Fructose-induced Inflammation And Increased Cortisol: A New Mechanism For How Sugar Induces Visceral

[Lokzo]

Fructose-induced inflammation and increased cortisol: A new mechanism for how sugar induces visceral adiposity. - PubMed - NCBI

 

[Fractality]

Do you have the full study? Relying on abstracts/titles can be misleading.

 

[Suikerbuik]

Regarding cortisol, skimming the article, this seems to be their evidence:

"Overall, the HPA-axis as well as 11β-HSD-1 is activated by an increasing amount of cytokines due to excess consumption of fructose, causing secretion of glucocorticoids to combat inflammation.[64,65]"

"H6PD preserves the oxo-reductase activity by generating NADPH, suggesting the importance of co-factor availability which can dictate the direction of activity of 11β-HSD-1.[82]"

So check out reference 64, 65 and 82.

(Albeit a very suggestive study)

 

[LeeLemonoil]

A study from 2013 concludes similar things

Fructose is a cortisol booster

 

[Animalinstinct]

Who consumes isolated fructose? Other than the poor lab rats.

 

[LeeLemonoil]

Context matters, hormesis exists. Fructose per se ain’t bad or good.


Suppversity has a lot of well-written articles about fructose, always analyzing corresponding studies. It’s a worthwhile blog

 

[rei]

Fructose is a toxin that can be milked for energy, much like alcohol. Both are metabolized very similarly, in sharp contrast to glucose. So i would expect them to have similar dynamics, moderate amounts being beneficial while too much is quickly detrimental, especially if the liver is under stress due to PUFA.

 

[Hans]

The study mentions that the fructose from fruits is not a problem, but only from industrial food products.

They also said that fructose increases 11bHSD1 by increase NADPH, but fructose and glucose produces the same amount of NADPH.
11bHSD2 requires NAD, and fructose increases the NAD to NADH ratio.

I also found this meta-analysis from 2018: Effect of Dietary Sugar Intake on Biomarkers of Subclinical Inflammation: A Systematic Review and Meta-Analysis of Intervention Studies

"Pooled effects of the different interventions (investigated as mean differences) revealed that fructose intervention groups showed no significant differences in (hs)CRP when compared to glucose control groups."

"The fact that there was often no difference observed between intervention and control groups in studies that administered supra-physiological doses [32,36,37,38,43] may be due to post-prandial stress, that activates low-grade inflammation due to extremely high energy intake."

"Fructose has a low glycemic index (GI), and there is evidence that suggests that consumption of foods with a lower dietary GL/GI is associated with anti-inflammatory effects. Accordingly, ingestion of fructose may contribute to a reduction of chronic inflammation, due to the avoidance of glycemic spikes"

"Two studies included in this review observed that weight loss resulting from energy-restricted diets was associated with greater improvements in inflammatory markers (regardless of fructose-intake amounts)"

Inflammation from fructose is due to overfeeding studies.

And this cortisol boosting effect is definitely not unique to fructose overfeeding (high fructose intake is not the problem, but caloric excess), but also to endotoxins, PUFAs, alcohol, etc.
And I think that fructose is less inflammatory than the other mentioned ones.

 

[General Orange]

 

[stargazer1111]

Fructose-induced inflammation and increased cortisol: A new mechanism for how sugar induces visceral adiposity. - PubMed - NCBI

Excessive Sugar Consumption May Be a Difficult Habit to Break: A View From the Brain and Body. - PubMed - NCBI

This study directly contradicts that review. The sample size is small, but it demonstrates what *might* actually be occurring in practice rather than mechanistic theory.

My n=1 is that sugar is a major stress buster. My waist size hasn't shrunk but it also hasn't expanded on a high-sugar diet either.

 

[LucH]

As already said, fruit fructose does not make any problem if ... Only the dose makes it poisonous.
Jason Fung says, in his book "Code Diabetes":
*) Fructose and insulin resistance
A 2009 study confirmed that fructose can easily induce insulin resistance in healthy volunteers. (10) They consumed 25% of their daily calories as a sweetened Kool-Aid (drink) with glucose or fructose. Although this quantity seems huge, many people consume such a proportion of sugar in their diet. The fructose-fed group - not the one fed with glucose - has seen its insulin resistance increase to such an extent that these volunteers were clinically able to be classified as pre-diabetic after only eight weeks of overconsumption of fructose.

It is astonishing to note that it only takes one week of an excess of fructose to cause insulin resistance. And it only takes eight weeks to allow prediabetes to carve out a place. So what happens after decades of high fructose consumption? The result is the disaster of diabetes, precisely the one we know right now.

