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Sucralose Double Whammy

 

All,

 

At some times in the past at least, sucralose (aka Splenda) has been considered by some CR folks to be one of the better artificial sweeteners due to it's apparent inert nature in the human digestive system. But that seems to have been called into question recently, as highlighted by two popular press pieces that came across my radar today.

 

The first is this story on the recent downgrade of Splenda from "Caution" to "Avoid" by the Center for Science in the Public Interest (CSPI), as announced here. Quoting the CSPI president:

 

“We recommend that consumers avoid sucralose, or Splenda, and we recommend consumers also avoid saccharin, aspartame, and acesulfame potassium,” said CSPI president Michael F. Jacobson. “That said, the risk posed by over-consumption of sugar and high-fructose corn syrup, particularly from soda and other sugar-sweetened beverages, of diabetes, heart disease, and obesity, far outweighs the cancer risk posed by sucralose and most other artificial sweeteners. Consumers are better off drinking water, seltzer, or flavored waters, but diet soda does beat regular soda.”

 

The CSPI cites concerns over Splenda as a result of this new study [1], which found mice fed daily doses of sucralose (supposedly equivalent to 10 cans of diet soda) developed leukemia. The conclusion of [1] is fairly alarming (alarmist?!):

 

These findings do not support previous data that sucralose is biologically inert. More studies are necessary to show the safety of sucralose, including new and more adequate carcinogenic bioassay on rats. Considering that millions of people are likely exposed, follow-up studies are urgent.

 

While I haven't looked at the full text, it seems this study alone might be sufficient to discourage the use of sucralose, especially on top of the troubling previous study [2] that found sucralose (along with nutrasweet/aspartame and Sweet-N-Low/saccharin) caused obesity-promoting changes in the gut microbial population. Dr. Greger highlights [2] as his motivation for recommending people avoid Splenda in today's video:

 

 

He also points to correlations between the introduction of sucralose and the rise in prevalence of irritable bowel syndrome (IBS) in several countries as potentially troubling as well.

 

--Dean

 

------------

[1] International Journal of Occupational and Environmental Health 

Published online: 29 Jan 2016
 
DOI:10.1080/10773525.2015.1106075
 
Sucralose administered in feed, beginning prenatally through lifespan, induces hematopoietic neoplasias in male swiss mice
 
Soffritti M. , Padovani M. , Tibaldi E. , Falcioni L. , Manservisi F. , Lauriola M. , Bua L. , Manservigi M. , Belpoggi F. 
 
Abstract 
 
Background: Sucralose is an organochlorine artificial sweetener approximately 600 times sweeter than sucrose and used in over 4,500 products. Long-term carcinogenicity bioassays on rats and mice conducted on behalf of the manufacturer have failed to show the evidence of carcinogenic effects.
 
Objective: The aim of this study was to evaluate the carcinogenic effect of sucralose in mice, using a sensitive experimental design.
 
Methods: Five groups of male (total n = 457) and five groups female (total n = 396) Swiss mice were treated from 12 days of gestation through the lifespan with sucralose in their feed at concentrations of 0, 500, 2,000, 8,000, and 16,000 ppm.
 
Results: We found a significant dose-related increased incidence of males bearing malignant tumors (p < 0.05) and a significant dose-related increased incidence (p < 0.01) of hematopoietic neoplasias in males, in particular at the dose levels of 2,000 ppm (p < 0.01) and 16,000 ppm (p < 0.01).
 
Conclusions: These findings do not support previous data that sucralose is biologically inert. More studies are necessary to show the safety of sucralose, including new and more adequate carcinogenic bioassay on rats. Considering that millions of people are likely exposed, follow-up studies are urgent.
 
------------
[2] Nature. 2014 Oct 9;514(7521):181-6. doi: 10.1038/nature13793. Epub 2014 Sep 17.
 
Artificial sweeteners induce glucose intolerance by altering the gut microbiota.
 
Suez J(1), Korem T(2), Zeevi D(2), Zilberman-Schapira G(3), Thaiss CA(1), Maza
O(1), Israeli D(4), Zmora N(5), Gilad S(6), Weinberger A(7), Kuperman Y(8),
Harmelin A(8), Kolodkin-Gal I(9), Shapiro H(1), Halpern Z(10), Segal E(7), Elinav
E(1).
 
Non-caloric artificial sweeteners (NAS) are among the most widely used food
additives worldwide, regularly consumed by lean and obese individuals alike. NAS 
consumption is considered safe and beneficial owing to their low caloric content,
yet supporting scientific data remain sparse and controversial. Here we
demonstrate that consumption of commonly used NAS formulations drives the
development of glucose intolerance through induction of compositional and
functional alterations to the intestinal microbiota. These NAS-mediated
deleterious metabolic effects are abrogated by antibiotic treatment, and are
fully transferrable to germ-free mice upon faecal transplantation of microbiota
configurations from NAS-consuming mice, or of microbiota anaerobically incubated 
in the presence of NAS. We identify NAS-altered microbial metabolic pathways that
are linked to host susceptibility to metabolic disease, and demonstrate similar
NAS-induced dysbiosis and glucose intolerance in healthy human subjects.
Collectively, our results link NAS consumption, dysbiosis and metabolic
abnormalities, thereby calling for a reassessment of massive NAS usage.
 
PMID: 25231862

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The below papers I think have not been included in the conversation yet, but let me say that I have averaged 50 packets of Sugar Twin daily for months if not a year with excellent fasting glucose and hemoglobin A1c levels.  Also, when I tried pro- and pre-biotics, I could never notice any effects.  I think when we eat a lot of plant foods including soluble and insoluble fiber we consume the great leveler of our microbiome population.  There are I believe enough bugs in there, as evidenced by gas and odor, but only digressing significantly from my diet seems to alter my GI friends.

 

 

Non-caloric artificial sweeteners and the microbiome: findings and challenges.
Suez J, Korem T, Zilberman-Schapira G, Segal E, Elinav E.
Gut Microbes. 2015;6(2):149-55. doi: 10.1080/19490976.2015.1017700. Epub 2015 Apr 1. Review.
PMID: 25831243
 
Metabolic effects of non-nutritive sweeteners.
Pepino MY.
Physiol Behav. 2015 Dec 1;152(Pt B):450-5. doi: 10.1016/j.physbeh.2015.06.024. Epub 2015 Jun 19. Review.
PMID: 26095119
 
Artificial Sweeteners: A systematic review and primer for gastroenterologists.
Spencer M, Gupta A, Dam LV, Shannon C, Menees S, Chey WD.
J Neurogastroenterol Motil. 2016 Feb 25. doi: 10.5056/jnm15206. [Epub ahead of print]
PMID: 26932837 Free Article

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I love it Al you saying this. For years and years I have ignored these newer sweeteners and stuck with plain old saccharine, but I am sure Dean will dig up some awful dirt on it now that I mention it-huh ha! Brace yourself!

