25 replies to this topic

[Sillewater]

Alan Aragon wrote a pretty damning post on the Lustig lecture on the dangers of fructose and argued that dosage was not considered. From my reading it seems that fructose regarding weight gain probably doesn't happen in a state of caloric deficiency. However I think many of us here are at very little risk of becoming diabetic so it might now apply to us. However what does apply (and is not usually discussed in the blogosphere [except for JLL's blog]) is the concept of glycation. If the study from 1968 is true and fructose glycates at 10x that of glucose then it is still probably more prudent to stay away from fructose.

Biochem Biophys Res Commun. 2010 Jan 7. [Epub ahead of print]
Fructated apolipoprotein A-I showed severe structural modification and loss of beneficial functions in lipid-free and lipid-bound state with acceleration of atherosclerosis and senescence.
Park KH, Jang W, Kim KY, Kim JR, Cho KH.

School of Biotechnology, Aging-associated Vascular Disease Research Center, Yeungnam University, Gyeongsan 712-749, Republic of Korea.
Non-enzymatic glycation of serum apolipoproteins is a main feature of diabetes mellitus under hyperglycemia. Advanced glycation end products are implicated in the development of aging and metabolic syndrome, including premature atherosclerosis in diabetic subjects. ApoA-I is the principal protein constituent of HDL. In this study, glycated human apoA-I (gA-I) by fructation was characterized on functional and structural correlations in lipid-free and lipid-bound states. The gA-I showed more spontaneous multimeric band formation up to pentamer and exhibited slower elution profile with more degraded fragments from fast protein liquid chromatography. The gA-I showed modified secondary structure from fluorescence and circular dichroism analysis. Reconstituted high-density lipoprotein (rHDL) containing the gA-I had less content of phospholipid with a much smaller particle size than those of rHDL-containing nA-I (nA-I-rHDL). The rHDL containing gA-I (gA-I-rHDL) consisted of less molecular number of apoA-I than nA-I-rHDL with decreased alpha-helical content. Treatment of the gA-I-rHDL induced more atherogenic process in macrophage cell and premature senescence in human dermal fibroblast cell. Conclusively, fructose-mediated apoA-I glycation resulted in severe loss of several beneficial functions of apoA-I and HDL regarding anti-senescence and anti-atherosclerosis activities due to a lack of anti-oxidant activity with increased susceptibility of protein degradation and structural modification. Copyright © 2010 Elsevier Inc. All rights reserved.

PMID: 20059975 [PubMed - as supplied by publisher]

I always thought that fructose was always packaged in lipids or converted to something else other than fructose. But that doesn't seem to be the case:

Diabetes Care. 2002 Feb;25(2):353-7.
Increased fructose concentrations in blood and urine in patients with diabetes.
Kawasaki T, Akanuma H, Yamanouchi T.

Department of Internal Medicine, Teikyo University, School of Medicine, 11-1, 2-chome Kaga, Itabashi-ku, Tokyo, Japan 173-0003. t-kawa@med.teikyo-u.ac.jp
OBJECTIVE: To investigate fructose metabolic changes in patients with diabetes. RESEARCH DESIGN AND METHODS: Serum and urinary fructose concentrations were determined in healthy subjects (n = 23) and in nondiabetic (n = 23) and diabetic patients (n = 26). Fructose was measured using our newly developed method, and (13)C(6)-fructose was used as the internal standard. After adding sample to a fixed amount of internal standard, ion-exchange resins and high-performance liquid chromatography pretreatments were performed. Then, the amount of fructose in the sample was measured by gas chromatography-mass spectrometry. RESULTS: Serum fructose concentrations in patients with diabetes (12.0 +/- 3.8 micromol/l) were significantly higher than those in healthy subjects (8.1 +/- 1.0 micromol/l, P < 0.001) and nondiabetic patients (7.7 +/- 1.6 micromol/l, P < 0.001), and daily urinary fructose excretion was significantly greater in patients with diabetes (127.8 +/- 106.7 micromol/day) than in nondiabetic patients (37.7 +/- 23.0 micromol/day, P < 0.001). In patients with diabetes (n = 20), serum fructose concentrations (8.6 +/- 1.8 micromol/l, P < 0.001) and daily urinary fructose excretion (63.4 +/- 63.8 micromol/day, P < 0.01) significantly decreased by week 2 after admission. CONCLUSIONS: The present results differed from those of previous studies in that we found that the serum and urinary fructose concentrations decreased rapidly, concomitant with an improvement in glycemia. Therefore, hyperglycemia was associated with increased serum and urinary fructose concentrations in patients with diabetes.

