Monday, April 17, 2023

Fructose (02) Obesogen

I guess we could do worse than to being this post here;

It's a follow on study after an initial dog study from 1998 which demonstrated that, much like glucose, in a tightly controlled somatostatin/insulin/glucagon model, low dose fructose markedly suppresses hepatic glucose output and markedly increases glycogen formation in healthy dogs. On a fixed insulin background, low dose fructose behaves as an insulin mimetic.

This follow on study in 2002 used hormonally intact dogs instrumented for portal vein, hepatic vein, femoral vein and femoral artery access. In addition they were cannulated to allow intra-duodenal infusion of glucose or glucose + fructose. This gets rid of all of the pesky delay in gastric emptying involved in an OGTT and allows time to assess effects under steady state conditions rather than the brief and dynamic changes which occur under an OGTT. Between the first and second canine studies the group had performed a couple of sets of human OGTT studies +/- fructose with somewhat challenging results, which I suspect is what led to this latest canine study, to really control as many variables as practical.

Aside: There is a horrible typo in the plasma glucose graphs throughout the study. For glucose they clearly mean milli moles/l, not micro moles/l. Arghhh. I think the fructose at 100micromoles/l is likely to be correct. I can't face trying to confirm whether their infusion rates are correct re micro vs milli. Ugh. I think their data are fine per se, unfortunate re typos. End aside.

The intra-duodenal glucose infusion was pitched to generate a modest, stable hyperglycaemia at ~10mmol/l. In the intervention section this glucose infusion remained unchanged at 44.4μmol/kg/min but an additional infusion of fructose was added at 2.2μmol/kg/min, ie around 5% fructose in addition to the original glucose. This is what happened to the systemic plasma glucose levels:

If anyone had developed a drug to produce this effect in diabetic patients it would be impressive. But that's not all. Look at what insulin levels were needed to achieve that drop in blood glucose:

Adding in 2.2μmol/kg/min of fructose to an hyperglycaemic glucose infusion profoundly lowers the insulin levels needed to maintain a modestly reduced hyperglycaemia value. In a hormonally intact dog preparation.

That's amazing if correct. Fructose appears to be profoundly insulin "sensitising" or mimicking.

Almost nothing is being "done" with the fructose. It enters the liver, drops though fructolysis and is excreted largely as lactate, well in excess of that produced by the glucose alone. I hope we're all aware that fructolysis bypasses those regulatory steps which make glycolysis a tightly regulated process. Here's the lactate change:

Next we can quickly doodle in the fructolysis pathway taken from here

Fructose Metabolism in Cancer

which has this as a generic cell capable of metabolising fructose. In the liver the various GLUTs will be different but the same principle applies:

We can add in fructolysis with its unregulated, high flow pathway to lactate as typically seen in our current discussion of hepatocytes. Like this:

Equally we can put in the tightly regulated glycolysis route to either ox phos and/or lactate, usually a bit of both. But regulated by pH, citrate, ATP or oxygen availability.

We can put both pathways in together and throw in the insulin receptor too:

We are now in a position to add in the core features to an understanding of what is going on. Like this:

and then we can fade the background to let us concentrate on the generation of ROS:

Here we have the situation under intra-duodenal glucose infusion alone. ROS are being generated by glucose ingress per se using NOX2 and also by insulin docking with the insulin receptor to activate NOX4. Both insulin level and the entrance of glucose in to cells without insulin are tightly controlled.

Neither glucose nor insulin are the signal to activate the insulin signalling cascade. That is purely the prerogative of ROS, at physiologically appropriate levels. The end result is a glucose value of around 10mmol/l and an insulin value at around 250pmol/l.

