64 replies to this topic

[playground]

interesting video on glycotoxins

 

obviously, i'm not endorsing this company or it's products.

 

Playground.

[playground]

And another good video on gylcotoxins

 

(it's another advert,  i'm not endorsing the company or their products)

 

 

 

Edited by playground, 24 June 2015 - 06:57 AM.

[playground]

Since T2D and AD are both variants of the same underlying glucose regulation

problem then meds for T2D are also meds for AD.

 

In consequence, drugs like resveratrol and pterostilbene (which act to regulate

diabetic glucose and insulin levels) are also appropriate for AD.

 

And further, any new drugs in the resveratrol / SIRT1 stimulating class are

also likely to be good for AD (that is, if they are good for T2D)

 

With that in mind....

 

An interesting presentation with David Sinclair at a Ted Med talk.

 

Zoom in around the 19:50

He's basically saying they have a drug going through trials

that's 1000 times more potent than resveratrol (as a SIRT1 agonist)

It's being developed for ostensibly for T2D.

 

 

Naturally, i'd be very interested to find out what that drug is and how

it's progressing through those trials.

 

Playground.

 

 

Edited by playground, 24 June 2015 - 07:54 PM.

[normalizing]

someone care to make a table of support which ones are good AGE breakers

[playground]

The people that consume the least amount of glycotoxins are vegans.

 

And amongst the vegans, those consuming the least glycotoxins are the raw food vegans.

 

This seems to have a definite longevity effect, see here:

 

All these people are vegans and over 70:

 

 

 

 

 

 

playground

[playground]

I  have created a new thread about Alzheimer's and Chlamydia Pneumoniae.

This thread is asserting that AD is caused by a bacterial infection.

(Note: the evidence for this is persuasive)

 

Interested readers will find it here:

http://www.longecity...ae-cp/?p=734003

 

playground.

Edited by playground, 25 June 2015 - 09:58 PM.

[resveratrol_guy]

The people that consume the least amount of glycotoxins are vegans.

 

And amongst the vegans, those consuming the least glycotoxins are the raw food vegans.

 

This seems to have a definite longevity effect, see here:

 

All these people are vegans and over 70:

playground

 

Those videos are pretty shocking, especially in light of the titanic amount of sugar that raw fooders actually ingest. In addition to the great benefits from all the phytochemicals in their diet, I suspect that their youthful looks and obviously intact brain function are a direct result of involuntary caloric restriction. In other words, their food takes so much effort to prepare (juicing is tedious) and contains so much water, that they find little interest in just sitting around eating.

 

Now here's a key question: what would happen if you ate 100% raw organic food, with no caloric constraints? And you could exercise if you felt like it, but had no obligation to do so. In other words, if you want another fructose-laden apple, you can eat it, or 10 more if you like. I think the diet would rapidly collapse into diabetes and obesity. But if it didn't, that would be a huge breakthrough, because it would accomplish the effects of CR without the hunger. The only thing that even comes close, AFAIK, is the ketogenic diet. Now, it might be the case that people on these diets have such spectacular insulin sensitivity that attempting to overeat would rapidly result in disgust and appetite shutdown. I don't know.

 

But yeah, I'm still in shock at their state of health, considering that they must be glycating the hell out of their circulating proteome.

Edited by resveratrol_guy, 26 June 2015 - 01:12 AM.

[ceridwen]

I'd join a campaign

[playground]

Hi Ceridwen,

 

Do you mean a vegan 'campaign' ?

 

I keep thinking about this vegan-ism business.

 

vegans have the least risk of T2D.

vegans have the least risk of AD.

 

vegans seem to look better ....for longer.

 

veganism and regular exercise is the recommendation of

Dr Ornish for reversing atherosclerosis and heart disease.

 

presumably vegans have almost zero risk of obesity.

 

I keep thinking about fish... and how i've believed for (literally) decades

that eating fish is one of the best foods you can eat from a brain health

point of view.... i've eaten fish, on average, approx twice a week, week in,

week out,  since about 2007.

 

There's also the vitamin B12 issue.

There's only tiny amounts of B12 in a vegan diet.

There's plenty of B12 in fish.  There's huge amounts in liver!

But..  there's B12 in my B-vitamin supplement too.