PMID: 11815509 [PubMed - indexed for MEDLINE]

In the meantime fructose is still something I'll try to limit within reason (such as part of my berry intake).

Edited by Sillewater, 15 February 2010 - 08:10 AM.

[kismet]

If the study from 1968 is true and fructose glycates at 10x that of glucose then it is still probably more prudent to stay away from fructose.

Sorry, but honestly, that's in vitro bullshit. One'd need much more knowledge about actual metabolism and kinetics to make such a call. Methylglyoxal, a potential intermediate of glucose (fructose) metabolism, is several thousand if not several tens of thousand times more reactive than glucose and what does it tell us? (not much w/o any knowledge about metabolism)


I think MR has quite often cited the study of long-lived rodents being fed different CHO sources. And there were hardly any effects on life or health span IIRC. In vivo & human data is what we need.

Edited by kismet, 15 February 2010 - 03:08 PM.

[Sillewater]

I think MR has quite often cited the study of long-lived rodents being fed different CHO sources. And there were hardly any effects on life or health span IIRC. In vivo & human data is what we need.

Really? Could you direct me towards some.

[niner]

If the study from 1968 is true and fructose glycates at 10x that of glucose then it is still probably more prudent to stay away from fructose.

Sorry, but honestly, that's in vitro bullshit. One'd need much more knowledge about actual metabolism and kinetics to make such a call. Methylglyoxal, a potential intermediate of glucose (fructose) metabolism, is several thousand if not several tens of thousand times more reactive than glucose and what does it tell us? (not much w/o any knowledge about metabolism)

I think MR has quite often cited the study of long-lived rodents being fed different CHO sources. And there were hardly any effects on life or health span IIRC. In vivo & human data is what we need.

Is this the paper in question? (1988, not '68)

Biochemistry. 1988 Mar 22;27(6):1901-7.
Role of fructose in glycation and cross-linking of proteins.

McPherson JD, Shilton BH, Walton DJ.

Department of Biochemistry, Queen's University, Kingston, Ontario, Canada.

Incubation of carbohydrate-free human serum albumin (HSA) with fructose in an aqueous buffer at pH 7.4 resulted in glycation of epsilon-amino groups of lysyl residues. A recently developed procedure, involving analysis of hexitol amino acids by high-performance liquid chromatography of phenylthiocarbamyl derivatives, was used to show that 85% of the bound hexose was attached to protein via carbon 2 (C-2). The remainder was attached to protein via carbon 1 (C-1). When incubations were conducted with glucose under identical conditions, all the hexose was attached via C-1. Examination of human ocular lens proteins showed that the majority of the covalently bound hexose was connected to epsilon-amino groups of lysyl residues via C-1; this was attributed mainly to nonenzymatic glucosylation in vivo, which has already been documented. A significant proportion (10-20%) of the bound hexose was connected via C-2. In view of the HSA-hexose incubation results (above), this indicated that the lens proteins had reacted with endogenous fructose; i.e., they had undergone nonenzymatic fructosylation in vivo. The model protein bovine pancreatic ribonuclease A reacted with fructose and glucose at similar rates under physiological conditions. However, covalent, non-disulfide cross-linking, which could be inhibited by D-penicillamine, was induced 10 times more rapidly by fructose than by glucose. It is postulated that some of the protein cross-linking that occurs in vivo is fructose-induced. The possible significance of these processes in diabetic subjects is discussed.

PMID: 3132203

I can't just dismiss this as the usual "in vitro bullshit", because fructose is a macronutrient. The usual bioavailability concerns don't apply here; we know it gets in. We can still question whether or not the concentration of fructose is as high as, or even in the ballpark of that of glucose. I'm sure that's known, but not by me at this moment. However, if we consume a large dose of fructose, it's a pretty good bet that we will soon be looking at a significant plasma fructose concentration. When the crosslinking potential is an order of magnitude higher than glucose under equivalent conditions in vitro, I have to take some notice. Everything I've seen about fructose so far tells me that eliminating refined forms of it (cane sugar, corn syrup, etc) from my diet is a good move. I still eat berries on a daily basis, eat larger fruits in moderation, and try to stay away from fruit juices. At worst I'm denying myself the pleasure of wolfing down a bunch of sugar, and more likely I'm avoiding some significant damage to my organism. This seems like a prudent bet, imho.

