- This topic has 27 replies, 6 voices, and was last updated 8 years, 10 months ago by
.
-
Posts
-
I wanted to submit a post about fructose malabsorption because it is something few on here have talked about, but was important for me to figure out. Long-story-short, my digestion has sucked for a long time (though it is slowly improving), and I find too much starch bothers me, but too much fruit/honey alone gives me heartburn from niflheim and a stiff neck.
So, I looked into fructose malabsorption–which has a lot of misinformation out there–and found a couple studies including this one below:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1433856/
I have access to the whole article. I wish I could attach the pdf here.
What this study shows is that, at least for most people (and recoverees may be worse than the study members here) fructose in very high amounts is ok and DOES NOT get malabsorbed (aka DOES NOT get fermented by bad bugs that release endotoxin and make your life miserable) PROVIDED THAT consumed glucose>= fructose. Sucrose, with is 50:50 was never malabsorbed in the subjects, and glucose:fructose ratios of 50:50 or greater were always absorbed without any trace of malabsorption even at very high amounts of sugar. However, some subjects had massive hydrogen breath positives (massive malabsorption and resultant intestinal fermentation) from consuming even 5g more fructose than glucose (such as 30g fructose, 25g glucose). In these very fructose-sensitive patients, simply adding glucose to the meal abolished symptoms and resulted in negative breath tests.
So, since most fruits except bananas have slightly more fructose than glucose, I thought perhaps fructose malabsorption might be my problem. So, I experimented eating some potatoes with a whole bunch of honey and raisins (about 50g starch, plus 100g sugar from each honey and raisins, which by nutritiondata.com would be about 105-110g fructose and 90-95g glucose). This worked fine and I had no symptoms. Normally, eating raisins or honey on their own ruin me, but combined with starch (which breaks down to glucose) helped me absorb my free fructose.
So, since then, I bought some dextrose powder and I dissolve 10-20 grams dextrose in some water and drink it with my meals when I’m having fruit/honey on their own. And now, NO SYMPTOMS.
This makes eating higher fruit and sugar loads more doable for me and I have really enjoyed the results.
I hope someone out there can benefit from a similar approach.
This is very fascinating, thank you for sharing.
Would this mean that if fructose were properly absorbed by consuming sufficient glucose, then there would be none of the bad effects as mentioned by Dr. Robert Lustig?
Based on my readings, I think it is overwhelmingly clear that the rise in triglycerides, the increased visceral adiposity (and concomitant insulin resistance and hypertension), and whatever other ill effects fructose has on humans is the result of malabsorption and selective fermentation by ‘bad bugs’ which produce various toxins (such as endotoxin) which we then absorb. Foods with digestive inhibitors, such as legumes and certain grains, may lead to a similar rise in endotoxin due to their inhibiting of the digestion of our foods.
My understanding with foods (or at least with carbs/protein/fat/alcohol/fibers/synthetic sweeteners/etc.) is that fermentation by bacteria WILL HAPPEN when we malabsorb the food. The result (good or bad) depends on the selectivity of the feeding. ‘Resistant starch’ and ‘inulin’ tend to feed ‘probiotic’ bifidobacteria and increase healthful substrates like butyrate and other short chain fats. Conversely, fructose, alcohol, (and other things) if malabsorbed will selectively feed ‘bad bugs’ and increase endotoxin absorption which goes to the liver and places a massive energy burden on the liver to detox the endotoxin. If the liver is given extra energy via, for example, short chain fats like MCTs and vinegar, the systemic effects of the endotoxemia are lessened. This, I think, is one of the reasons vinegar lowers postprandial glucose in diabetics and pre-diabetics (it helps the liver cope with postprandial endotoxemia).
As an aside to this last point, I one time recommended my med school roommate take some apple cider vinegar capsules and coconut oil right before he went out drinking. He is a small Asian guy who said he normally feels ?buzzed? after one beer. Well, I challenged him to see how much he could drink by taking some ACV and MCTs. I had him take 10 ACV caps and 20g coconut oil. He said he got up to 6 beers and stopped because he thought he should, but felt nothing. I am not a drinker, but I think this is a proof of principle: supporting the liver’s energy status with short chain fats and absorbable carbs can eliminate most negative effects of malabsorbed foods. But better would be to absorb the food properly in the first place!