This is what happens if we add 2.2μmol/kg/min of fructose to the glucose infusion. We achieve a portal vein fructose concentration of 100μmol/l which will generate significant ROS, in direct proportion to the rate of entry of fructose to the cell, which will be high:

The fructose generated ROS will increase the ROS signal. This is the activator of the insulin cascade. The ROS signal will result in the phosphorylation of AKT, the activation of glycogen synthesis and will decrease the penetration of glucose past the liver and in to the systemic circulation. Systemic glucose will fall, less pancreatic secretion of insulin will be needed.

We get what we see in the study.

My personal definition of an obesogenic drug is one which activates "insulin" signalling in the absence of insulin. Fructose generates "unexpected" ROS when entering liver cells at a concentration of 100μmol/l. I think it is perfectly likely that, should one achieve an adipocyte exposure of 100μmol/l of fructose, that a similar effect might occur.

In Laughlin's 2014 review

there is the suggestion that peak systemic fructose concentrations healthy men after a high sugar exposure might be about 0.5mmol/l, ie 500μmol/l and a fasting level might be a fraction of a μmol/l.

There are a number of studies showing fasting fructose levels as high as 2.0mmol/l (ie 100 times Laughlin's accepted level) with post fructose loading reaching over 17.0mmol/l. That makes life easy for everyone. If you want to show fructose is harmless or beneficial you chose the low studies. If you want toxicities you choose the high studies.

But are low doses of fructose beneficial at all? Is insulin cascade activation good or bad? Are the benefits of reduced absolute insulin exposure offset by the ROS mediated activation of insulin cascade?

Whichever fructose measurement camp you fall in to, a normal human being can easily maintain systemic fructose levels > 100μmol/l in the aftermath of even a modest fructose load, which in the dog studies I consider generates enough ROS to be markedly facilitating of what we could call an insulin sensitising or mimetic exposure. Perhaps we should apply this to adipocytes.

Does fructose make you insulin sensitive? Of course it does. Does activating insulin signalling make you fat? Of course it does.

Except, of course, when it does the opposite.



Passthecream said...

There's a great business opportunity there for therapeutic low dose sugar pills :)))

(If we could just get people to stop taking them when they've had enough ...)


Passthecream said...

Brilliant stuff btw.

Peter said...

I recall a homeopathic vet once who used prednisolone tablets as the "vehicle" for his homeopathic dilutions. Worked well for atopic skin disease compared to boring sugar tablets. So yes, a weight loss white powder, Passthecoke(tm)....... Might work!


Passthecream said...

Anything which makes it taste awful should work. A spoonfull of medicine helps the sugar pill go down. I'll stop now.

mct4health said...

Peter, very interesting, nice work. Would it be too heretic to say that glucose uptake could be not limited by GLUT4 here? Almost all rates are the same but diversion of glucose to lactate and to glycogen are elevated by tiny amount of fructose. It looks like processes that convert glucose to something else are the limiting factor in this case, fructose just helps them to divert. There could be plenty of H2O2, so no need for extra supply, just heathy animals.

Peter said...

Not sure Jaromir, the effect is present in some but not all human type 2 diabetics while in "healthy" humans it's not obvious in those with excellent OGTT results but very clear in those with poorest (but still normal) OGTT results. As far as I can see no one has used tracer studies to see where the lactate is coming from but the track from fructose to lactate under normal circumstances seems quite plausible. I'd have to hunt tracer studies to get any further. All work from Cherrington's group.

The effect discussed here is hepatic, I think the ROS principle is generic but clearly which GLUTs are involved (2 and 5 in the liver?) and whether we are talking glucose uptake in adipocytes (GLUT4 & 5, and GLUT1?) or suppression of release from hepatocytes will all be ROS mediated. I look to ROS because they are simple, none of that complicated molecular switching of intermediary metabolism... The ROS signal, metabolism obeys. Just my view.


lapis_exilis said...

LOL, love this - Passthecoke(tm)! Maybe I should try this instead of the boring meat diet... :P

(Super interesting post Peter! Thank you!)

mct4health said...