[Sillewater]

Great reply Niner, always able to put it so succintly. Awesome. I totally agree with that.

[s123]

If the study from 1968 is true and fructose glycates at 10x that of glucose then it is still probably more prudent to stay away from fructose.

Sorry, but honestly, that's in vitro bullshit. One'd need much more knowledge about actual metabolism and kinetics to make such a call. Methylglyoxal, a potential intermediate of glucose (fructose) metabolism, is several thousand if not several tens of thousand times more reactive than glucose and what does it tell us? (not much w/o any knowledge about metabolism)

We (me and Johan) also came across this study while doing research for our glucosepane paper. Several factors have to be taken into account when comparing the glycation potential of glucose versus fructose.

(i) The aldehyde group of glucose is more reactive than the ketone group of fructose.
(ii) Only the open chain form is reactive. 0,002% of glucose is present in an open chain form compared to 0,7% for fructose.
(iii) Glucose is present in millimolar concentrations while fructose is in the micromolar range.

This makes it quite difficult to compare the glycation potential of both sugars in vivo.

Glyoxal, methylglyoxal, malondialdehyde and 4-HNE are much more reactive than sugars. The primary source of these reactive molecules is not carbohydrate metabolism but lipid peroxidation. The AGE content of high carbohydrate foods is typical low compared to high fat foods.

For example the AGE content measured as CML:

- Whole-wheat bread (center): 0,54 kU/g
- Pancake (home made): 10 kU/g
- Chicken breast, broiled for 15 min.: 58 kU/g
- Roasted almonds: 66,5 kU/g
- Cheese, American: 87 kU/g
- Butter: 265 kU/g

Source: Goldberg et al. Advanced glycoxidation end products in commonly consumed Foods. Journal of the American Dietetic Association, 2004, 104(8): 1287-1291.

Free link: http://www.newcastle...d AGEs text.pdf

Edited by s123, 16 February 2010 - 10:06 AM.

[e Volution]

Does this mean there would potentially be benefit to substituting a solid nutrition heavyweight like berries to a whole food (but fructose-free) supplement version to get all the benefits? Currently the view would be berries are a lifelong dietary inclusion so this could save a fair bit of exposure over a lifetime and my very simplistic understanding is the effect is cumulative. Or is the exposure so small that the berries and low/moderate fruit consumption that's common around here sufficient enough?

[Skötkonung]

Here is an interesting list of fructose (mg) per 200cal serving in common fruits and fruit products:
http://www.nutrition...00000000-1.html?

[niner]

We (me and Johan) also came across this study while doing research for our glucosepane paper. Several factors have to be taken into account when comparing the glycation potential of glucose versus fructose.

(i) The aldehyde group of glucose is more reactive than the ketone group of fructose.
(ii) Only the open chain form is reactive. 0,002% of glucose is present in an open chain form compared to 0,7% for fructose.
(iii) Glucose is present in millimolar concentrations while fructose is in the micromolar range.

This makes it quite difficult to compare the glycation potential of both sugars in vivo.

s123, thanks for a great post. From this and other information, we might be able to take a stab at the in vivo danger of fructose. Points (i) and (ii) would appear to net out to a factor of ten higher fructation potential than glucation, on the basis of the in vitro experiment. That only leaves the question of (iii) the concentration differences. Micromolar concentrations sound very low for a macronutrient consumed in multi-gram doses. I found this methodology paper that finds a plasma fructose level much higher in healthy human volunteers. In fact, the observed peak post-prandial fructose levels were higher by over a factor of two than typical peak post-prandial glucose levels, which might be as much as 7.8 mM, but maybe 6 mM after a healthy meal. The observed fasting fructose was a bit less than half of a typical fasting glucose level. If these numbers are correct, they point a very large and incriminating finger at fructose; perhaps even worse than I had earlier thought.

Pancreas. 2009 Aug;38(6):706-12.
Direct spectrophotometric determination of serum fructose in pancreatic cancer patients.

Hui H, Huang D, McArthur D, Nissen N, Boros LG, Heaney AP.

Division of Endocrinology, David Geffen School of Medicine at UCLA, Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA 90024, USA.