 

Of course kidding aside I totally appreciate Dean, you and Michael Rae for all you guys do.

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It does seem that stevia beats aspartame and especially glucose for glucose/insulin effects.

 

And yes, Michael, 50 packets Sugar Twin is what I took daily, along with =/> 10 liters of water.

 

 

Effects of stevia, aspartame, and sucrose on food intake, satiety, and postprandial glucose and insulin levels.

Anton SD, Martin CK, Han H, Coulon S, Cefalu WT, Geiselman P, Williamson DA.

Appetite. 2010 Aug;55(1):37-43. doi: 10.1016/j.appet.2010.03.009. Epub 2010 Mar 18.

PMID: 20303371 Free PMC Article



 

Abstract

 

Consumption of sugar-sweetened beverages may be one of the dietary causes of metabolic disorders, such as obesity. Therefore, substituting sugar with low calorie sweeteners may be an efficacious weight management strategy. We tested the effect of preloads containing stevia, aspartame, or sucrose on food intake, satiety, and postprandial glucose and insulin levels. DESIGN:

19 healthy lean (BMI=20.0-24.9) and 12 obese (BMI=30.0-39.9) individuals 18-50 years old completed three separate food test days during which they received preloads containing stevia (290kcal), aspartame (290kcal), or sucrose (493kcal) before the lunch and dinner meal. The preload order was balanced, and food intake (kcal) was directly calculated. Hunger and satiety levels were reported before and after meals, and every hour throughout the afternoon. Participants provided blood samples immediately before and 20min after the lunch preload. Despite the caloric difference in preloads (290kcal vs. 493kcal), participants did not compensate by eating more at their lunch and dinner meals when they consumed stevia and aspartame versus sucrose in preloads (mean differences in food intake over entire day between sucrose and stevia=301kcal, p<.01; aspartame=330kcal, p<.01). Self-reported hunger and satiety levels did not differ by condition. Stevia preloads significantly reduced postprandial glucose levels compared to sucrose preloads (p<.01), and postprandial insulin levels compared to both aspartame and sucrose preloads (p<.05). When consuming stevia and aspartame preloads, participants did not compensate by eating more at either their lunch or dinner meal and reported similar levels of satiety compared to when they consumed the higher calorie sucrose preload.

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hello, I don't use stevia or other sweeteners but recently I listened to a noted italian epidemiologist and expert in nutrition (Franco Berrino) saying that people using  zero-calorie drinks get more often sick of diabetes. He said also about stevia that  it is ok to use stevia if you don't eat noting, so the glycemia can't to go up, but if you eat at the same time, glycemia probably will go up more than using sugar.

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Cloud,

hello, I don't use stevia or other sweeteners but recently I listened to a noted italian epidemiologist and expert in nutrition (Franco Berrino) saying that people using  zero-calorie drinks get more often sick of diabetes. He said also about stevia that  it is ok to use stevia if you don't eat noting, so the glycemia can't to go up, but if you eat at the same time, glycemia probably will go up more than using sugar.

 

Apparently it's time to stop listening to Dr. Berrino. Did he really say "glycemia will go up more [using stevia] than using sugar"?! That's just plain ignorant, given sugar is (in large part) glucose!

 

In fact, quite the opposite appears to be true in fact. Not just that stevia has less of an increase on blood glucose than sugar, but in fact stevia reduces blood glucose in response to a meal or glucose challenge.

 

From [1] in humans:

 

 The extract of Stevia rebaudiana increased glucose tolerance. The [stevia] extract significantly decreased plasma glucose levels during the test and after overnight fasting in all volunteers.

 

From [2] in rats:

 

[stevia] produced a delayed but significant (P < 0.01) decrease in the blood glucose level, without producing condition of hypoglycemia after treatment...

 

From [3] in rats:

 

Stevioside (0.5 mg/kg), lowered the blood glucose levels in STZ-induced diabetic rats, peaking at 90 min. Stevioside administered twice daily also demonstrated dose-dependent effects in lowering the glucose levels in both diabetic rat models. Stevioside reduced the rise in glucose during glucose tolerance testing in normal rats... Stevioside also reduced insulin resistance in the diabetic animals as shown by the glucose lowering effects of tolbutamide. In conclusion, stevioside was able to regulate blood glucose levels by enhancing not only insulin secretion, but also insulin utilization in insulin-deficient rats...

 

--Dean

 

-------

[1] Braz J Med Biol Res. 1986;19(6):771-4.

 
Effect of Stevia rebaudiana on glucose tolerance in normal adult humans.
 
Curi R(1), Alvarez M, Bazotte RB, Botion LM, Godoy JL, Bracht A.
 
Author information: 
(1)Departamento de Farmácia-Bioquímica, Universidade de Maringá, Brasil.
 
The effect of aqueous extracts of Stevia rebaudiana leaves on a glucose tolerance
test was investigated in 16 normal volunteers. Aqueous extracts of 5 grams of
leaves were administered to volunteers at regular 6-h intervals for 3 days.
Glucose tolerance tests were performed before and after extract administration. A
second group of 6 normal volunteers who ingested an aqueous arabinose solution
was also studied to eliminate possible stress effects. The extract of Stevia
rebaudiana increased glucose tolerance. The extract significantly decreased
plasma glucose levels during the test and after overnight fasting in all
volunteers.
 
PMID: 3651629 
 
-----------
[2] J Pharm Bioallied Sci. 2011 Apr;3(2):242-8. doi: 10.4103/0975-7406.80779.
 
Antidiabetic activity of medium-polar extract from the leaves of Stevia
rebaudiana Bert. (Bertoni) on alloxan-induced diabetic rats.
 
Misra H(1), Soni M, Silawat N, Mehta D, Mehta BK, Jain DC.
 
Author information: 
(1)School of Studies in Chemistry and Biochemistry, Vikram University, Ujjain -
456 010, Madhya Pradesh, India.
 