 

I don't believe in 'big bang' life-style changes, they never work.

A series of small changes... seems to work (for me at least).

 

I might switch to fish once per week.... for some unspecified period.

Then consider moving to once per month.  And then review things.

 

I find it quite motivating and encouraging to think that i can make

small changes now.. and reap the benefits for years and years

into the future.

 

I have some suggestions for how you might beat your sugar cravings Ceridwen.

(1) Whenever you feel a sugar craving eat a piece of fruit.

peach, banana, fig, orange ... or berries or grapes.. etc.  Whatever you like.

The benefit of this is that you wont feel the 're-bound' sugar cravings 20 minutes later.

This tactic works, but be warned, in the first few days,  you'll eat huge quantities of fruit.

This will die back as your sugar cravings recede.

Also, fruit wont 100% satisfy your sugar craving, it only gets about 70-80% of the way there.

On the other hand, you only have to show self-discipline for the loss of this 20-30% satisfaction.

Your sugar cravings will fade away surprisingly quickly... just a few weeks... perhaps a month.

but it gets easier and easier the more you persist.  

A bit like giving up smoking, the first week is the hardest.

 

(2)  Resveratrol and Pterostilbene both help to regulate blood sugar.

People taking these supplements report less intense sugar cravings. 

 

Hope this helps

 

Playground.

 

Edited by playground, 26 June 2015 - 11:31 AM.

[Jackhill41]

Very interesting post, in addition to the thread  re: CPN association with Alzheimers.  FWIW, some information in this paper on how to minimize AGEs in cooked meat.  

 

http://www.ncbi.nlm....les/PMC3704564/

 

Acidic marinades, low temperatures, and moisture-intensive cooking methods (e.g., poaching) significantly decrease AGEs.  I try to cook all my meat in a slow cooker now, but there is no denying it does not taste as good as grilled or fried meat.

[playground]

Very interesting post, in addition to the thread  re: CPN association with Alzheimers.  FWIW, some information in this paper on how to minimize AGEs in cooked meat.  

 

http://www.ncbi.nlm....les/PMC3704564/

 

Acidic marinades, low temperatures, and moisture-intensive cooking methods (e.g., poaching) significantly decrease AGEs.  I try to cook all my meat in a slow cooker now, but there is no denying it does not taste as good as grilled or fried meat.

 

Interestingly, the abstract to the article you link to also suggests adding an AGE inhibitory

chemical, called aminoguandine, to food when cooking.

 

Abstract

Modern diets are largely heat-processed and as a result contain high levels of advanced glycation end products (AGEs). Dietary advanced glycation end products (dAGEs) are known to contribute to increased oxidant stress and inflammation, which are linked to the recent epidemics of diabetes and cardiovascular disease. This report significantly expands the available dAGE database, validates the dAGE testing methodology, compares cooking procedures and inhibitory agents on new dAGE formation, and introduces practical approaches for reducing dAGE consumption in daily life. Based on the findings, dry heat promotes new dAGE formation by >10- to 100-fold above the uncooked state across food categories. Animal-derived foods that are high in fat and protein are generally AGE-rich and prone to new AGE formation during cooking. In contrast, carbohydrate-rich foods such as vegetables, fruits, whole grains, and milk contain relatively few AGEs, even after cooking. The formation of new dAGEs during cooking was prevented by the AGE inhibitory compound aminoguanidine and significantly reduced by cooking with moist heat, using shorter cooking times, cooking at lower temperatures, and by use of acidic ingredients such as lemon juice or vinegar. The new dAGE database provides a valuable instrument for estimating dAGE intake and for guiding food choices to reduce dAGE intake.

 

Playground

Edited by playground, 26 June 2015 - 10:40 PM.

[ceridwen]

Have you heard of the MIND diet? It is a preventative against Alzheimers. You eat fish once a week. Poultry no more than twice a week. Leafy green vegetables 6 times a week. Berries twice a week. Nuts 5 times a week. Whole grains 3 times a day. Wine once a day. These are minimal servings so for green vegetables it's 6 times a week or more. Cheese less than once a week. Maybe that might be a good diet on the way to a vegetarian diet. The longer people stayed on the diet the better their chances became of avoiding the disease.

I think the vegan diet obviously has much more appeal as it is the most protective but the above sounds good for people intending to cut their meat consumption.