In any case, specific to fructose, provided it is absorbed, it’s all good. And making sure you eat enough glucose WITH the fructose will help most absorb the fructose without problem. The exact mechanism of this is not worked out, but appears to involve a ‘cotransport’ mechanism by which one molecule each of fructose and glucose are carried together.
What foods could I eat that are high in dextrose, so that I can combine them with the high fructose foods? It would be nice to not have to take a dextrose powder if I don’t have to, so are there any combinations you’d recommend? Maybe just putting some sugar on my fruit?
Sugar is 50:50 glucose:fructose so that wouldn’t help boost the glucose side of the ratio. Lactose however is glucose and galactose so as far as this is concerned a glass of milk ought to boost your glucose:fructose ratio easily. Huh, maybe just found yet another reason why both my husband and I just can’t seem to get enough milk.
elfman5150, like ErinElizabeth said, cane sugar or ‘sugar’ or ‘sucrose’ is one part glucose and one part fructose. Based on the studies I’ve seen, most people handle this just fine ALONE. However, it will not help you absorb an excess of fructose from fruit/honey. ‘Dextrose’ is just free glucose made in a lab by enzymatically breaking down starch.
Unfortunately, very few foods contain free glucose, and the reason is that everything (bacteria, fungus, animals, etc.) can all easily eat free glucose, so storing free glucose would be suicide. (Besides that, free glucose attracts water moreso than sucrose or starch, so it is more wasteful of space to have free glucose). Ripe bananas are about as good as it gets, with about 1/3 fructose, the rest glucose or starch (depending on ripeness). If you can’t buy dextrose (I use NOW Foods dextrose powder), you could try eating some starch with your fruit. Or, you could try rice syrup, which is rice starch broken down via enzymes to shorter ‘oligosaccharides’ of glucose chains (not straight glucose, but easier to digest than long starch). I eat rice syrup like I do honey, by just taking a big spoonful. Essentially all the carbs in rice syrup metabolize to glucose, so it should help balance fruit nicely.
ErinElizabeth, yeah that’s interesting what you say about milk. Galactose absorbs just dandy in most people on its own, so the cleaved glucose from lactose would assist in fructose absorption from fruit/honey.
However, I suspect many people who are fructose malabsorbers as a result of unhealth (few are genetic malabsorbers) will also be lactose intolerant, since the same hypothyroid, intestinal overgrowth, high stress situation that results in low fructose transporters (low glut5) will result in low lactase activity. In this case, the milk won’t help. But, hey, if it works for you stick with it!
Thanks to both of you for your knowledgeable responses. I do love to drink whole milk with food, especially salty foods like PB&J and pizza, so maybe I’ll just drink some whole milk when I’m eating high fructose foods. I might not have a fructose malabsorption problem, but it never hurts to drink some whole milk.
Celticphoenix, are/were you a biology student? You seem to know a lot about this stuff. It really fascinates me as well, and will be useful since I am a pre-med student right now.
Thanks again.elfman5150,
Definitely drink milk if it agrees with you! It tastes delish and is high in many valuable nutrients. Unfortunately, it does not agree with everyone, for one reason or another.I was a biochem major, which really helped give me the background to better do my own research and understand scientific literature on my own. No class I ever took (undergrad or med school) taught me anything particularly practical, but I can’t say that is was completely unhelpful. I think the hardest thing, and the thing to be most careful about, is to be critical with the textbook stuff taught in schools, on encyclopedias, and disseminated through ‘popular’ culture/doctors/television. I may be wrong, but I have come through my own investigation to disagree with the vast majority of stuff considered ‘fact’ by the authorities. I think that’s the same for Matt Stone and others.
I do recommend that you take the premed courses that you need, but also don’t shy away from other courses that you just WANT to take. I regret not taking more history and language courses, for instance. You may never get the chance to take some of these again. So have fun!