OBJECTIVE: To investigate the medicative effects of medium-polar
(benzene:acetone, 1:1, v/v) extract of leaves from Stevia rebaudiana (family
Asteraceae) on alloxan-induced diabetic rats.
MATERIALS AND METHODS: Diabetes was induced in adult albino Wistar rats by
intraperitoneal (i.p.) injection of alloxan (180 mg/kg). Medium-polar extract was
administered orally at daily dose of 200 and 400 mg/kg body wt. basis for 10
days. The control group received normal saline (0.9%) for the same duration.
Glibenclamide was used as positive control reference drug against Stevia extract.
RESULTS: Medium-polar leaf extract of S. rebaudiana (200 and 400 mg/kg) produced 
a delayed but significant (P < 0.01) decrease in the blood glucose level, without
producing condition of hypoglycemia after treatment, together with lesser loss in
the body weight as compared with standard positive control drug glibenclamide.
CONCLUSIONS: Treatment of diabetes with sulfonylurea drugs (glibenclamide) causes
hypoglycemia followed by greater reduction in body weight, which are the most
worrisome effects of these drugs. Stevia extract was found to antagonize the
necrotic action of alloxan and thus had a re-vitalizing effect on β-cells of
pancreas.
 
PMCID: PMC3103919
PMID: 21687353
 
----------
[3] Planta Med. 2005 Feb;71(2):108-13.
 
Mechanism of the hypoglycemic effect of stevioside, a glycoside of Stevia
rebaudiana.
 
Chen TH(1), Chen SC, Chan P, Chu YL, Yang HY, Cheng JT.
 
Author information: 
(1)Department of Medicine, Taipei Medical University-Wan Fang Hospital, Taipei,
Taiwan.
 
We have studied the effects of stevioside on the glucose and insulin metabolism
in 2 models of diabetes in rats, STZ-induced diabetic rats and NIDDM diabetic
rats induced by feeding with fructose. Stevioside (0.5 mg/kg), lowered the blood 
glucose levels in STZ-induced diabetic rats, peaking at 90 min. Stevioside
administered twice daily also demonstrated dose-dependent effects in lowering the
glucose levels in both diabetic rat models. Stevioside reduced the rise in
glucose during glucose tolerance testing in normal rats. Stevioside
dose-dependently decreased protein levels of phosphoenol pyruvate carboxykinase
(PEPCK) and PEPCK mRNA after 15 days of treatment. Stevioside also reduced
insulin resistance in the diabetic animals as shown by the glucose lowering
effects of tolbutamide. In conclusion, stevioside was able to regulate blood
glucose levels by enhancing not only insulin secretion, but also insulin
utilization in insulin-deficient rats; the latter was due to decreased PEPCK gene
expression in rat liver by stevioside's action of slowing down gluconeogenesis.
Further studies of this agent for the treatment of diabetes appear warranted.
 
PMID: 15729617

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Hello Dean, Dr. Berrino is a respected epidemiologist and researcher in the field of cancer and nutrition, you can find his studies on pubmed.

I have tried to translate what he said in a recent seminar (for doctors) answering a question about the use of  artificial sweeteners.  

he said that zero-calorie drinks are not a good solution, people drinking these drinks get sick more often of diabetes

and regarding stevia he said that it is fine sweeten a drink with stevia but only  if you do not eat anything, in this case blood glucose can not increase, but if you, at the same time, eat some food probably the blood glucose will increase more than if you use sugar.

Probably it is only his opinion but I do not think he ignores the studies on the subject.

 

The research on the subject maybe is not so conclusive, I have just remembered the following transcript of an interview with V. Longo and M.Mattson, do you know it? https://thedianerehmshow.org/shows/2014-01-09/latest-research-intermittent-fasting-0  

 

In the transcription you can find: 

  • REHMDr. Longo, where do you come in on diet drinks?

  • 11:36:10

    LONGOWell, first of all, the diet drinks can have effects on your endocrine system even though it doesn't have sugar in it. So insulin could be released. And also there's a number of studies showing that you gain weight by being under diet drinks. So...

  • REHMWhy would that be? Why would people gain weight using diet drinks?

  • 11:36:33

    MATTSONWell, Dr. Mosley pointed out -- so when you're taking something that's like sugar that your body has responses to the like sugar and may make you more hungry. But the research hasn't been done with relation to intermittent fasting and whether, you know, taking at least, unless Valter know something I don't know about. No one's done a study to critically ask the question whether it makes any difference whether on the days you're not eating much...

     

    (sorry for the format)

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Cloud,

 

Respectfully - your, Berrino's and Longo's responses sound like arguments from authority, pure speculation and non-sequiturs with respect to the Stevia evidence I posted, respectively.

 

--Dean

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Dean, 

 

As I said I am not used to consume sweeteners, and so I don't know and follow the scientific literature on the argument but I thought could be useful for the CR forum posting the opinions of Berrino and Longo on the subject I came across.  The scientific studies are not always  without bias and limitations and so I think that sometime the opinions (or pure speculations as you say) of experts of value, even if not yet supported by peer-reviewed journals, are worthy of attention.

-Cloud

Edited by Cloud

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I was surprised by the below quotation from the last below paper, having thought that artificial sweeteners raised blood sugar levels.  What do you think?
 

". Fasting
blood glucose was not different between treatment groups after 12
weeks or one year and there was no indication that LCS had an adverse
effect on glucose homeostasis [31,32]."
 
[31] The effects of water and non-nutritive sweetened beverages on weight loss during a 12-week weight loss treatment program.
Peters JC, Wyatt HR, Foster GD, Pan Z, Wojtanowski AC, Vander Veur SS, Herring SJ, Brill C, Hill JO.
Obesity (Silver Spring). 2014 Jun;22(6):1415-21. doi: 10.1002/oby.20737.
PMID: 24862170 Free Article
http://onlinelibrary.wiley.com/doi/10.1002/oby.20737/full
http://onlinelibrary.wiley.com/doi/10.1002/oby.20737/pdf
 
Abstract
 
OBJECTIVE:
 
To compare the efficacy of non-nutritive sweetened beverages (NNS) or water for weight loss during a 12-week behavioral weight loss treatment program.
 
METHODS:
 
An equivalence trial design with water or NNS beverages as the main factor in a prospective randomized trial among 303 men and women was employed. All participants participated in a behavioral weight loss treatment program. The results of the weight loss phase (12 weeks) of an ongoing trial (1 year) that is also evaluating the effects of these two treatments on weight loss maintenance were reported.
 
RESULTS:
 
The two treatments were not equivalent with the NNS beverage treatment group losing significantly more weight compared to the water group (5.95 kg versus 4.09 kg; P < 0.0001) after 12 weeks. Participants in the NNS beverage group reported significantly greater reductions in subjective feelings of hunger than those in the water group during 12 weeks.
 