[normalizing]

if a person start obsessing with what to consume weekly, at one point during day or night, how much, how often to the exact measurements, grams, milligrams, seperating specificaly one food from the other in count and keep thinking about health, then i believe they will just become psychotic

Edited by normalizing, 27 June 2015 - 09:08 AM.

[playground]

An interesting study:

source: http://www.pnas.org/...3/4940.abstract

title: Oral glycotoxins are a modifiable cause of dementia and the metabolic syndrome in mice and humans

Abstract:  Age-associated dementia and Alzheimer’s disease (AD) are currently epidemic.

Neither their cause nor connection to the metabolic syndrome (MS) is clear. Suppression of deacetylase

survival factor sirtuin 1 (SIRT1), a key host defense, is a central feature of AD. Age-related MS and diabetes

are also causally associated with suppressed SIRT1 partly due to oxidant glycotoxins [advanced glycation

end products (AGEs)]. Changes in the modern diet include excessive nutrient-bound AGEs, such as neurotoxic

methyl-glyoxal derivatives (MG). To determine whether dietary AGEs promote AD, we evaluated WT mice

pair-fed three diets throughout life: low-AGE (MG⁻), MG-supplemented low-AGE (MG⁺), and regular (Reg) chow.

Older MG⁺-fed mice, similar to old Reg controls, developed MS, increased brain amyloid-β₄₂, deposits of AGEs,

gliosis, and cognitive deficits, accompanied by suppressed SIRT1, nicotinamide phosphoribosyltransferase,

AGE receptor 1, and PPARγ. These changes were not due to aging or caloric intake, as neither these changes

nor the MS were present in age-matched, pair-fed MG⁻ mice. The mouse data were enhanced by significant

temporal correlations between high circulating AGEs and impaired cognition, as well as insulin sensitivity in older

humans, in whom dietary and serum MG levels strongly and inversely associated with SIRT1 gene expression.

The data identify a specific AGE (MG) as a modifiable risk factor for AD and MS, possibly acting via suppressed

SIRT1 and other host defenses, to promote chronic oxidant stress and inflammation. Because SIRT1 deficiency

in humans is both preventable and reversible by AGE reduction, a therapeutic strategy that includes AGE reduction

may offer a new strategy to combat the epidemics of AD and MS.

 

playground.

[playground]

source:  http://www.pnas.org/.../15888.full.pdf

 

title:  Oral advanced glycation endproducts (AGEs) promote
insulin resistance and diabetes by depleting the
antioxidant defenses AGE receptor-1 and sirtuin 1

 

There's no point quoting from the abstract, the title sums it up perfectly.

 

 

 

[playground]

To my mind this paper could be a central clue to  understanding how

AGEs are linked to T2D and AD (T3D)

 

In short, AGEs in food upsets glucose regulation, which in turn leads

to T2D and T3D.

 

 

source:  http://care.diabetes...8.full.pdf html

 

title:  Consumption of a Diet Low in Advanced Glycation
End Products for 4 Weeks Improves Insulin
Sensitivity in Overweight Women

 

OBJECTIVE
High-heat cooking of food induces the formation of advanced glycation end
products (AGEs), which are thought to impair glucose metabolism in type 2 di-
abetic patients. High intake of fructose might additionally affect endogenous
formation of AGEs. This parallel intervention study investigated whether the ad-
dition of fructose or cooking methods influencing the AGE content of food affect
insulin sensitivity in overweight individuals.

RESEARCH DESIGN AND METHODS
Seventy-four overweight women were randomized to follow either a high- or low-
AGE diet for 4 weeks, together with consumption of either fructose or glucose
drinks. Glucose and insulin concentrations d
after fasting and 2 h after an oral glucose tolerance test d
were measured before and after the intervention. Ho-
meostasis model assessment of insulin resistance (HOMA-IR) and insulin sensi-
tivity index were calculated. Dietary and urinary AGE concentrations were
measured (liquid chromatography tandem mass spectrometry) to estimate AGE
intake and excretion.

RESULTS
When adjusted for changes in anthropometric measures during the intervention,
the low-AGE diet decreased urinary AGEs, fasting insulin concentrations, and
HOMA-IR, compared with the high-AGE diet. Addition of fructose did not affect
any outcomes.