Peter, it is very complex, who knows. But here some tracing study, about 30% of lactate from fructose, about 50% glucose from fructose.
Fructose metabolism in humans – what isotopic
tracer studies tell us

And the switching mechanism is very real, it was traced on intestinal cells, practically no lactate was produced from fructose, all from glucose and caused by fructose, but not hepatic tissue.

Peter said...

Yes, excellent review. I started with something looking at the end result here

I also started an initial version of the post with microbiota metabolism to acetate (ie this fructose doesn't exist as far as the gut is concerned, let alone the liver, it's just acetate (and CO2 -> bloating). Then I looked at enterocytes and fructose -> palmitate -> ApoB48 -> thoracic duct, ie the liver never sees this fructose. Then I went to liver fructose -> glycogen +/- DNL (tiny). Then I asked myself what actually controls all of this.

Why does low dose fructose markedly improve hepatic glucose retention? W/o fructose what hormone does this? And that hormone is just an overlay over ROS controlling the lovely processes detailed in the N&M article. All of those processes integrate and are, for me, far too complex to try and work out step by step. But ROS are simple.

As you realise there is a huge literature based around high dose fructose intake in rodents and it provides mild obesity, marked redistribution of fat to visceral adipose and fatty liver. Plus metabolic syndrome “illnesses”. None of this is easily comprehensible in terms of the N&M diagram, to me. Certainly hepatic DNL from fructose is trivial. And of course the whole of metabolic syndrome in these rodent models of high fructose ingestion is largely reversible by oral co-ingestion of almost any antioxidant you care to mention or any NOX inhibitor you care to mention.

Anyone not viewing this from the ROS perspective will not generate a plausible mechanism. And low dose ROS -> insulin mimetic, high dose ROS -> insulin resistance is also essential.

That's how my brain works. Keep it simple.


mct4health said...

As Richard Johnson says, speed of fructose intake makes the poison. By slow intake it is converted to something else.

Passthecream said...

This is one of those many studies but seems to be dosing on the cusp so that insulin mimetic effect occurs and acts to inhibit beta ox.


"In Brief Softic et al. show that in addition to its well-described effects to increase hepatic fatty acid synthesis and malonyl-CoA levels, consumption of fructose-sweetened water decreases dietary fat oxidation. "

I thunk.

Tucker Goodrich said...

Interesting. I've wondered why fructose has the effects it does, and unregulated generation of ROS in the liver would certainly do the trick.

"Regulatory landscape of AGE-RAGE-oxidative stress axis and its modulation by PPARγ activation in high fructose diet-induced metabolic syndrome"

"The severity of rat liver injury by fructose and high fat depends on the degree of respiratory dysfunction and oxidative stress induced in mitochondria"

"Fructose and Oxidized LDL in Pediatric Nonalcoholic Fatty Liver Disease: A Pilot Study"

Just like with ethanol, I'd love to see some studies comparing fructose ingestion against different fatty acid backgrounds.

It seems like we'd see the same thing.

"Dietary linoleic acid is required for development of experimentally induced alcoholic liver injury"

Peter said...

Tucker, I have absolutely no doubt this will be the case. The most glaring example of ethanol as an insulin mimetic is the fall in blood glucose than makes you hungry.

Low dose of ethanol and fructose will provide "insulomimetic" ROS. High doses will provide lipid peroxidising levels, converting the stored liver fat from above in to NASH.

Obviously LA potentiates the first role and is crucial to the second.

But first we need to look at NADH oxidase(s) vs mitochondria and location/targeting of "ROS". Location might matter too.


Peter said...


Yes, getting on the "cusp" is okay. Getting a study through ethics board review for grossly hepatotoxic levels of fructose ingestion for humans on a par with rodent high fructose diets would be impossible. That job is for marketing execs working for McDs et al!


Peter said...

Jaromir, slow uptake fructose -> palmitic acid [heart emoji]


mct4health said...

