. Epub 2011 May 18. PubMed PMID: 21593196; PubMed Central PMCID: PMC3131443.

18: Molon-Noblot S, Keenan KP, Coleman JB, Hoe CM, Laroque P. The effects of ad libitum overfeeding and moderate and marked dietary restriction on age-related spontaneous pancreatic islet pathology in Sprague-Dawley rats. Toxicol Pathol. 2001 May-Jun;29(3):353-62. PubMed PMID: 11442021.

19: Birt DF, Pour PM, Nagel DL, Barnett T, Blackwood D, Duysen E. Dietary energy restriction does not inhibit pancreatic carcinogenesis by N-nitrosobis-2-(oxopropyl)amine in the Syrian hamster. Carcinogenesis. 1997 Nov;18(11):2107-11. PubMed PMID: 9395209.

20: Roebuck BD, Baumgartner KJ, MacMillan DL. Caloric restriction and intervention in pancreatic carcinogenesis in the rat. Cancer Res. 1993 Jan 1;53(1):46-52. PubMed PMID: 8416749.

21: Hass BS, Hart RW, Gaylor DW, Poirier LA, Lyn-Cook BD. An in vitro pancreas acinar cell model for testing the modulating effects of caloric restriction and ageing on cellular proliferation and transformation. Carcinogenesis. 1992 Dec;13(12):2419-25. PubMed PMID: 1473253.

22: Howe GR, Ghadirian P, Bueno de Mesquita HB, Zatonski WA, Baghurst PA, Miller AB, Simard A, Baillargeon J, de Waard F, Przewozniak K, et al. A collaborative case-control study of nutrient intake and pancreatic cancer within the search programme. Int J Cancer. 1992 May 28;51(3):365-72. PubMed PMID: 1317361.

23: Giles TC, Roebuck BD. Effects of voluntary exercise and/or food restriction on pancreatic tumorigenesis in male rats. Adv Exp Med Biol. 1992;322:17-27. PubMed PMID: 1442294.

24: Bueno de Mesquita HB, Moerman CJ, Runia S, Maisonneuve P. Are energy and energy-providing nutrients related to exocrine carcinoma of the pancreas? Int J Cancer. 1990 Sep 15;46(3):435-44. PubMed PMID: 2394510.

25: Howe GR, Jain M, Miller AB. Dietary factors and risk of pancreatic cancer: results of a Canadian population-based case-control study. Int J Cancer. 1990 Apr 15;45(4):604-8. PubMed PMID: 2157670.

26: Roebuck BD, Yager JD Jr, Longnecker DS. Dietary modulation of azaserine-induced pancreatic carcinogenesis in the rat. Cancer Res. 1981 Mar;41(3):888-93. PubMed PMID: 7459874.

 

Edited by Michael R
removing strikethrough

Share this post


Link to post
Share on other sites

Michael,

 

Thanks once again for a huge and helpful post about the subtle but potentially important distinctions between impaired glucose tolerance (IGT) and impaired fasting glucose (IFT), as well as the potential relationship between diabetes and pancreatic cancer.

 

A couple of things.

 

In response to Tasbin's calling my good postprandial glucose control "cheating", you wrote:

... I actually have to agree with Tasbin's overall point here, Dean. An OGTT is performed first thing in the morning, fasting, when counterregulatory hormones (glucagon and catecholamines) are elevated, is performed while quietly sitting or lying down, and uses a 75 g bolus of liquid glucose solution. By contrast, you were consuming much lower-glycemic carbs, along with protein and plenty of fat, and you took 2 hours to consume it, giving your tissues time to absorb the glucose slowly dripping into your bloodstream and your glucagon and catecholamines time to lay off.

 
Moreover, were you really inactive that whole time? You've certainly written in the past that you often make almost continuous use of your treadmill desk or under-desk pedaling machine. At the very least, you've got to shovel all that food into your maw and chew — and, yes, mess with your teeth ;) . And then, for your later results, you exercised — and (as my half-completed post reviews) there is now good evidence that the bulk of the benefit of post-meal exercise comes starting about half an hour after finishing a regular meal (tho' CR meals may vary), and that you're actually better off resting a bit immediately after finishing and only engaging in moderate (rather than intense) exercise.
 
Your glucose levels clearly reflect good glucose management, albeit not your complete glucose management protocol: they don't tell us much about your response to an OGTT, when all of those management strategies are denied to you.

 

From a technical perspective Michael, you are clearly correct. The formal diagnosis of IGT (or conversely, normal glucose tolerance) is made using a very controlled oral glucose tolerance test (OGTT), not the informal post-meal glucose measurements than many of us do. So you are right that technically I'm comparing apples to oranges, and the content of my meal (many high fiber, low-GI fruits and vegetables, with protein and fats from nuts and seeds which slow down absorption and potential insulin release, not to mention 3400kcal vs. 300kcal for a formal OGTT) as well as the way I consume it (over several hours, while standing and doing light kitchen work), is quite different from a traditional OGTT.