CONCLUSION:
 
These results show that water is not superior to NNS beverages for weight loss during a comprehensive behavioral weight loss program.
 

[32] The effects of water and non-nutritive sweetened beverages on weight loss and weight maintenance: A randomized clinical trial.
Peters JC, Beck J, Cardel M, Wyatt HR, Foster GD, Pan Z, Wojtanowski AC, Vander Veur SS, Herring SJ, Brill C, Hill JO.
Obesity (Silver Spring). 2016 Feb;24(2):297-304. doi: 10.1002/oby.21327. Epub 2015 Dec 26.
PMID: 26708700 Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4744961/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4744961/pdf/OBY-24-297.pdf
 
Abstract
 
OBJECTIVE:
 
To evaluate the effects of water versus beverages sweetened with non-nutritive sweeteners (NNS) on body weight in subjects enrolled in a year-long behavioral weight loss treatment program.
 
METHODS:
 
The study used a randomized equivalence design with NNS or water beverages as the main factor in a trial among 303 weight-stable people with overweight and obesity. All participants participated in a weight loss program plus assignment to consume 24 ounces (710 ml) of water or NNS beverages daily for 1 year.
 
RESULTS:
 
NNS and water treatments were non-equivalent, with NNS treatment showing greater weight loss at the end of 1 year. At 1 year subjects receiving water had maintained a 2.45 ± 5.59 kg weight loss while those receiving NNS beverages maintained a loss of 6.21 ± 7.65 kg (P < 0.001 for difference).
 
CONCLUSIONS:
 
Water and NNS beverages were not equivalent for weight loss and maintenance during a 1-year behavioral treatment program. NNS beverages were superior for weight loss and weight maintenance in a population consisting of regular users of NNS beverages who either maintained or discontinued consumption of these beverages and consumed water during a structured weight loss program. These results suggest that NNS beverages can be an effective tool for weight loss and maintenance within the context of a weight management program.
 

Low Calorie Sweetener (LCS) use and energy balance.
Peters JC, Beck J.
Physiol Behav. 2016 Apr 7. pii: S0031-9384(16)30111-1. doi: 10.1016/j.physbeh.2016.03.024. [Epub ahead of print] Review.
PMID: 27061939
http://sci-hub.io/10.1016/j.physbeh.2016.03.024
 
Abstract
 
For thirty years there has been a debate about whether low calorie sweeteners (LCS) provide a benefit for body weight management. Early studies showed that when consumed alone in a beverage appetite and food intake were increased. Some, observational longitudinal cohort studies reported an association between LCS usage and increasing BMI, suggesting that LCS may actually promote weight gain. In the ensuing decades numerous additional observational and experimental trials have been conducted with the experimental trials nearly uniformly showing a benefit for LCS, either in weight loss or weight gain prevention. The observational trials have been more inconsistent with two recent meta-analyses indicating either a small positive association between LCS usage and BMI (weighted group mean correlation, p=0.03) or an inverse association with body weight change (-1.35 kg, p=.004). Numerous potential mechanisms have been explored, mostly in animal models, in an attempt to explain this association but none have yet been proven in humans. It is also possible that the association between LCS and BMI increase in the observational studies may be due to reverse causality or residual confounding. Randomized controlled trials are consistent in showing a benefit of LCS which suggests that simple behavioral engagement by individuals attempting to control their weight is a sufficiently strong signal to overcome any potential mechanism that might act to promote energy intake and weight gain. Based on existing evidence, LCS can be a useful tool for people actively engaged in managing their body weight for weight loss and maintenance.
 
KEYWORDS:
 
Body weight; Diet beverages; Low calorie sweeteners; Observational trials; Randomized trials

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Al,

 

I was surprised by the below quotation from the last below paper, having thought that artificial sweeteners raised blood sugar levels.  What do you think?

 

I'm surprised you thought that. I'm never had that impression from the published data, nor did I find it to be true in my own case, based on glucose testing I did after ingesting Splenda - back when I used to eat Splenda.

 

It's not that non-caloric sweeteners like Splenda are bad for blood glucose, or even weight gain as long as one is careful not to fall prey to "real sugar binging" effect that can result from trying to maintain a "sweet" low-calorie diet with artificial sweeteners.

 

Instead, the "gotcha" with Splenda is the potential association with cancer (leukemia) and detrimental changes in gut microbes, as discussed in the first post in this thread.

 

--Dean

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Very interesting, I thought CSPI would be less biased with it's advertisement free model ( like consumer reports ), scientific panel, and extensive use of references. Any thoughts on ulterior motives and biases vs. error on either side of the analysis?

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New Aspartame Study - Does it Really Cause Diabetes?

 

[Admin Note: I changed the title of this thread from "Sucralose Double Whammy" to the more generic "Artificial Sweeteners - CR Friendly or Toxic?" to reflect the broader discussions that have been covered in this thread]

 

I'm not a big fan of several of the most popular artificial sweeteners like Splenda, Aspartame or Saccharin for reasons discussed above (mostly their apparent effect on gut microbiome) . But I do use Stevia and xylitol/erythritol in modest amounts.

 

So when this Care2.com story Diet Soda May Actually Help Cause Type 2 Diabetes came across my radar yesterday, I figured I'd take a look, thinking I might dig up some new dirt on the common artificial sweeteners. What I found shocked me. And no, it had nothing to do with any harm from the sweeteners involved (saccharine and especially aspartame, it turns out). It had to do with the unbelievably shoddy "journalism" the story's author used to support her bogus headline. I guess I shouldn't be surprised, given how frequently this sort of thing happens.

 

Here is the study [1], and how the writer, Michelle Schoffro (supposedly a Board Certified "Doctor of Natural Medicine" (DNM) - see her bio at the bottom) misinterpreted it. Note I'll use "writer" for Ms. Schoffro, who penned the popular press article, and "authors" or "researchers" to refer to those who did the research and published the results of [1].

 

Here is how the writer describes [1] and its results:

 

The study had two phases: The first one examined a possible correlation between blood sugar impairment and artificial sweetener consumption in 33,994 people over several years. The second component assessed 2856 individuals aged 40 to 74 with no diagnosis of diabetes who fasted and then were given either sugars or artificial sweeteners, the latter of which included aspartame and saccharin. Their blood sugar levels were monitored. Of course, we’d expect those who took the sugar to have blood sugar issues afterward but those individuals who had the artificial sweeteners had even worse blood sugar problems. There was a significant correlation between artificial sweetener use, excessive weight and glucose intolerance.

 

So what did the researchers in [1] actually do and what did they find?