CONCLUSIONS
Diets with high AGE content may increase the development of insulin resistance.
AGEs can be reduced by modulation of cooking methods but is unaffected by
moderate fructose intake.

Edited by playground, 28 June 2015 - 02:11 PM.

[playground]

This is an important paper:

 

AGEs _initiate_  amyloid plaque formation.  The argument here

is that it is AGEs' ability to glue proteins to glucose that is basically

the _seed_ of what turns out to be an amyloid plaque.

 

source: http://okdentalwelln...AGE-Amyloid.pdf

 

title:  Advanced glycation end products contribute to amyloidosis in
Alzheimer disease

 

some quotes from the abstract:

 

AGE-modified flAP-nucleation seeds further accelerated aggregation of soluble flAP compared to

non-modiflied "seed" material. Over time, nonenzymatic advanced glycation also results in the

gradual accumulation of a set of post translational covalent adducts on long-lived proteins in vivo.

 

In a standardized competitive ELISA, plaque fractions of AD brains were found to contain about

3-fold more AGE adducts per mg of protein than preparations from healthy, age-matched controls.

These results suggest that the in vivo half-life of fi-amyloid is prolonged in AD, resulting in greater

accumulation of AGE modifications which in turn may act to promote accumulation of additional amyloid.

 

Playground.

 

 

[playground]

This 2015 paper is showing how Tau formation is accelerated in the presence of AGE, and that

Tau formation is inhibited an AGE blocker (aminoquanidine).

 

 

source: http://www.ncbi.nlm....pubmed/26095350

 

TITLE:  Ribosylation triggering Alzheimer's disease-like Tau hyperphosphorylation via activation of CaMKII.

 

ABSTRACT: Type 2 diabetes mellitus (T2DM) is regarded as one of the serious risk factors for age-related cognitive impairment; however, a causal link between these two diseases has so far not been established. It was recently discovered that, apart from high D-glucose levels, T2DM patients also display abnormally high concentrations of uric D-ribose. Here, we show for the first time that the administration of D-ribose, the most active glycator among monosaccharides, produces high levels of advanced glycation end products (AGEs) and, importantly, triggers hyperphosphorylation of Tau in the brain of C57BL/6 mouse and neuroblastoma N2a cells. However, the administration of D-glucose showed no significant changes in Tau phosphorylation under the same experimental conditions. Crucially, suppression of AGE formation using an AGEs inhibitor (aminoguanidine) effectively prevents hyperphosphorylation of Tau protein. Further study shows AGEs resulted from ribosylation activate calcium-/calmodulin-dependent protein kinase type II (CaMKII), a key kinase responsible for Tau hyperphosphorylation. These data suggest that there is indeed a mechanistic link between ribosylation and Tau hyperphosphorylation. Targeting ribosylation by inhibiting AGE formation may be a promising therapeutic strategy to prevent Alzheimer's disease-like Tau hyperphosphorylation and diabetic encephalopathies.

 

 

[playground]

There are lots of papers on gylcotoxins  that mention aminoguanidine as the

preferred anti-glycation compound.  However, Genentech abandoned stage 3 trails

with aminoguanidine in 1999 (on the grounds of 'lack of efficacy' --- sounds familiar, huh)

 

This paper is suggesting that Quercetin is a better anti-glycation compound than aminoguanidine.

 

So at the moment it looks like..... if you want to  supplement with something that's going to

reduce the glycotoxin load on your body.... use Quercetin.   It's a readily available supplement.

 

 

Int J Biol Macromol. 2015 Jun;77:188-92. doi: 10.1016/j.ijbiomac.2015.03.021. Epub 2015 Mar 20.

Quercetin as a finer substitute to aminoguanidine in the inhibition of glycation products.