OBJECTIVES: We sought to develop an assay to measure circulating fructose concentrations in pancreatic cancer patients. METHODS: Using fructose dehydrogenase-catalyzed conversion of d-fructose to 5-ketofructose, followed by quantitation of MTT [3-(4,5-dimethylthiaze-syl)-2,5-diphenyltetrazolium bromide] formazan production by direct spectrophotometry, an assay to measure serum fructose concentration was developed, and assay sensitivity and specificity were tested. Validity of the assay was confirmed by gas chromatography-mass spectroscopy, and the assay was tested in healthy subjects and pancreatic cancer patients. RESULTS: The assay was highly specific, exhibiting no cross-reactivity with other sugars. Mean serum fructose concentration in fasting healthy volunteers was 1.9+/-0.4 mM and after ingestion of a fructose and glucose-containing drink rose to 16.3+/-1.2 mM at 15 minutes and peaked at 30 minutes when serum fructose was 17.2+/-1.1 mM. Mean fasting serum fructose level was significantly higher at 5.7+/-2.5 mM in patients with pancreatic cancer than those with no pancreatic cancer. The fructose dehydrogenase-based enzymatic assay correlated highly with gas chromatography-mass spectroscopic analysis of serum fructose with a correlation coefficient of 0.94. CONCLUSION: This spectrophotometric assay for fructose is easy to perform and well suited to determination of serum fructose. Measurement of serum fructose concentration may provide insight into the relationship between refined fructose intake and diseases including pancreatic cancer.

PMID: 19506535

[kismet]

It certainly is not "the usual" in vitro BS, but in vitro and ex vivo data is always guilty until proven innocent. 

The plasma concentrations are surprising. But what about the area under the curve? Tried to confirm it with a quick pubmed, but something's off with the data (a typo?) 

Look at:

Metabolism. 2004 May;53(5):583-8.
Postprandial plasma fructose level is associated with retinopathy in patients with type 2 diabetes.
Kawasaki T, Ogata N, Akanuma H, Sakai T, Watanabe H, Ichiyanagi K, Yamanouchi T.
"concentrations were simultaneously measured 3 times within a 24-hour period (2 hours after each meal)...The mean postprandial plasma fructose concentrations (MPPF) and the mean postprandial plasma glucose concentrations (MPPG) were calculated. Fructose was measured by gas chromatography-mass spectrometry (GCMS). Based solely on MPPF, we were able to divide the patients into three groups: the high MPPF (31.9 +/- 6.5 micromol/L) group (n = 12), the middle MPPF (21.2 +/- 1.8 micromol/L) group (n = 13), and the low MPPF (15.2 +/- 2.4 micromol/L) group [note how similar the numbers are between the studies, it's just the units. Either fructose shows *thousand fold* higher peaks than steady state/AUC levels or maybe it really is a typo in the pancreas journal I can't access] (n = 13)."
Mean plasma glucose is as expected in the milimolar range. Plus, see their ref. 16, which is the reason why I am so vehement about *actually understanding pharmakokinetics and metabolism before jumping to conclusions*:
"fructose disappears from the circulation twice as fast as glucose, with its half-life being about 18 minutes as compared with 43 minutes for glucose."

Found the post about the different dietary CHO sources (no clear evidence of an effect on life span in animal models, see ref. 4 I believe the summary to be accurate, but didn't read the paper(s)). Taken together with the epidemiology evidence in favour of fruit, including "large" fruit like apples and pears with no hint of a ceiling effect (AFAIK), it would be almost crazy to consider limiting fruits that were shown to be beneficial. Although, fruit juices and high GI/GL fruits are a different story.

Apparently there are also some awfully strange results for glucose per se, see ref. 1. The whole AGE story is pretty complicated it seems.

EDIT: repeated edits

Edited by kismet, 16 February 2010 - 08:59 PM.

[niner]

This is a puzzle. I thought I had it figured out, that it was just a bad translation from a Greek character, and whoops, there goes three orders of magnitude! But no... I went to the Pancreas website and looked at their version of the abstract, and it reads the same. They can't both be right; it's either milli- or micro-. Micromolar levels still sound low to me. Glucose levels are tightly controlled; does the body have any mechanism to control fructose concentration?