I wish you the best of luck in your studies! We’re all students! As a look ahead, you may find as you move forward with formal education that teachers and the ‘system’ are increasingly hard on free thinkers, and that just regurgitating what the system wants is easier for you than swimming upstream all the time. Following orders would not be so bad in this case. But do please keep an open mind and, at least to yourself in your own head, be critical of what is being taught. I don’t think there is a stronger propaganda program in existence than what is fed premeds and med students in our country.
You sound a lot like me! I actually graduated from university in 2012 with my bachelor’s in philosophy, so I certainly am not afraid to think for myself, and take everything I hear/read with a grain of salt (and not only for the metabolic advantage ;)
I took a bunch of languages; French, Spanish, Latin, Greek, and have learned several on my own, though to a much lesser extent. Some of my favorite classes had nothing to do with my major; I think I enjoyed psychology the most, and that has persuaded me to consider going to med school to be a psychiatrist. I am primarily focused on psychotherapy (CBT, REBT, etc), and believe medication should be a last resort. However, I do have hope in the future of medicine and pharmacy, especially the non-conventional treatments such as Ketamine for instance. I think my true passion in life is to get others to feel good about themselves. Our society is a breeding ground for self-doubt and lack of confidence, and I want to remedy that. And heck, psychology/psychiatry can be quite philosophical, so I can take advantage of my undergrad degree. No education is meaningless.
Looking forward to your new, informative posts.
ChrisThanks, Chris. It’s a pleasure meeting you here online! I wish I had the aptitude for languages like you! I took a couple years of Latin, one semester Old Norse, and I learned Old English on my own. My preferences for ancient languages meshes with my preference for ancient/medieval history. But modern languages require faster processing speed, and mouth/tongue ‘dexterity’, and I find that very difficult for me.
I don’t know much formally about psychology, but it sure is an important field. However, in medicine, psychiatry is rarely respected among ‘normal’ doctors. (Most doctors (most people) are highly biased.) I always found psychiatrists to be the most agreeable to me, and surgeons the least.
Ave atque vale!
-JI always wanted to learn Old English, but never got around to it with the exception of attempting to read Beowulf in its original. One of the ‘nerdiest’ languages I learned was Elvish (Quenya to be exact), and I occasionally browse through my resources on that; my current studies are preventing me from spending too much time on it though – which is probably not a bad thing.
Anyway, I do agree with what you said about pyshciatrists and surgeons. On the one hand, IN GENERAL psychiatrists tend to be more personable, while surgery seems so removed from the individual. Of course, in the medical field it is apparently ‘best’ to not become too invested in the patient, or so I’m told, but that just isn’t my natural inclination. I’d rather try to get to know my patients as well as I can, because that sort of relationship seems most meaningful and therapeutic, in my opinion.
Just realized this is the “Fructose Mal-absorption” thread. So to be relevant somewhat, I LOVE BLUEBERRIES.
If you ever find some cool information, feel free to email the articles to me:
rowleyca@dukes.jmu.edu
“Ad Astra Per Aspera”“In any case, specific to fructose, provided it is absorbed, it’s all good.”
Okay, late to the game here, but from what I’ve read lately, fructose is what causes metabolic syndrome/pre-diabetes (not glucose), plus all sorts of inflammation, and issues with collage breakdown, not to mention it binds to tryptophan, which then can cause anxiety/depression issues.
CelticPhoenix — if you find this thread again — I’d love to hear your thoughts on this.
Hey DannyJ,
I haven’t been on the site for a while, but I do get emails from continued activity, so I’m happy to respond.
There are certainly a lot of studies on fructose and its problems–not to mention the public media’s banter.
Let me post some links to several studies and then comment a bit at the end. Some of these articles have free access to the whole article. I have full access to everything I post here, unless I state otherwise. I wish I could just attach a pdf, but a web link will have to do. Some really appreciate the primary scientific references, while it burdens others. But I think it’s good to include them whenever possible.