 

But as your quote from me indicates, I wasn't literally claiming to have beaten IGT per se, only that "Given my history of IGT, It looks like I'm doing something right" based on my postprandial (pre-exercise) glucose readings. In particular, there have been times in the past when I've measured my own post-meal glucose levels, and they've looked a whole lot worse than they do now, even when I was eating much less of basically the same diet.

 

Just a couple minor clarification. You wrote:

... were you really inactive that whole time? You've certainly written in the past that you often make almost continuous use of your treadmill desk or under-desk pedaling machine.

 

Eating is one of the few times of the days (besides sleeping), when I'm not actively engaged in deliberate physical exercise (i.e. pedalling, walking, jogging, swimming or resistance training). I do stand when I eat, and engage in light kitchen activities (chopping, tending sprouts, making witches brew coffee/tea/cacao, mixing, etc.). So I'm obviously not resting reclined like during a formal OGTT, that's for sure. So again, some degree of apples vs. oranges.

 

Next you said:

...there is now good evidence that the bulk of the benefit of post-meal exercise comes starting about half an hour after finishing a regular meal (tho' CR meals may vary), and that you're actually better off resting a bit immediately after finishing and only engaging in moderate (rather than intense) exercise.

 

Interesting. Have we discussed said evidence? I can potentially believe it, although I can also imagine it being like the old adage "don't swim for an hour after eating" - perhaps a practical aphorism (since you'll feel like crap swimming on a full stomach), but not necessarily well-supported by rigorous evidence. I'd be curious to see (again?) what evidence that claim is based on.

 

Moreover, as your quip "(tho' CR meals may vary)" suggests, it is especially hard to interpret "about half an hour after finishing a regular meal" in the context of a normal CR meal, to say nothing of my once-a-day, 2-hour mega-feast ☺. Since my meal is 3-4 times as big (in calories), at least an order of magnitude greater in volume, and 8 times as long in duration than a typical person's meal, does the ½ hour rule really translate?

 

In any case, except for swimming lately (where I've been pushing it to set personal bests and because I enjoy the way it feels), I never engage in intense exercise. And while it's not a full ½ hour, I do putter around for 15-20 minutes after eating, doing very light activities (i.e. cleaning up dishes, brushing teeth, sowing new sprouts & microgreens, taking the dog out for a morning potty break), before engaging in my moderate post-meal exercise regime of jogging, resistance training and pedalling.

 

Regarding diabetes and pancreatic cancer - thanks for the deep dive into the more recent evidence. Both epidemiological and mechanistic studies appear to support your assessment, namely that the causal linkage between pancreatic cancer and diabetes probably goes in → direction rather than ← direction.

 

Moreover, as a result of the evidence you point to, I too suspect Paul's observation of several allegedly CR practitioners having impair glucose metabolism and a short time later dying from pancreatic cancer is likely a coincidence, or possibly the result of selection bias - i.e. people with early health problems caused by undiagnosed pancreatic cancer, including impaired glucose metabolism, seek out Paul's help to improve their diet and lifestyle, only to discover a short time later they have pancreatic cancer that likely caused their metabolic dysfunction. 

 

Nevertheless, or perhaps even because of the likely direction of causality you've elucidated (i.e. pancreatic cancer → diabetes), 

it seems like it might be prudent for someone who believes they have experienced a recent and sudden onset of diabetes-like symptoms (including impaired glucose) to consult with their doctor and perhaps ask to get tested for pancreatic cancer. But obviously I'm not a doctor so consult your healthcare professional...

 

Next you said:

Clarifying one related point:

 

While Steve Jobs had a slow growing form of pancreatic cancer, generally it grows very quickly - 80% of pancreatic cancer patients die within one year of diagnosis.

 

Not sure where you got this, but it doesn't seem to be true (all emphasis mine):

....

 

"When you have a pancreatic neuroendocrine tumor, that is substantially different from pancreatic cancer," Saltz says.

etc.

 

Hmmm... I can't quite tell Michael if we are agreeing and you are misinterpreting what I meant, or you are picking nits. What I meant by my statement was that despite Jobs' unusual longevity with pancreatic cancer, in general pancreatic cancer kills very quickly. That seems to be what your quotes are suggesting as well. So I'm a bit confused.

 

Perhaps the nit you are picking is the distinction between the common form of pancreatic cancer that most people get (which kills very quickly) and the rare disorder Jobs actually had, namely "a pancreatic neuroendocrine tumor" (which kills slowly and is sometimes even curable). 

 

If so, I stand corrected. But my point (and yours too, I think) remains - namely that pancreatic cancer almost always kills swiftly.  As a corollary, since the latest evidence from meta-analyses you point to shows that risk of a pancreatic cancer diagnosis is associated with short-term (but not long-term) diabetes, this suggests swiftly-growing pancreatic cancer may kill off beta cells, causing diabetes in the short months or year before it is diagnosed, and before it becomes lethal.

 

Finally, after all that scholarship Michael, I was hoping for some kind of satisfying wrap-up on your part at the end of your post. I'm sure I was not alone in feeling a bit let down by the geeky and abrupt end to your post, without any sort of summary. I know you put a lot of research into it, and I'm very appreciative. I'm just left wondering what the upshot of your post really was.