 

The authors looked at the NHANES group of ~34K people, which the writer got right. Yippie! But there weren't really two phases to the study, and they certainly didn't follow the subjects "over several years" as the writer says. The NHANES cohorts have been followed for many years, but this was a one-time study. They used a mobile trailers to interview and do basic bloodwork on the NHANES subjects. The "first phase" the writer refers to is simply looking at the baseline demographic data and correlating these measures with self-reported sweetener consumption via a food frequency questionnaire, the accuracy of which is always suspect, as we've discussed before, even specifically wrt NHANES - but let's ignore that weakness.

 

All I can figure is that the writer is interpreting the following from the demographic data with "excessive weight" in her one-sentence summary of the results in the last sentence of the quote above:

 

Individuals consuming artificial sweeteners (aspartame or saccharin) had a subtly higher BMI (28 vs. 27 kg/m2), and were more likely to be female (Table 1, P < 0.05). 

 

First off, a BMI of 28 vs. 27 is a pretty small difference - both in the overweight category. And there is a huge risk of reverse causality here. Rather than artificial sweeteners causing excessive weight as the writer suggests, excessive weight motivates people to go on a diet, causing them to consume (or report consuming) more artificial sweetener relative to sugar. From the same table, the aspartame consumers were also 2 years younger on average and more likely to be female. So does aspartame also slow aging and feminize you as well? ☺ Seriously, without controlling for demographics (which the authors didn't apparently do), you can't even remotely conclude that even the small BMI difference between aspartame and non-aspartame consumers is due to the aspartame - although even if they had controlled for other demographic confounders, a causal link between aspartame and excessive weight still couldn't be claimed.

 

But believe it or not it gets worse.

 

First, notice this statement by the writer:

 

The second component assessed 2856 individuals aged 40 to 74 with no diagnosis of diabetes who fasted and then were given either sugars or artificial sweeteners, the latter of which included aspartame and saccharin. Their blood sugar levels were monitored.

 

This is total bullsh*t. 

 

The authors did a 2-hour oral glucose tolerance test (OGTT) on a subset of the 34K NHANES participants, almost 3000 people in all (quite an undertaking...), and then correlated performance on the OGTT with their sweetener habits. In an OGTT, the subjected were given glucose, and glucose only silly writer, not "...and then were given either sugars or artificial sweeteners, the latter of which included aspartame and saccharin."

 

Next notice the writer's other statement at the end of her summary paragraph "...significant correlation between artificial sweetener use, excessive weight and and glucose intolerance". What was the evidence from [1] on which the writer bases that statement?

 

Here are the results, in graphical form, showing glucose level at 2h as a function of BMI and sweetener consumption:

 

MiPn43Q.png

 

 

Now right off the bat something about these graphs makes me suspicious, this time of the authors. Notice there are only two points for each condition, with a straight line between them? What's up with that? There is nothing in the methods section saying they split the NHANES folks into two groups, the skinny and chubby folks for the 2h OGTT:

 

Secondary analyses conducted for this study utilized 2856 adults with complete data for oral glucose tolerance, weight, height, and diet, and who were not taking medications for diabetes....
 
The oral glucose tolerance test was conducted at the mobile examination centre and was limited to a subset of individuals aged 40–74 years old without previously diagnosed type 2 diabetes and who were not taking insulin. Participants fasted overnight (>8 h) and blood was drawn from the antecubital vein by a trained phlebotomist according to a standardized protocol. Participants received a 75-g glucose-equivalent oral glucose challenge and a second blood sample was drawn 2 h later. 

 

We can only presume they binned the 3000 OGTT subjects into skinny and chubby groups, and analysed them separately to generate these graphs. 

 

About the graphs themselves, they appear to show that neither high (vs. low) consumption of sucrose or fructose is associated with any worse performance on an oral glucose tolerance test. The upward slopes in all the graphs simply shows that fatter people have worse glucose control. The author's confirm this:

 

Sucrose and fructose intake were not significantly related to glucose tolerance, HOMA-IR, or fasting glucose independent of BMI (P > 0.10).

 

So much for the fructose/HFCS bashers, to say nothing of the fruit haters...

 

But the real action is in the bottom two graphs, for saccharin and especially aspartame. Notice the stats on the saccharin graph "BMI x Saccharin: P > 0.05; BMI: P < 0.01; Saccharin: P = 0.30"? This basically says fatter people have worse glucose tolerance than skinny folks, but saccharin has nothing to do with it. That is, the difference between the two parallel lines in the graph wasn't statistically significant. So this data doesn't support a link between saccharin and impaired glucose tolerance / diabetes at any BMI. So much of the over-general "Diet Soda" (which would include saccharine-sweetened soda) reference in the title of the writer's story...

 

But what about aspartame? That's the really interesting part. As you can see from the greater slope of the high-aspartame consumers, thin folks who consumed a lot of aspartame actually exhibited improved 2h glucose control relative to low/non-aspartame consumers! On the other end, the chubby high-aspartame consumers did look a little worse than the chubby low-consumers, but the disadvantage on the high end appears to be (slightly) smaller than the advantage on the low end! Extrapolating, you'd expect someone with an intermediate, "normal" weight (~BMI 25) to do a bit better on an OGTT if they consumed aspartame than if they didn't! And this is even more the case for really skinny folks like many of us. 

 

Here is how the authors themselves spin their results in the discussion:

 

The results of the current study illustrate that aspartame consumption is associated with augmented obesity-related deteriorations in glucose tolerance and fasting glucose. 

 

In other words, they appear to be claiming that if you're fat, consuming aspartame is associated with an increased risk of being (pre)diabetic. But if we look at the table (albeit not broken down by BMI - a simple analysis which the authors apparently did not do, or at least report), we see that aspartame consumers in general (independent of BMI) had no worse (or better) glucose metabolism than the non-consumers - see highlighted cells below:

 

X0BAbSK.png

 

So the claim about worse fasting glucose for (fatter) aspartame eaters seems at best unsupported by the data provided, and at worse just plain wrong. In fact, earlier in the paper, in the results section, the authors acknowledge as much, seeming to me to contradict the statement they make in the conclusion:

 

There were no differences in glucose tolerance, HOMA-IR, or fasting plasma glucose between those consuming high sugars or artificial sweeteners and those who did not.

 

Perhaps their statement in the discussion section isn't entirely wrong, but it is certainly misleading / hard to parse correctly. 