Peter, yes, but how? PA will mostly be formed from acetyl-CoA and glucose. Fructose seems to divert glucose to fermentation and to lactate (PKM2 modification?). The response to lactate seems to be very important, releasing Mg2+ from the endoplasmic reticulum and changing cellular preferences to suppress OXPHOS and increase glycolytic (and gluconeogenic and fat synthesis, HIF-1?) pathways. This activates SCD1 desaturase and creates a substrate for peroxisomes, so more H2O2 is produced. Now we are in the same situation as with glucose and unsaturated FA with overactivated peroxisomes suppressing almost all mitochondrial inputs. Modification of PKM2 bv fructose appears to be the key, but research is early and it could all be wrong.

Passthecream said...

Peter the idea of putting heaps of fructose in all of the rats drinking water is appalling but well matched by the 'doyouwantacokewiththat' of contemporary provisioning.

I had a gran like yours, very very sweet cups of tea with a side of insulin from one of those big glass and stainless steel jobbies. Ugh. But it reminds me that one of the comforts offered to diabetics in the pre-insulin days was barley water which sounds innocent albeit starchy, however it was usually loaded up with sugar and fruit juice. The rat diet looks totally ethical in comparison.

Passthecream said...

Hmmm thinking about what I just wrote versus the theme of this blog essay, perhaps a fructose intake at some level can act in lieu of the missing insulin system in frank t1dm. (The glucose component of sucrose would be a fly in that ointment??)

karl said...

Too many moving parts for me...

So Fructose is sweeter than sucrose or glucose :
Type Relative sweetness.
Lactose 40
Dextrose 70–80
Fructose 150–170
Sucrose 100

I'm thinking about the insulin response to sweetness here. Add to this that it appears there are genetic variations in these receptors. Does the intestinal insulin response change between fructose and sucrose.

The enteric nervous system is separate from our other nervous system - adding yet another layer to thinking about this - the pancreas is controlled by the enteric nervous system.

I link to this paper mainly for the references:

If we evolved to sense sweetness, from the breakdown of starches - and fruits were intermittent - I think it is safe to say that we are not adapted for the western diet full of sucrose.

There is also the problem of glucose vs fructose metabolism by intestinal bacteria flora - the flora is NOT a constant thing - evolving to the changing environment or the foods eaten.

A study looking at receptor response to different sweeteners vs insulin response would help.

So I'm wondering how to look at the direct response to fructose in the cell plus more insulin from the sweetness receptor response adds up?

(lots of feedback loops)..

Then I think about the effect of antibiotics on the intestinal flora - could they change the ability of the E. coli to digest glucose and fructose?

What happens if we test instead by putting the glucose and fructose directly into the blood stream?

So I'm thinking there is an intestinal-endocrine control loop under this cellular control loop - and we need tricky experiments to keep this all clear.

cavenewt said...

All of this makes my brain hurt.

I'm left wondering if the dried figs and wine I indulged in last night were a secretly suicidal impulse. Or if I'ive inoculated myself by not ingesting any extra linoleic acid?

Peter said...

cave and karl,

No doubt


Peter said...


Not sure why yet, but it wouldn't work (methinks). Probably about 3 posts down the road if I can get my head round it. No promises...


mct4health said...

Yes, it is complicated. I simlify it for myself as peroxisomal / mitochondrial activity ratio, the ratio of potential problems.
Unsaturated fats -> peroxisomes
Saturated fats -> mitochondria
Fructose -> peroxisomes
Glucose -> mitochondria

Peroxisomes are fat making machines, add little bit of glucose and you make triglyceride to store. It must be much more glucose to suppress peroxisomes. High peroxisomal activity suppress mitochondiral activity and vice versa.

If you are already obese, you convert almost all saturated fat to unsaturated. So reversing with saturated fat is problematic. Saturated fats are blocked from mitochondria unless they are unsaturated and accepted by peroxisomes.

The paper form Passthecream pefectly support this. Fructose = fat (unsaturated), Glucose without fructose can ballance unsaturated fat. Don't combine fructose with (poly)unsaturated fats!