[niner]

Here's a pretty good paper. They find both plasma fructose and glucose in the mM range in rats, as per their table 1. They look at a number of significant parameters, and conclude that fructose is worse with respect to aging than either sucrose or glucose. The link is to the full text of the paper. Of course, the caveat here is that rats aren't furry little humans, though the opposite sometimes holds.

The Journal of Nutrition Vol. 128 No. 9 September 1998, pp. 1442-1449Long-Term Fructose Consumption Accelerates Glycation and Several Age-Related Variables in Male Rats

[Sillewater]

I think the one that measured micromolar concentrations of fructose didn't actually test post-prandial. Like they didn't give patients like 30g of fructose and other patients 30g of glucose. It was the fasting levels they were measuring. Most studies I've seen are in the millimol for both glucose and fructose.

[kismet]

I think the one that measured micromolar concentrations of fructose didn't actually test post-prandial. Like they didn't give patients like 30g of fructose and other patients 30g of glucose. It was the fasting levels they were measuring.

Most studies I've seen are in the millimol for both glucose and fructose.

Can you post them? I've seen other *fasting* measurements in the micromolar range by GC/MS so the data is likely accurate.
This would then suggest that fructose indeed peaks 1000 fold higher compared to steady fasting levels. (which definitely suggests never to binge on anything, esp. fructose...)

Niner, re. their methodology see the post I linked to (first few paragraphs). Their methodology may (*may*) be flawed and the results (re. longevity) definitely are at odds with some other studies.

Edited by kismet, 17 February 2010 - 06:45 PM.

[niner]

I think the one that measured micromolar concentrations of fructose didn't actually test post-prandial. Like they didn't give patients like 30g of fructose and other patients 30g of glucose. It was the fasting levels they were measuring.

Most studies I've seen are in the millimol for both glucose and fructose.

Can you post them? I've seen other *fasting* measurements in the micromolar range by GC/MS so the data is likely accurate.
This would then suggest that fructose indeed peaks 1000 fold higher compared to steady fasting levels. (which definitely suggests never to binge on anything, esp. fructose...)

Niner, re. their methodology see the post I linked to (first few paragraphs). Their methodology may (*may*) be flawed and the results (re. longevity) definitely are at odds with some other studies.

Levi & Werman's methodology? The most serious of MR's complaints are addressed by the fact that L&M also had rats consuming glucose and sucrose ad lib in water, and they didn't have the problems that the fructose-drinking rats did. I suppose rats might like the taste of fructose way more than the others. Don't we sometimes argue that it's addictive? Anyway, I can't believe that there are three orders of magnitude between these numbers in the literature. What's up with that? I have one question: How the hell can anyone assay fructose by GC? Do they first derivatize it? To get a compound through a GC, it has to vaporize. Fructose would caramelize and gunk up the column, I'd think. Wouldn't LC/MS have been more appropriate? That's a little too blatant to explain the 1000X discrepancy, though. (I hope...)

[kismet]

It sez "methyloxime peracetate derivatized aldose and ketose" (Clin Biochem. 2010 Jan;43(1-2):198-207. Epub 2009 Sep 8.) They probably didn't screw up their methodology (tho' this is a different paper reporting similar values).

The problem is that the rodent data is at odds with a better controlled, not ad lib study, showing no effects of CHO source (although, according to MR's post the one may have been flawed itself; bla, bla, etc, ...).

Skimmed a few other studies:
http://www.ajcn.org/...t/48/6/1424.pdf
After 50g of fructose postprandial fructose peaked at <1mM or 20mg/dl (more than 5 times lower than postprandial glucose?) and after 120 min decreased to 0.25mM. The peak data is still an order of magnitude lower than in the study you found.

http://www.ajcn.org/...t/50/5/1008.pdf
up to 0.25mM postprandially on a fructose diet (20% fructose calories)

"For example, plasma fructose concentrations are usually in the range of 0.1 to 0.25 mM but can rise to levels of 0.25 to 0.8 mM at 30 to 60 min after the oral administration of dosages ranging from 18 to 100 g of fructose.16,17 In other words, 1 mM serum fructose concentration can be achieved when a large amount of fructose is ingested.16 As such, a 20-oz soft drink, which contains 32.6 g of fructose, would be expected to increase serum fructose concentrations in this range. "
http://jasn.asnjourn.../full/19/9/1712

The pancreas data still looks way off.