Many of the immediately deleterious effects commonly associated with fructose are abolished if given with an antibiotic, implying that it is fructose fermentation after mal-absorption resulting in endotoxemia is causing these problems (I do not have full access to the first here):
http://www.ncbi.nlm.nih.gov/pubmed/18395289
Endotoxemia induced any number of other ways has similarly negative effects typically associated with fructose; this endotoxemia can be induced fundamentally by screwing the gut flora with high protein diets (leading to protein ‘putrefaction’, which is just fermentation but of protein instead of carbs), digestion inhibitors such as wheat that lead to increased protein putrefaction, and even high fat diets which increases absorption of the fat-soluble endotoxin once made in the intestinal lumen:
http://www.ncbi.nlm.nih.gov/pubmed/17991637
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3526354/
http://www.ncbi.nlm.nih.gov/pubmed/17456850
And here are a couple blog posts along these lines (the author of this blog has some perspectives I don’t fully agree with, but it has some good info, I think):
http://humanfoodproject.com/sorry-low-carbers-your-microbiome-is-just-not-that-into-you/
http://humanfoodproject.com/can-a-high-fat-paleo-diet-cause-obesity-and-diabetes/
Fructose is mal-absorbed by most unless taking simultaneously with equal parts glucose (or starch glucose), as measured by hydrogen and methane breath test:
http://www.ncbi.nlm.nih.gov/pubmed/8213606
http://www.ncbi.nlm.nih.gov/pubmed/21793722
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1433856/
Certain ‘good’ prebiotic fibers, such as inulin, seem to induce a favorable shift in the gut flora (up to a point), which can temper the negative effects of substrates that fuel pathogenic strains:
http://www.ncbi.nlm.nih.gov/pubmed/24332524
http://www.ncbi.nlm.nih.gov/pubmed/24059649
http://www.ncbi.nlm.nih.gov/pubmed/12088526
Now, there have been some studies where inulin has reversed the endotoxemia-induced obesity in mice:
http://www.nutritionandmetabolism.com/content/9/1/60
http://www.nature.com/ismej/journal/v8/n10/full/ismej201445a.html
But, rats really can’t digest fat well and the fat mal-absorption leads to a deficiency of certain minerals; inulin increases colon fermentation and cecal mineral absorption, which may counter-balance the decrease in mineral absorption from the mal-absorbed fat (indicating that the reverse in health of inulin-fed rats/mice may be more to do with alleviating a nutrient deficiency than correcting gut flora directly):
http://www.ncbi.nlm.nih.gov/pubmed/15340751
http://www.ncbi.nlm.nih.gov/pubmed/16365069
http://www.ncbi.nlm.nih.gov/pubmed/1941180
Once nutrient, in particular, that I think deserves a lot of attention is copper. Copper deficiency is induced in rats and mice on a high fat and/or high sugar/fructose diet; and copper supplementation counters ALL of the effects of a high sugar, high fat diet, including obesity and metabolic syndrome and heart dysfunction:
http://www.ncbi.nlm.nih.gov/pubmed/23512597
http://www.ncbi.nlm.nih.gov/pubmed/6695829
http://www.ncbi.nlm.nih.gov/pubmed/17495201
http://www.ncbi.nlm.nih.gov/pubmed/21781943
http://ajcn.nutrition.org/content/76/5/911.full
http://ajcn.nutrition.org/content/61/1/105.full.pdf
On its own, copper deficiency causes massively increased lipogenesis and cholesterol synthesis, which would result (practically speaking) in increased triglycerides, LDL-c, and fatty liver. (I don’t have full access to the third article below). Presumably acetyl CoA substrates would worsen this, meaning that diets high in fat or fructose would worsen these effects, but not glucose or protein or starch. That being said, simply avoiding sugar and fat but not actually correcting the copper deficiency is trouble. So, I would say to keep eating fruit and fats as desired, but get copper status up if this were a problem.