(And it has also ROS aspect, peroxisomes also make lot of ROS, so it must be ballanced by NNT and GPx or CAT)


Passthecream said...


"as any fule kno"
N. Molesworth, How to be Topp.

Hoggwarts was first mentioned by Molesworth, Op. Cit.

Tucker Goodrich said...


"I'm left wondering if the dried figs and wine I indulged in last night were a secretly suicidal impulse. Or if I'ive inoculated myself by not ingesting any extra linoleic acid?"

That's my bet. We evolved from frugivores, who would have eaten a lot of fructose and a good bit of alcohol from fermented surgars. In moderation, should be no problem.

"These Monkeys' Taste For Boozy Fruit Could Explain Why Humans Love Alcohol, Too"

Tucker Goodrich said...

@Peter: "But first we need to look at NADH oxidase(s) vs mitochondria and location/targeting of "ROS". Location might matter too."

Somewhat off-topic, but I came across this in my Twitter feed. I'd forgotten all about it.

"Rapid increase in serum lipid peroxide 4-hydroxynonenal (HNE) through monocyte NADPH oxidase in early endo-toxemia"

"By this assay, we found that a low dose of bacterial lipo-polysaccharide (LPS), injected intra-peritoneally (0.5 mg/kg), increased serum HNE level by 28-folds, with a peak at 20 min."

That would certainly make for a rather inhospitable environment if you were an invading microbe!

mct4health said...

One more note, we can eat bad things as long as they are accompanied with an antidote. I know that flavonols can suppress the overexpression of HIF-1, which can completely prevent obesity. Honey and fruit also surely have some of these flavonols or other antidotes. On the other hand, there are components that works the same as fructose, without beeng sweet, such as autoxidation products of linoleic acid (9-ONA), LPS or other poisons. That's why the whole food idea applies.

Peter said...

cave and Tucker, we have a fig tree. I eat the figs fresh. It's a routine but limited excursion from carnivore each August. There will be none this year as we had a very warm November last year and this year's fruit ripened then, so zero overwintering figs. I also tend to occasionally make my own extremely low carb alcohol, usually honey based. I'm thinking low L6 might excuse such misdemeanors.

Jaromir, I've long hated antidotes such as flavanols. Just not poisoning myself more than occasionally seems a better plan. Plants hate us. They will punish us for eating them... Occasional recreational use might be worth the costs. So it seems to me...


karl said...

Peter said: " I've long hated antidotes such as flavanols. Just not poisoning myself more than occasionally seems a better plan. Plants hate us. They will punish us for eating them."

This quote fits two themes that I've written about.

One - much better to prevent exposure than to look for a magic pill/supplement. (thus my great-grandmother rule (don't eat anything she didn't))).

Two - Plants and especially fungi have been using chemical warfare for a long time - chemicals to effect behavior or to just kill you are common. Antibiotics came from mycotoxins - which can save your life at the right dosage - but clearly they are poisons. My hunch is that the narrative to 'eat your vegetables' was for saving the high value food for the hunters - let the kids fill up on the greens and roots.

Earlier I meant to say that while fructose is utter complex - confounded with feedback loops at different levels - the right approach is to understand the low level bits first as Petro is focused on.

Thinking about why did plants evolve fruits with fructose? I suppose because it is sweeter, it is less expensive to promote consumption to spread seeds?

One other bit that I ran into years ago - I was talking to one of our host students doing cancer cell research - it turned out that fructose really helped in culturing these cell lines.

I think the reason so many cancer rates are correlated with BG is that it fuels cancer growth fast enough to get past the immune response.

Fructose seems different in this as the body removes it faster than glucose. I remember one other difference between Glucose and fructose as the rate in which they form AGE(advanced glycation End-products) - fructose being something like 10x faster. The formation of AGEs appears to increase ROS (not sure how sure we know this). Taken as a whole, I don't think we are at all well adapted to handle a high fructose exposure.