 

I'll take a shot at summarizing what I think you may have been saying:

  • It is important to distinguish between impaired glucose tolerance (in response to a challenge meal or OGTT), and impaired fasting glucose. The former appears reasonably common among serious CR practitioners, while the latter (and especially its onset while practicing CR) seems very rare or non-existent among our cohort.
  • Tasbin should not jump to conclusions about the cause or temporal onset/progression of his apparent glucoregulatory dysfunction, at least based on the limited self-testing he has reported to us. He might also want to get an OGTT to see whether or not he officially has OGTT.
  • The most likely connection between diabetes and pancreatic cancer is not (as Paul seems to suggest) diabetes causes pancreatic cancer, but instead pancreatic cancer causes diabetes. But lest we unnecessarily alarm anybody, we should keep in mind that pancreatic cancer is quite rare, and therefore unlikely to be the cause of any particular individual's problems with glucose metabolism.

Please correct me if I'm wrong, or elaborate if I've left important stuff out.

 

--Dean

Share this post


Link to post
Share on other sites

Ihanks, Michael, for your helpful post.  You confirm my suspicion, that the do-it-yourself procedures suggested by several well-meaning people on the Forums --putting together postprandial glucose tests with a fasting glucose test, is no substitute for a formal GTT.  I intend to get such a test.  I'm having a little difficulty convincing my new GP to prescribe it -- but I'll probably have no trouble getting it from my CR-friendly endocrinologist.

 

  -- Saul

Share this post


Link to post
Share on other sites

First off, one more thing I forgot to acknowledge about Michael's post. It did not go unnoticed that he said:

And long before these reported cases, he [Paul] was stridently opposed to anyone reaching BMIs <18.5, on a far cruder basis than your (Dean's) generally quite reasoned arguments.

 

Aww shucks. Thanks Michael. I take that as a compliment, given how we haven't always (and almost certainly still don't) quite seen eye-to-eye on this topic. It's heartening to know that you respect at least some of my arguments, at least when I'm being reasonable ☺.

 

Saul, regarding your statement:

 

You [Michael] confirm my suspicion, that the do-it-yourself procedures suggested by several well-meaning people on the Forums --putting together postprandial glucose tests with a fasting glucose test, is no substitute for a formal GTT.  I intend to get such a test.

 

I really do think it would be worth you getting an OGTT, and that's why I pinged you about it recently. It is certainly the case that for diagnosing impaired glucose tolerance (IGT), there is no substitute for a formal OGTT, since IGT is defined as failure on just such a test. And it's important part of determining if you've progressed to frank diabetes (along with fasting glucose and insulin), as well as qualifying for treatment (e.g. metformin) if you and your doctor decide it's appropriate.

 

However, if you (or anyone else) is suspicious about IGT, whether or not you've been formally diagnosed with it, in order to manage IGT many of us have found postprandial glucose testing to be very valuable, and eye-opening.

 

Michael can correct me if I'm wrong about the following, but I think he'll agree given his observations about the low-carbers above (i.e. they are metabolically pretty healthy, despite transient IGT to an OGTT):

 

What matters ultimately is not whether you pass or fail a formal OGTT. What matters for health and longevity is long-term exposure to high glucose and insulin. People like the low-carbers, and those of us who employ cold exposure and post-meal exercise to effectively manage glucose despite eating lots of healthy carbs, can be quite healthy despite the fact that we might fail a formally-administered "pop quiz" OGTT. Post-meal glucose testing to see where we're at wrt glucose excursions, and to gauge the effectiveness of various glucose management strategies, can be quite valuable (unless you are like Michael and allegedly can't bleed...).

 

So go ahead and get your prescription for an OGTT, but don't rule out using home glucose monitoring to manage your glucose metabolism. This seems like it would be particularly germane for you Saul, given the very high proportion of carbs in your diet, via the whole "fruit vegetables" (e.g. sweet peppers) that you consume.

 

--Dean

Share this post


Link to post
Share on other sites

Hi Dean!

 

I, like you, thought that I was on a "high carb" diet -- since we both (and most in the Forums) eat a lot of raw vegetables.

 

But dietary fiber (and of course there's a lot of that in raw veggies) (which doesn't  contribute the same number of calories as simple carbs (of which of course we eat very litte).

 

Some of the speakers at CR IX spoke considerably about a high ketotic diet.  In a private conversation with Prof. Speakman, he suggested that most of us are on a ketotic diet, not a "high carb" diet-- the fiber doesn't count much in his definition of a "high carb" diet.

 

I had my keytones tested shortly aftr CR IX  -- it showed "ketosis" -- which doesn't really mean ketosis, but that I'm on a ketotic diet -- feeding my cells with keytones rather than glucose -- which is consistent with my fasting glucose of 60.

 

So, according to Speakman's definitions, I'm on a low carb diet.

 

  --  Saul

Share this post


Link to post
Share on other sites

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!

Register a new account

Sign in

Already have an account? Sign in here.

Sign In Now

×