http://www.ncbi.nlm.nih.gov/pubmed/11110846
http://www.ncbi.nlm.nih.gov/pubmed/1563598
http://www.ncbi.nlm.nih.gov/pubmed/1559618
Now, in humans, since we typically digest fat better than mice and rats, copper is not obliterated by high fat, and inulin doesn’t boost our mineral absorption to such a great extent. Since inulin DOES improve our bifido numbers, but does not seem to help our metabolic syndrome to as great an extent as in mice/rats, I think it is safe to assume that it may NOT be the gut flora as much as nutrient status (copper status) that is leading to obesity and the metabolic syndrome. In humans, at least in a couple case studies, copper deficiency has been induced by a high intake of fructose-containing diets, indicating that fructose (not fat) definitely does play a negative role for copper status. The question I can’t answer for right now is whether it is fructose mal-absorption or fructose as is (even in sucrose) that is increasing copper requirements.
http://gut.bmj.com/content/62/8/1112.full.pdf+html
http://onlinelibrary.wiley.com/doi/10.1002/ajh.20647/pdf
http://www.ncbi.nlm.nih.gov/pubmed/17298707
http://www.ncbi.nlm.nih.gov/pubmed/16365069
I haven’t seen anything about fructose and collagen as in your question; but considering that copper is essential for collagen and elastin formation, anecdotal reports of fructose harming collagen may in fact be observations of fructose detrimental effect on copper status, in which case simply adding several milligrams of copper as a supplement per day should correct this. Since copper status has already been obliterated in our food system over the past 100 years, I would recommend this anyway.
http://www.emeraldinsight.com/doi/abs/10.1108/00070709710181540
http://hortsci.ashspublications.org/content/44/1/15.full
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2137915/pdf/jem2040657.pdf
http://www.ncbi.nlm.nih.gov/pubmed/8613882
http://www.ncbi.nlm.nih.gov/pubmed/6125118
(this last link shows copper deficiency induces collagen hyperproliferation due to a lack of lysyl oxidase ability, resulting in emphysema in lungs, but presumably would causes similar derangements in other tissues; in skin collagen hyperproliferation is called ‘scars’ and when the collagen is laid perpendicular to the epidermis called ‘hypotrophic scars’, such as with acne scars.)
As for tryptophan and fructose, I haven’t seen anything on that specifically, either. However, tryptophan is converted to many of the necessary amines via tryptophan hydroxylase which is a copper/iron enzyme (copper is needed for iron transport, and copper deficiency induces a brain iron deficiency, which could effect this). But copper is also needed to break down neurotransmitters histamine (diamine oxidase, aka histiminase). In fact, catecholamines, tryptophan metabolites, and histamine use many of the same enzymes for catabolism, so high dose Trp, for instance, can induce excessive blood histamine and eosinophilic myalgia. Methylation (which I often think is overrated in blogs and popular websites, and about which there is more misinformation than most topics in health, I think) can be hurt via copper deficiency, since copper is needed in one way or another for COMT and Methionine Synthase. These methylation pathways are important for many things, including amine degradation. However, since copper deficiency also leads to increased transulfuration (pulling methionine down towards glutathione and cysteine, and away from methylation, presumably because they body needs the extra antioxidant power of glutathione while copper is out), it may be that increasing methylation supplements like choline, betaine, or methyl b12 and folate would do more harm than good, as they would try to pull methionine back towards methylation and away from glutathione; I don’t know about this, but I would think copper deficiency is creating a bigger need for methionine and glycine (and perhaps a little b6), and these should be supplemented over the methyl donors per se. And copper is clearly needed for niacin synthesis from Trp, so anyone who thinks they may be deficient in copper should consider supplementing niacinamide in the meantime (maybe 50-100mg 1-3 times daily), while they also supplement copper of course.
http://www.ebi.ac.uk/interpro/entry/IPR018301
http://www.ncbi.nlm.nih.gov/pubmed/15836628
http://www.ncbi.nlm.nih.gov/pubmed/18178529
http://www.ncbi.nlm.nih.gov/pubmed/17287146
http://www.ncbi.nlm.nih.gov/pubmed/10613762
http://www.journalofanimalscience.org/content/85/9/2198.full.pdf
http://www.ncbi.nlm.nih.gov/pubmed/11029965
http://www.ncbi.nlm.nih.gov/pubmed/16307217
http://www.ncbi.nlm.nih.gov/pubmed/17513393
http://www.scopemed.org/?jft=61&ft=61-1368828754
http://www.ncbi.nlm.nih.gov/pubmed/1563598
http://jn.nutrition.org/content/103/12/1764.full.pdf
More than likely, I have missed some key references that would make this response more thoroughly ‘a priori’. But, let me now sum things up a bit.