Fructose also spikes trygly - not just a little - my take is the expensive cholesterol panels is mostly just recording fructose exposure. This was not a problem of our ancestors - In the time of Columbus, an ounce of gold would buy only 40LBs of sugar - for most Europeans fruits were a once a year thing.

For some reason, the work of Winitz and others was ignored (messy old page with good links):

As per flavinols - polyphenols I'm not seeing that they are well absorbed - I'm suspicious that they work in the intestinal flora - perhaps binding to metals preventing absorption? These are sheet like molecules with hydroxides that are happy to find a free metal atom - hang on to it - let it pass on out??

RE DLPA - I remember trying phenylalanine back about 1980 - came in as a reagent a powder in a glass bottle (perhaps Kodak made it?). The narrative (I think from Wurtman) was it was a catecholamine precursor - Something like =>tyrosine => L-DOPA => dopamine - might make one smarter. Never noticed much - but that pathway does not only end with dopamine - but norepinephrine and epinephrine as well. I could see it effecting heart rate.

Passthecream said...

Fig season here right now!

Bush walking recently we stumbled across some blue agaves, gigantic things and more so when they get to flowering and they are a terrible feral pest in Aus but a serious (fermentable) crop species in Mexico.

There is a heap of b/s about agave syrup, available at supermarket near you which is supposedly a " vegan sweetener" --- are there many animal sources of fructose and sucrose? = dubious claims department. (only bees, naturally, but I always thought that sugarcane and beets were vegetables???)

Can vegans not eat grasshoppers?

Along with fructose, sucrose, glucose in that syrup you get fructans, saponenes, oligosacharides and various other plant chemicals ie fodmaps with attitude. It sounds like hell in a bottle. I'm sure the tequila and mezcal would be far healthier to consume than the unfermented hell-brew.

Being a vegan must be very hard on the bowells.

Peter said...

karl, yes, plants want a seed vector. At exactly the same time they want to disable the seed digestion process. These are inseparable. For green parts of plants they just need a toxin w/o any sweetener. As I consider ROS, fructose and palmitate there is an idea forming of why carbihydrate restriction may have some long term benefits.

Pass, ah, vegan logic. What's to wonder about?

Jaromir, take care!


Passthecream said...

Peter, "vegan logic" is one of those phrases where the noun and the adjective are at right angles to each other.

Plants and animals have worked out some pretty interesting symbioses involving seeds and fruit. This is a three way love-fest involving fruits + emus, seeds + ants:

There are some other types of seeds which can't germinate until they have passed through the digestive system of an emu.

This reminds a bit of human farming, the behaviours are complex by which grains get what they need from us --- obviously we are being farmed by wheat, barley, bananas...

mct4health said...

Peter, totally agree. But sometimes it works, so very interesting.
Myricetin protects against diet-induced obesity
Substituting Honey for Refined Carbohydrates Protects Rats from Hypertriglyceridemic and Prooxidative Effects of Fructose
Flavonoids induce HIF-1α but impair its nuclear accumulation and activity

Passthecream said...

As with many natural materials honey is not monolithic, there can be variable quantities of the different sugars and other content depending on the season and pollen source. I'm thinking of one particular neutral honey beekeepers use for blending with stronger varietals derived from echium spp, purple bugloss, a plant which is toxic to stock, and hepatotoxic to humans. You might get a benefit but at some cost!

Peter said...

Haha, Jaromir. I'm currently learning all about bee keeping through evening classes with these guys

Its fascinating. We have a lot of ground and abut several acres of wilderness. I'm not intending to go full-on Hadza honey eating. We're more interested in how honeybees "work", ie learning "bee-logic". Might make some very, very dry mead. They're a cool system, like ants, the colony is almost one organism. Mostly we'll give the honey away to non LC family members (like the crab apple jelly and damson jam, or quince jelly when the tree sets fruit).


cavenewt said...