Edited by kismet, 18 February 2010 - 12:55 AM.

[niner]

The pancreas data still looks way off.

Yes, I believe it is. I think I know what happened, too. If you change the units in the Pancreas paper to mg/dL, then the numbers make sense and match the other reports. Wow, what a F-up! I emailed the author to ask him about it, and sent him a link to Truswell et al. Truswell gives units both in mg/dL and mM in his graph of plasma fructose conc. I think we know a bit more about fructose absorption than we did a couple days ago, eh? Thanks for the papers.

[Sillewater]

Thanks Niner for that discovery. Well after all this I'm going to stay away from Fructose still.

[Sillewater]

Can you post them? I've seen other *fasting* measurements in the micromolar range by GC/MS so the data is likely accurate.
This would then suggest that fructose indeed peaks 1000 fold higher compared to steady fasting levels. (which definitely suggests never to binge on anything, esp. fructose...)

Missed this, yea at the time the millimole levels I was thinking about were <1.0mM.

On another note, has anyone read this study? I find the results odd.

J Gerontol A Biol Sci Med Sci. 1995 May;50(3):B148-54.

Source of dietary carbohydrate affects life span of Fischer 344 rats independent of caloric restriction.

Murtagh-Mark CM, Reiser KM, Harris R Jr, McDonald RB.

Edited by Sillewater, 24 December 2011 - 07:31 AM.

[Werner]

Thanks Niner for that discovery. Well after all this I'm going to stay away from Fructose still.

I eat lots of fructose (fruits) since at least ten years. If I read niners article text:

"Dietary fructose has adverse effects on certain segments of the population. The rapid hepatic fructose utilization leads to far-reaching consequences for carbohydrate, lipid and purine metabolism. Fructose elevates triglycerides, cholesterol, uric acid, urea nitrogen and carnitine in blood (Hallfrisch 1990). It also increases hepatic pyruvate and lactate production, decreases glucose tolerance, increases insulin resistance and causes a shift in balance from oxidation to esterification of nonesterified fatty acids, resulting in elevated secretion of VLDL (Mayes 1993)."

I must say that FOR ME it is not true. I have record low triglyceride and LDL cholesterol
numbers.

[1kgcoffee]

What kinds of fruits do you eat Werner?
The flavonoids in fruit, especially things like blueberries are known to have the opposite effect of fructose on triglycerides, cholesterol and LDL. If you were ingesting something like straight agave nectar or refined fruit juices, and had great numbers I would be very surprised. Fruit juicies <<<< Fruit <<<< Green smoothies

[rwac]

Source of dietary carbohydrate affects life span of Fischer 344 rats independent of caloric restriction.

http://stan-heretic....ast-cancer.html

“The results show that it’s not just overall carbohydrates, but particularly starch,” said Jennifer A. Emond, M.S., a public health doctoral student at the University of California, San Diego. “Women who increased their starch intake over one year were at a much likelier risk for recurring [breast cancer].”
Researchers conducted a subset analysis of 2,651 women who participated in the Women’s Healthy Eating and Living (WHEL) Dietary Intervention Trial, a plant-based intervention trial that enrolled about 3,088 survivors of breast cancer. WHEL researchers studied breast cancer recurrence and followed the participants for an average of seven years.

Edited by rwac, 24 December 2011 - 09:24 PM.

[Sillewater]

Ah yes, it makes a bit more sense but I would like to read the entire study. However some of CR's effect may be the lack of insulin signalling thus a starch diet would counteract that. But that really doesn't make much sense to me considering (as MR always says) its the calories that matter in the end. I just find it extremely odd that the CR lived just about the same, a little less, then AL.

[Werner]

What kinds of fruits do you eat Werner?
The flavonoids in fruit, especially things like blueberries are known to have the opposite effect of fructose on triglycerides, cholesterol and LDL. If you were ingesting something like straight agave nectar or refined fruit juices, and had great numbers I would be very surprised. Fruit juicies <<<< Fruit <<<< Green smoothies

According to the season I eat oranges, grapes, cherries, strawberries, mango,
peaches, nectarines, apples und dried fruit - no blueberries. Fruit juices only
without added sugar.
Furthermore, no meat, no bread, not much dairy.

[1kgcoffee]

Are you doing calorie restriction, or the raw food diet?

[Werner]

Are you doing calorie restriction, or the raw food diet?

No, nothing.