Take Figure 8.3, underneath: When the consumption of cereals and fructose began to increase in the late 1970s, the result was the beginning of the epidemic of obesity and type 2 diabetes. Sugar is more fattening than any other refined carbs and leads precisely to type 2 diabetes. The prevalence of diabetes rises by 1.1% for each surplus of 150 daily calories of sugar per person. (15) Each additional serving of 355 milliliters (12 ounces) of a soft drink increases the risk of diabetes by 25% and the risk of metabolic syndrome by 20%. (16) No other food group, neither lipids nor proteins, demonstrates such a significant link with diabetes.

Diabetes is strongly correlated with sugar, not with other sources of calories. The overconsumption of fructose directly stimulates the fatty liver and leads directly to insulin resistance. The consumption of high fructose corn syrup, chemically similar to table sugar, has the same high correlation with diabetes. (17)

Figure 8.3 Whole Grain Carbohydrate Substitution by SGHF in the United States (corn syrup) (18)


For Dr. Robert Lustig, “the dose is poisonous”. Why?
- Only the liver is able to metabolize fructose effectively.
- If you exceed the storage capacity of the liver, or if you do not practice alternating glycolysis / lipolysis (with intermittent fasting or 16.8), you will stimulate de novo lipogenesis (LPN). Fructose has no alternative route of elimination. The body can only handle small amounts of fructose. If you saturate the liver, a defense mechanism will then be put in place to avoid accentuating the visceral fat: Transfer of storage to the muscles, then to the pancreas, then at the end of the race to the liver. Hepatotoxicity that will lead to type 2 diabetes (progressive insensitivity to insulin).

*) The dose make the poison.
Editor's note: It is generally accepted that 25 to 50 gr of fructose are a maximum tolerable, at least half of which must come from fruits and vegetables. But if you ingest more calories than you spend, such as 2-thirds of people, it would be better to limit to 25 grams, especially if your BMI is above 23 and your waist is more than half your size. (Waist up to 90 if you measure 1m80).

Sources and references from Jason Fung's book Obesity Code.
1. Lustig, R. «Sugar: the bitter truth». Vidéo 90’

Robert H. Lustig M.D., M. S. L., professor of pediatrics, Division of Endocrinology, University of California, San Francisco.

10. Stanhope KL, et coll. «Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans». Journal of Clinical Investigation, 2009; 119(5): 1322-1334.

15. Basu S, et coll. «The relationship of sugar to population-level diabetes prevalence: an econometric analysis of repeated cross-sectional data». PLoS One, 2013; 8(2): e57873. doi: 10.1371/journal.pone.0057873.

16. Malik VS, et coll. «Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes». Diabetes Care, 2010; 33(11): 2477-2483.

17. Goran MI, et coll. «High fructose corn syrup and diabetes prevalence: A global perspective». Global Public Health, 2013; 8(1): 55-64.

18. Gross LS, et coll. «Increased consumption of carbohydrates and the epidemic of type 2 diabetes in the United States: an ecologic assessment». American Journal of Clinical Nutrition, mai 2004; 79(5): 774-779. .

 

[stargazer1111]

This stuff has largely been debunked.

Check out Alan Argon's debate with Lustig online. He wipes the floor with him.

Actually, and I have shown this in other threads before, sugar does NOT correlate at all with diabetes risk if you expand your time frame back to 1909. Sugar intake increased dramatically at around 1930 and leveled off. The only macronutrient that increased between 1909 and 1999 was polyunsaturated fat, particularly omega-6 from soybean oil and canola oil (corn oil as well).

Additionally, Lustig has a fundamental misunderstanding of the biochemistry of fructose metabolism. He claims fructose is "alcohol without the buzz." This is patently false. The only similarity between fructose and alcohol is that they are both primarily metabolized by the liver. This is where the similarities end. Alcohol is oxidized to acetaldehyde which is markedly toxic and eventually acetic acid by the alcohol dehydrogenases. Fructose is mostly either converted into glucose or directly oxidized. A small percentage ends up as uric acid which could be a potential problem if one is deficient in vitamin C. A very small percentage, on the order of 3-4 percent, becomes triglycerides.

Randle et al. discovered the competition between fat and glucose in the early 1960's which shows a marked increase in insulin resistance depending on fat intake. The more fat a person consumes, the harder it is to get glucose into cells and hence the more insulin required to get the job done.

Fat is the problem. Not sugar.

Citation number 10 is a study that relied on outpatient data which is tenuous at best. Also, they gave them glucose-sweetened and fructose-sweetened drinks. This does not reflect natural fructose consumption as fructose is always packaged with glucose. Not always at a 50/50 ratio, but there is always glucose packaged with fructose. Fructose requires glucose to be absorbed in the intestine so feeding people pure fructose will likely lead to bacterial fermentation and issues with endotoxin in the gut. This confounds the results of their study.