 

In short it appears to me the authors exaggerated the meaning / significance of their results (i.e. P-hacking) to get it published and to make headlines. Then the writer took the ball and ran with it - hyper-exaggerating the very questionable results of [1] and turning it into the click-bait headline Diet Soda May Actually Help Cause Type 2 Diabetes. At least this is better than the apparent original title of the popular press story, which from it's URL appears to have been Diet Soda May Actually CAUSE Type 2 Diabetes (ALL-CAPs in the original). 

 

If I were to put it charitably, I'd call actions of the authors and the writer a "comedy of errors" where mistakes are ignored and weak findings exaggerated. But I'm more inclined to call it the type of "unholy alliance" between researchers and the media that I discussed in this post. This kind of dirt poor coverage and misinterpretation of questionable nutrition studies is shockingly common. It seems the researchers conduct them to get/maintain funding, and the authors write them mostly as click-bait, with an inflammatory title which compels people concerned with their health to read them. It really gets my goat. In fact, I've decided to start maintaining a list of posts about this kind of bogus reporting, here. This is the first one on my list, although I know we'd talked about many others over the years. If you come across others either that we've discussed before or new studies, please let me know.

 

Bottom line though - this study shows no association between diabetes and aspartame or Saccharin, to say nothing of "Diet Soda", despite the popular press claim to the contrary. In fact, for skinny folks like most of us, it could be argued the data in [1] suggests that aspartame may improve glucose metabolism, although I still don't recommend it since the results here were weak, and due to the potential adverse effect it may have on one's gut microbiome, as discussed previously in this thread. 

 

--Dean

 

P.S. I posted this comment below the Care2 story discussed above. We'll see if Ms. Schoffro replies...

 

Dear Michelle the author of this story. I'm not an advocate for consuming aspartame or other artificial sweeteners, but you TOTALLY messed up your analysis of this study. Whether it was intentional or not I can't tell. But you really should completely retract what you said here. See here for details of what you got so terribly wrong. The study doesn't support virtually anything you said above. https://www.crsociety.org/topic/11605-artificial-sweeteners-cr-friendly-or-toxic/?do=findComment&comment=17138
 

----------

Here is the writer's impressive sounding bio. Look at all those degrees! Of course the titles of her books, which include words like Slim, Detox, Vitality, Life Force, and pH Solution, should have given it away from the start...

 

 Michelle Schoffro Cook, MSc, RNCP, ROHP, DNM, PhD is an international best-selling and 17-time book author and board-certified doctor of natural medicine, whose works include: 60 Seconds to Slim, Weekend Wonder Detox, Healing Recipes, The Vitality Diet, Allergy-Proof, Arthritis-Proof, Total Body Detox, The Life Force Diet, The Ultimate pH Solution, The 4-Week Ultimate Body Detox Plan, and her new book The Probiotic Promise. 

 

----------

[1] Appl Physiol Nutr Metab. 2016 May 24:1-4. [Epub ahead of print]

Aspartame intake is associated with greater glucose intolerance in individuals
with obesity.

Kuk JL(1,)(2), Brown RE(2,)(2).

Author information:
(1)School of Kinesiology and Health Science, York University, Toronto, ON M3J
1P3, Canada.

This study examined whether sucrose, fructose, aspartame, and saccharin
influences the association between obesity and glucose tolerance in 2856 adults
from the NHANES III survey. Aspartame intake significantly influenced the
association between body mass index (BMI) and glucose tolerance (interaction: P =
0.004), wherein only those reporting aspartame intake had a steeper positive
association between BMI and glucose tolerance than those reporting no aspartame
intake. Therefore, consumption of aspartame is associated with greater
obesity-related impairments in glucose tolerance.

PMID: 27216413

 

----------

[1] Appl Physiol Nutr Metab. 2016 May 24:1-4. [Epub ahead of print]

Aspartame intake is associated with greater glucose intolerance in individuals
with obesity.

Kuk JL(1,)(2), Brown RE(2,)(2).

Author information:
(1)School of Kinesiology and Health Science, York University, Toronto, ON M3J
1P3, Canada.

This study examined whether sucrose, fructose, aspartame, and saccharin
influences the association between obesity and glucose tolerance in 2856 adults
from the NHANES III survey. Aspartame intake significantly influenced the
association between body mass index (BMI) and glucose tolerance (interaction: P =
0.004), wherein only those reporting aspartame intake had a steeper positive
association between BMI and glucose tolerance than those reporting no aspartame
intake. Therefore, consumption of aspartame is associated with greater
obesity-related impairments in glucose tolerance.

PMID: 27216413

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Hi Dean!

 

I use neotame as an artificial sweetener.  Neotame is 18 times sweeter than sucralose, which is (I think) 600 times sweeter than sugar.  As a result, I consume so little of the stuff that I doubt that it could have any effect on my gut microbiome.  (Of course, no studies have been done on the effects of neotame on the gut microbiome; my guess:  A huge dose would have zero impact -- but that's just my guess).

 

I rarely use Splenda tablets -- but again, I don't worry about it.  I believe that the studies made are unconvincing.  I like Michael Rae's comment:  "In an abundance of caution", he avoids artificial sweeteners.

 

The negative data on aspartame also appears week, IMO.  But there IS some evidence that there might be a negative effect with sacharine.

 

IMO, much more thorough studies are necessary before any definitive conclusions can be made.

 

What IS true is that sugar has terrible effects on both your metabolism and your gut microbiome -- and that includes the natural sugars that you ingest when you eat most fruits.  So, IMO, you're much better off eating a non-starchy, non-sugary vegetable -- and sweetening it with your favorite non-caloric sweetener -- than eating most fruits.  (And much better off eating a fruit than adding sugar to your tea or coffee.)

 

:)xyz

 

  --  Saul

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Saul,

 

You and I agree that refined sugar is unhealthy, and that there is some (but not overwhelming) evidence suggesting avoidance of many of today's popular artificial sweeteners based (at least) on apparent impact on the gut microbiome. I'll leave aside any discussion of neotame, since I don't want to bother researching it. To me it seems like a freakishly potent and rarely used artificial compound, making me suspicious of it's long term effects. But I don't have any evidence one way or the other, and don't feel like bothering to research it since it seem you're the only one around here that uses it. I admire your willingness to be an N=1 experiment with it. I'll be curious to see how it works out for you.

 

But your dissing of fruit is just more of your usual ill-informed drivel that I can't let go by unchallenged. ["sorry honey, I can't come to bed yet, someone just said something stupid on the internet."]