Fructose does clearly in both human and animal studies precipitate many metabolic disturbances, including the ones most often talked about like metabolic syndrome, fatty liver, visceral fat accumulation, and even increased blood pressure. I haven’t seen anything directly on tryptophan or collagen, per se. What studies do also show, however, is that the majority of the problems with fructose are related to the effect fructose has on gut flora and mineral absorption. In terms of postprandial (post meal) endotoxemia, simply eating fructose with equal parts glucose corrects for this, and I think that is pretty straight forward. Some white rice, oats, or even dextrose or rice syrup should all be equally effective in being able to temper fructose mal-absorption. Inulin or other prebiotics may also help temper any negative consequences of fructose (or wheat or whatever) on the gut flora; however, in humans, this effect seems to be less important than in rats with respect to metabolic syndrome and obesity, and even mineral absorption, but some individuals may find it really helps. I do not know exactly why glucose helps increase fructose absorption, but the model that has been proposed is the ‘piggy back’ model, whereby one glucose molecule helps carry fructose with it through a more readily available glucose transporter. Once absorbed, fructose WILL increase the requirement for choline, since it is a building block fro bio-synthesized triglycerides, which (like dietary fat) require extra choline for proper transport out of the liver. Glucose, whether as starch or free fructose, doesn’t do this.
So, when I originally said that simply eating more glucose with fructose is ALL ONE HAS TO DO, this was a oversimplification; I would like to amend it to say one must ensure proper absorption by eating enough glucose, but then also intake enough extra choline (and perhaps other nutrients like copper) in order to compensate for the particular pathways that fructose uses over that of glucose. This is not all bad, since different pathways require different nutrients. For instance, glucose, by increasing insulin to a greater extent, relies more on Mg, potassium, and thiamine than fructose (glucose relies on the cofactors for glycolysis to a greater extent; fructose more on the fat cofactors like choline and potentially coenzyme A from B5 and copper and cysteine).
For individuals with high triglycerides from whatever reason, I would highly recommend considering supplementation or increased intake of copper and choline (choline is high in egg yolks and liver).
Fructose, and also potentially other dietary factors (and presumably many things that are poorly digested including cellulose) may decrease absorption of certain minerals, and copper deficiency is so strongly and causally linked with fructose and high fat diets that it may just be that copper deficiency can explain many of the deleterious effects of fructose in both humans and rats. And yet, the negative consequences of fructose, at least in rats, can be corrected for with modest copper supplementation; in human,s something like 3-6mg per day I would think appropriate (copper glycinate likely better than sulfate or gluconate, in my opinion), depending on the rest of the diet. Let’s first, though, take a step back and ask the question: “is it reasonable to think that copper deficiency COULD BE responsible for modern obesity and metabolic syndrome epidemics?” The answer to this, I would think, is a resounding yes. Copper status in foodstuffs has decreased 50-70% on average, and the most copper rich foods (beef liver, for instance) nobody eats anymore. On top of that, it is not just an obesity epidemic that we have. We also have a greater increase in acne scars (collagen hyperproliferation), stretch marks (weak elastin), arthritis, and whatever else that are related to copper status. Interestingly, copper peptides (copper chloride dissolved in a hydrozlyed protein carrier) are being used for spider veins, skin, scars, and stretch marks quite successfully. And since copper deficiency clearly disturbs catecholamine and amine neurotransmitters, mindful experimentation should be considered to help correct copper deficiency, whether or nor fructose was at the root of its deficiency.
Anyhoo, those are my thoughts. I’d love to know your own thoughts if you think differently on the matter. And please forgive my no-doubt ubiquitous typos.
-CP
- You must be logged in to reply to this topic.