Citation 15 is epidemiology. This is good for generating hypotheses but not good for determining causality because it's very difficult to control for confounders.

Citation 16 is a meta-analysis. Meta-analyses are usually quite flawed because there is usually some level of bias in how they choose to include or exclude studies.

Many of the mechanistic/experimental studies show fructose to be harmless at physiological doses (generally doses up to 100 grams per day).

As already said, fruit fructose does not make any problem if ... Only the dose makes it poisonous.
Jason Fung says, in his book "Code Diabetes":
*) Fructose and insulin resistance
A 2009 study confirmed that fructose can easily induce insulin resistance in healthy volunteers. (10) They consumed 25% of their daily calories as a sweetened Kool-Aid (drink) with glucose or fructose. Although this quantity seems huge, many people consume such a proportion of sugar in their diet. The fructose-fed group - not the one fed with glucose - has seen its insulin resistance increase to such an extent that these volunteers were clinically able to be classified as pre-diabetic after only eight weeks of overconsumption of fructose.

It is astonishing to note that it only takes one week of an excess of fructose to cause insulin resistance. And it only takes eight weeks to allow prediabetes to carve out a place. So what happens after decades of high fructose consumption? The result is the disaster of diabetes, precisely the one we know right now.

Take Figure 8.3, underneath: When the consumption of cereals and fructose began to increase in the late 1970s, the result was the beginning of the epidemic of obesity and type 2 diabetes. Sugar is more fattening than any other refined carbs and leads precisely to type 2 diabetes. The prevalence of diabetes rises by 1.1% for each surplus of 150 daily calories of sugar per person. (15) Each additional serving of 355 milliliters (12 ounces) of a soft drink increases the risk of diabetes by 25% and the risk of metabolic syndrome by 20%. (16) No other food group, neither lipids nor proteins, demonstrates such a significant link with diabetes.

Diabetes is strongly correlated with sugar, not with other sources of calories. The overconsumption of fructose directly stimulates the fatty liver and leads directly to insulin resistance. The consumption of high fructose corn syrup, chemically similar to table sugar, has the same high correlation with diabetes. (17)

Figure 8.3 Whole Grain Carbohydrate Substitution by SGHF in the United States (corn syrup) (18)

View attachment 15063
For Dr. Robert Lustig, “the dose is poisonous”. Why?
- Only the liver is able to metabolize fructose effectively.
- If you exceed the storage capacity of the liver, or if you do not practice alternating glycolysis / lipolysis (with intermittent fasting or 16.8), you will stimulate de novo lipogenesis (LPN). Fructose has no alternative route of elimination. The body can only handle small amounts of fructose. If you saturate the liver, a defense mechanism will then be put in place to avoid accentuating the visceral fat: Transfer of storage to the muscles, then to the pancreas, then at the end of the race to the liver. Hepatotoxicity that will lead to type 2 diabetes (progressive insensitivity to insulin).

*) The dose make the poison.
Editor's note: It is generally accepted that 25 to 50 gr of fructose are a maximum tolerable, at least half of which must come from fruits and vegetables. But if you ingest more calories than you spend, such as 2-thirds of people, it would be better to limit to 25 grams, especially if your BMI is above 23 and your waist is more than half your size. (Waist up to 90 if you measure 1m80).

Sources and references from Jason Fung's book Obesity Code.
1. Lustig, R. «Sugar: the bitter truth». Vidéo 90’

Robert H. Lustig M.D., M. S. L., professor of pediatrics, Division of Endocrinology, University of California, San Francisco.

10. Stanhope KL, et coll. «Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans». Journal of Clinical Investigation, 2009; 119(5): 1322-1334.

15. Basu S, et coll. «The relationship of sugar to population-level diabetes prevalence: an econometric analysis of repeated cross-sectional data». PLoS One, 2013; 8(2): e57873. doi: 10.1371/journal.pone.0057873.

16. Malik VS, et coll. «Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes». Diabetes Care, 2010; 33(11): 2477-2483.

17. Goran MI, et coll. «High fructose corn syrup and diabetes prevalence: A global perspective». Global Public Health, 2013; 8(1): 55-64.

18. Gross LS, et coll. «Increased consumption of carbohydrates and the epidemic of type 2 diabetes in the United States: an ecologic assessment». American Journal of Clinical Nutrition, mai 2004; 79(5): 774-779. .

 

[stargazer1111]

Here is one example. Fructose, in an isocaloric context, does not appear to damage the liver.