 

I'm sure Saul you won't bother to read it (much less search for evidence for yourself), but we've got a whole thread documenting the benefits of fruit, even in some instances relative to non-starchy vegetables. But I will point to one study that (quite surprisingly) we haven't apparently discussed before, but which shows just how completely lacking in credibility your claim about fruit being worse than "veggies + neotame", to say nothing of your (possible?) suggestion that eating fruit is worse than not eating fruit due to the "terrible effects" from the "natural sugar" it contains.

 

In short, fruit is about the best damn thing you can do for you health.

 

That's not hyperbole, and you don't have to take my word for it. I'll let this report [1] of health risk factors in 187 countries around the world, sponsored by the Bill & Melinda Gates foundation and published in the The Lancet in 2012 speak for me.

 

It shows the enormous benefits of fruit consumption quite plainly. In short, low fruit consumption was the #1 dietary factor contributing to worldwide mortality between 1990 and 2010, resulting in an excess of 4.9 million deaths per year worldwide. Here is the fascinating chart of the percentage of deaths (x-axis) and "Disability-Adjusted Life Years" (DALYs - y-axis) lost as a result of the top 10 detrimental lifestyle factors (red) and diseases (blue). I've highlighted the dietary factors for easy parsing:

 

TDbcwFG.png

 

As you can see, of the dietary risk factors, "low fruit consumption" leads the pack - by a mile in fact. And Yes, I confirmed in the full text of the appendix that "low vegetable intake" was part of the study, and didn't even make the top 10 list of lifestyle factors shown (in red) above. Interestingly, "low legume intake" was also considered, but didn't measure up by the methodology employed. However low "Low nuts / seeds intake" did make the top 10 list, although was less than half as detrimental as low fruit intake.

 

Whatever way you slice it Saul, based on this and a mountain of other evidence (only some of which is documented in the thread pointed to above), fruit is tremendously healthy for you, despite the "natural sugars" you malign above, and despite what ill-informed folks like you continue to ignorantly claim.

 

Sorry once again for being so blunt Saul. If you'd only stop making such silly (mis)statements, I'd be happy to back off. You do seem a glutton for punishment.

 

--Dean

 

---------

[1] 1. Lancet. 2012 Dec 15;380(9859):2095-128. doi: 10.1016/S0140-6736(12)61728-0.

 
Global and regional mortality from 235 causes of death for 20 age groups in 1990 
and 2010: a systematic analysis for the Global Burden of Disease Study 2010.
 
Lozano R, [+ ~100 other authors].
 
Free full text of Appendix (where fruit data is): http://www.thelancet.com/cms/attachment/2017336178/2037711222/mmc1.pdf
 
BACKGROUND: Reliable and timely information on the leading causes of death in
populations, and how these are changing, is a crucial input into health policy
debates. In the Global Burden of Diseases, Injuries, and Risk Factors Study 2010 
(GBD 2010), we aimed to estimate annual deaths for the world and 21 regions
between 1980 and 2010 for 235 causes, with uncertainty intervals (UIs),
separately by age and sex.
 
METHODS: We attempted to identify all available data on causes of death for 187
countries from 1980 to 2010 from vital registration, verbal autopsy, mortality
surveillance, censuses, surveys, hospitals, police records, and mortuaries. We
assessed data quality for completeness, diagnostic accuracy, missing data,
stochastic variations, and probable causes of death. We applied six different
modelling strategies to estimate cause-specific mortality trends depending on the
strength of the data. For 133 causes and three special aggregates we used the
Cause of Death Ensemble model (CODEm) approach, which uses four families of
statistical models testing a large set of different models using different
permutations of covariates. Model ensembles were developed from these component
models. We assessed model performance with rigorous out-of-sample testing of
prediction error and the validity of 95% UIs. For 13 causes with low observed
numbers of deaths, we developed negative binomial models with plausible
covariates. For 27 causes for which death is rare, we modelled the higher level
cause in the cause hierarchy of the GBD 2010 and then allocated deaths across
component causes proportionately, estimated from all available data in the
database. For selected causes (African trypanosomiasis, congenital syphilis,
whooping cough, measles, typhoid and parathyroid, leishmaniasis, acute hepatitis 
E, and HIV/AIDS), we used natural history models based on information on
incidence, prevalence, and case-fatality. We separately estimated cause fractions
by aetiology for diarrhoea, lower respiratory infections, and meningitis, as well
as disaggregations by subcause for chronic kidney disease, maternal disorders,
cirrhosis, and liver cancer. For deaths due to collective violence and natural
disasters, we used mortality shock regressions. For every cause, we estimated 95%
UIs that captured both parameter estimation uncertainty and uncertainty due to
model specification where CODEm was used. We constrained cause-specific fractions
within every age-sex group to sum to total mortality based on draws from the
uncertainty distributions.
FINDINGS: In 2010, there were 52·8 million deaths globally. At the most aggregate
level, communicable, maternal, neonatal, and nutritional causes were 24·9% of
deaths worldwide in 2010, down from 15·9 million (34·1%) of 46·5 million in 1990.
This decrease was largely due to decreases in mortality from diarrhoeal disease
(from 2·5 to 1·4 million), lower respiratory infections (from 3·4 to 2·8
million), neonatal disorders (from 3·1 to 2·2 million), measles (from 0·63 to
0·13 million), and tetanus (from 0·27 to 0·06 million). Deaths from HIV/AIDS
increased from 0·30 million in 1990 to 1·5 million in 2010, reaching a peak of
1·7 million in 2006. Malaria mortality also rose by an estimated 19·9% since 1990
to 1·17 million deaths in 2010. Tuberculosis killed 1·2 million people in 2010.
Deaths from non-communicable diseases rose by just under 8 million between 1990
and 2010, accounting for two of every three deaths (34·5 million) worldwide by
2010. 8 million people died from cancer in 2010, 38% more than two decades ago;
of these, 1·5 million (19%) were from trachea, bronchus, and lung cancer.
Ischaemic heart disease and stroke collectively killed 12·9 million people in
2010, or one in four deaths worldwide, compared with one in five in 1990; 1·3
million deaths were due to diabetes, twice as many as in 1990. The fraction of
global deaths due to injuries (5·1 million deaths) was marginally higher in 2010 
(9·6%) compared with two decades earlier (8·8%). This was driven by a 46% rise in
deaths worldwide due to road traffic accidents (1·3 million in 2010) and a rise
in deaths from falls. Ischaemic heart disease, stroke, chronic obstructive
pulmonary disease (COPD), lower respiratory infections, lung cancer, and HIV/AIDS
were the leading causes of death in 2010. Ischaemic heart disease, lower
respiratory infections, stroke, diarrhoeal disease, malaria, and HIV/AIDS were
the leading causes of years of life lost due to premature mortality (YLLs) in
2010, similar to what was estimated for 1990, except for HIV/AIDS and preterm
birth complications. YLLs from lower respiratory infections and diarrhoea
decreased by 45-54% since 1990; ischaemic heart disease and stroke YLLs increased
by 17-28%. Regional variations in leading causes of death were substantial.
Communicable, maternal, neonatal, and nutritional causes still accounted for 76% 
of premature mortality in sub-Saharan Africa in 2010. Age standardised death
rates from some key disorders rose (HIV/AIDS, Alzheimer's disease, diabetes
mellitus, and chronic kidney disease in particular), but for most diseases, death
rates fell in the past two decades; including major vascular diseases, COPD, most
forms of cancer, liver cirrhosis, and maternal disorders. For other conditions,
notably malaria, prostate cancer, and injuries, little change was noted.
INTERPRETATION: Population growth, increased average age of the world's
population, and largely decreasing age-specific, sex-specific, and cause-specific
death rates combine to drive a broad shift from communicable, maternal, neonatal,
and nutritional causes towards non-communicable diseases. Nevertheless,
communicable, maternal, neonatal, and nutritional causes remain the dominant
causes of YLLs in sub-Saharan Africa. Overlaid on this general pattern of the
epidemiological transition, marked regional variation exists in many causes, such
as interpersonal violence, suicide, liver cancer, diabetes, cirrhosis, Chagas
disease, African trypanosomiasis, melanoma, and others. Regional heterogeneity
highlights the importance of sound epidemiological assessments of the causes of
death on a regular basis.
FUNDING: Bill & Melinda Gates Foundation.
 