I use local raw unfiltered honey to make kombucha (technically jun?), which ferments till the sweetness is gone. Hopefully no evil residue left after that.

Your mention of mead is very intriguing. Now I need to look up how to make that! I do love countertop farming.

Peter said...

I made a trial batch with supermarket honey. You just add honey to the ferment mix to give the alcohol target you want then ferment it to an SG well under 1.0, all the toxic fructose goes to toxic ethanol. The latter is more fun!


cavenewt said...

Peter, you're a bad influence. Re making mead, I looked up some instructions which seemed very fiddly and technologically-oriented. This dissatisfaction inspired a search for how medieval people managed their fermentations with more primitive technology. An article about traditional bochet elicited an immediate desire to try it, unlike the modern recipes. "The Quest to Recreate a Lost and ‘Terrifying’ Medieval Mead" (the scare-quotes are just clickbait.)

My biggest challenge will be finding a cool enough location. Before long we'll be in triple digit temperatures and I have no air conditioning. Hmm.

This recipe comes from an indispensable 13th-century bride's bible, The Good Wife's Guide (Le Ménagier de Paris)

Passthecream said...

Peter I'm surprised that you can fit evening classes in with everything else!

I made mead when I was a teenager, because. I found that relying on wild yeast made a very bitter drink with the wild type yeasts that live here, but like it is with the sourdough fanatics I'm sure you could scrape bloom off various fruits until you find an agreeable one, or make metheglyn instead which uses honey plus fruit juices. Eventually I got good results with a cultured white wine yeast, and the usual degree of careful cleanining, sterilisation of equipment as you would for wine.

My cousin used to brew a feisty ginger beer of the sort which blows up thick glass bottles, with the aid of a ginger beer plant which was kept alive through thick and thin. I saw the other day where someone in the US is offering a starter culture of these. Its an ancient yeast/bacteria symbiosis similar to keffir and water keffir, but different specific organisms

Peter said...

I've had a few demijohns lying around in a shed for years. Cleaned them up last autumn and made some cider by chopping apples in water and throwing wine yeast on them. Cider-like is the best description! When Mel mentioned getting bees I trialed the mead, wine yeast again. Works for me. Not quite carnivore but I'm no purist. Obvs the mead is slightly more so than the cider.


Passthecream said...

I was horrified to find out that cider in the USA seems to refer to plain apple juice and the real thing is known as hard cider.

Peter, you could have just mushed up all your apples in a juicer, filtered the pulp to make a must and not added any water and it would have turned into fantastic dry cider - it will ferment close to completion in a demijohn with an airlock if you use tart apples. I discovered a wild roadside apple tree recently with apples that are close to being cider apples and picked a couple of bags. I'm inclined to brew them up now. But maybe I'll add some honey?

Peter said...

Ah, two (or more) nations divided by a common language...

I've made a must by boiling chopped apples and filtering. Hard to clear the end product. I don't have a juicer (unsurprisingly) but am considering chopping apples or pears in a blender and using some added water as before. Main problem is you have no idea of the original gravity, though the carb count from final gravity is still easy. I guess a glass will allow assessment of ethanol content!


Passthecream said...

Cider brews are quite prone to acetobacter unless you add sulfite (and use sulfite resistant wine yeast) but that means you could take it one stage further to cider vinegar which is probably more nutritious, but less fun. Check the pH. A bit of malolactic ferment is good to make it less mouth puckering but doesnt happen at too low a pH, or too high.

cavenewt said...

'made some cider by chopping apples in water and throwing wine yeast on them'

There are a lot of fruit trees here, but because of our climate (frequent light frost) only about one year in three yields fruit. Having a surfeit of local peaches a few years ago, I chopped up a couple quarts in airlock jars and added some yeast given me by a friend who makes his own booze. The resulting alcoholic fruit was not sweet, and made a fine wintertime dessert treat when heavy cream was added.