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):
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:
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):
Fructose is mal-absorbed by most unless taking simultaneously with equal parts glucose (or starch glucose), as measured by hydrogen and methane breath test:
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:
Now, there have been some studies where inulin has reversed the endotoxemia-induced obesity in mice:
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):
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:
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.
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.
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.
(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.
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.