Copyright © 2012 Elsevier Ltd. All rights reserved.
 
PMID: 23245604  [PubMed - indexed for MEDLINE]

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A very important caveat here. Dean, you've read this as if they were reporting the impact of these various things on an individual's relative risk of lost Disability-Adjusted Life Years. But that isn't what they're reporting on: they're reporting on the percent of global deaths attributable to these things (or what is called the population-attributable fraction, globally): that is, how much they in aggregate are responsible for such loss across the entire global population.

 

To illustrate the difference: recent cocaine use increase's an individual's acute risk of heart attack by 2370%. Yowsa! As an individual, you should not snort coke!

 

You will also be at greater acute risk of a heart attack if your city has a lot of particulate matter in the air, but the effect on your risk is much less than that of recent cocaine use: the difference of 30 μg/m³ in particulate matter is just 5%.

 

The message to you is to be much more scrupulous not to hang out with the Notorious BIG than to spend an afternoon in Los Angeles smog.

 

However, very, very few people around the world are using cocaine at any given moment, whereas many people are exposed to air pollution. So even though the increased risk to the individual of air pollution is tiny, the population attributable fraction (prevalence x risk) is reversed: 4.76% of all deaths from MI can be attributed to that level of excess air pollution, vs. just 0.90% to cocaine use.

 

So the message to public health authorities is to pay a lot more attention to cleaning up excess air pollution than stamping out cocaine, at least from the perspective of avoiding heart attacks across the population.

 

I haven't looked at the full text to see if they break this down, but the point here is that the effect of fruit is the product of both how great the effect on an individual's risk is, and how common it is to be exposed to it – and we all know that many people don't meet the guidelines for fruit intake.

 

Reference

1: Nawrot TS, Perez L, Künzli N, Munters E, Nemery B. Public health importance of triggers of myocardial infarction: a comparative risk assessment. Lancet. 2011 Feb 26;377(9767):732-40. doi: 10.1016/S0140-6736(10)62296-9. PubMed PMID: 21353301.

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Michael,

 

...the point here is that the effect of fruit is the product of both how great the effect on an individual's risk is, and how common it is to be exposed to it – and we all know that many people don't meet the guidelines for fruit intake.

 

Fair point Michael. But do you think the diet of most people worldwide meets the dietary guidelines for vegetable intake, and that's why vegetables don't show up on the list? That doesn't seem very plausible. But I admit I'm not an expert on diets around the world so I could be woefully mistaken.

 

--Dean

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Well, you've got the full text ;) . But No, I doubt very much that many people globally meet vegetable intake either: indeed, while I'm not sure that we can extrapolate, certainly average Americans come closer to meeting the ftuit than the vegetable guidelne. I'm just saying that one mustn't equate the two (individual risk and PAF).

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 Hi Dean!

 

Sorry that I angered you.

 

A couple of details:  A lot of CRONnies use neotame; you can find a lot of posts on the subject in the Archives of the mailing list.

 

Also, I don't eat vegetables with neotame; my point was that there would be less damage done by this than by eating a very sweet fruit.

 

Also, many of my favorite vegetables are actually fruits (such as red, yellow and orange bell peppers),

 

Also, I do eat other fruits -- but I eat more vegetables.

 

It is certainly true that most fruits have goodies of their own. 

 

  --  Saul

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Saul wrote:

Sorry that I angered you.

 

Saul you ignorant slut.

 

You certainly did (and do) make me angry. My blood is boiling I'm so angry. And to make matters worse, you've been doing it for years. That was the last straw. I'm tired of your shenanigans and I'm done flogging you with words. If only I could engineer a way to reach through these damn intertubes to strangle you, I would. But wait, I know where you live - upstate NY. So perhaps instead, like a Ninja  :ph34r:, I'll quietly slip into your room at night and strangle you in your sleep, either while you're at home, or at that sissy Yoga Retreat you like so much.  

 

And after I get done with you, I'm gonna go after the new guy - that "Dr. Bennett" character. What kind of doctor does he think he is!? And what's with that beard anyway? Does he think he's Gandalf? And most of all, who does he think he is, eating animals. He's gonna get it worse than you for that. When I get ahold of him I'm gonna put him in a full Nelson! Then he'll feel my full wrath!!  :angry:

 

After I get done with the two of you, I'm goin' after my arch nemesis, Michael. Don't even ask what I'm gonna do to him!!!

 

Oh you think I'm kidding!? I pity the fool who thinks I'm kidding.  

 

--Dean

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^^^ actually this uncomfortable moment -- "quietly slip into your room at night and strangle..." -- sounds like that durian rider creep who eats like thousands of bananas and is himself an example of why to avoid fruit if eating fruit leads to...

 

Eat fruit if it doesn't send your own precious indie blood sugar crazy high rather than eat fruit because it's healthy for other people. I guess this is the message on loan from Michael? Cocaine? Air pollution?

Edited by Sthira

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