Abstract

Non-enzymatic glycation is the addition of a free carbonyl group of a reducing sugar to the free amino groups of proteins, which results in the formation of early and advanced glycation end-products (AGEs). Glycation reaction is profoundly associated with diabetes and its secondary complications, such as nephropathy and neuropathy. Glyoxal is a carbonyl species that reacts rapidly with the free amino groups of proteins to form AGEs. While the formation of AGEs with various glycating agents has previously been demonstrated, no extensive studies have been conducted to assess the role of quercetin in all three stages of glycation (early, intermediate and late). In this study, we report the glycation of HSA (human serum albumin) and its characterization by several spectroscopic techniques. Furthermore, inhibition of products at all stages of glycation was studied by various assays. Spectroscopic analysis suggests structural perturbations in the HSA macromolecule as a result of modification, which might be due to the generation of free radicals and the formation of AGEs. Inhibition in the formation of glycation has established that quercetin is a better and a more potent antiglycating agent than aminoguanidine at all stages of glycation.

 

 

 

[resveratrol_guy]

 

There are lots of papers on gylcotoxins  that mention aminoguanidine as the

preferred anti-glycation compound.  However, Genentech abandoned stage 3 trails

with aminoguanidine in 1999 (on the grounds of 'lack of efficacy' --- sounds familiar, huh)

 

This paper is suggesting that Quercetin is a better anti-glycation compound than aminoguanidine.

 

So at the moment it looks like..... if you want to  supplement with something that's going to

reduce the glycotoxin load on your body.... use Quercetin.   It's a readily available supplement.

 

 

Int J Biol Macromol. 2015 Jun;77:188-92. doi: 10.1016/j.ijbiomac.2015.03.021. Epub 2015 Mar 20.

Quercetin as a finer substitute to aminoguanidine in the inhibition of glycation products.

Abstract

Non-enzymatic glycation is the addition of a free carbonyl group of a reducing sugar to the free amino groups of proteins, which results in the formation of early and advanced glycation end-products (AGEs). Glycation reaction is profoundly associated with diabetes and its secondary complications, such as nephropathy and neuropathy. Glyoxal is a carbonyl species that reacts rapidly with the free amino groups of proteins to form AGEs. While the formation of AGEs with various glycating agents has previously been demonstrated, no extensive studies have been conducted to assess the role of quercetin in all three stages of glycation (early, intermediate and late). In this study, we report the glycation of HSA (human serum albumin) and its characterization by several spectroscopic techniques. Furthermore, inhibition of products at all stages of glycation was studied by various assays. Spectroscopic analysis suggests structural perturbations in the HSA macromolecule as a result of modification, which might be due to the generation of free radicals and the formation of AGEs. Inhibition in the formation of glycation has established that quercetin is a better and a more potent antiglycating agent than aminoguanidine at all stages of glycation.

 

 

 

This is interesting, although I've heard that quercetin has poor absorption (and perhaps might benefit from lipidation, like curcumin). So what's the best way to take advantage of its antiglycation properties?

 

Oh, and anyone discussing this should be aware of this.

Edited by resveratrol_guy, 29 June 2015 - 02:27 AM.

[playground]

I like this study.... It suggests that regular B-vitamins are AGE inhibitors.

 

The AGEs Inhibitor in this study is made up from vitamins: B1, B6 and B12:

 

benfotiamine [50 mg] = synthetic, fat-soluble vitamin B1.

pyridoxamine [50 mg] = vitamin B6

+methylcobalamin [500 µg]; = vitamin B12.

 

I strongly suspect this study is just a marketing exercise for some commercial product.

(consequently, the results are probably exaggerated ... or.. completely fictitious)

 

 

 

Clin J Pain. 2013 Aug;29(8):717-24. doi: 10.1097/AJP.0b013e318272ebec.

Efficacy and tolerability of advanced glycation end-products inhibitor in osteoarthritis: a randomized, double-blind, placebo-controlled study.

Garg S¹, Syngle A, Vohra K.

Author information

Abstract

OBJECTIVES:

Advanced glycation end-products (AGEs) play an important role in pathogenesis of osteoarthritis (OA). The objective of this study was to evaluate the efficacy and tolerability of AGEs inhibitor (benfotiamine [50 mg]+pyridoxamine [50 mg]+methylcobalamin [500 µg]; Vonder [Cosme Farma Laboratories Limited, Goa, India]) in OA patients.

METHODS:

A 24-week, double-blind, randomized placebo-controlled study in primary OA patients (n=30 [F/M=26/4; mean age, 57.26±2.16 y]) meeting the classification criteria of American College of Rheumatology, was conducted. Inflammatory disease activity scores on the Western Ontario and McMaster University (WOMAC) Osteoarthritis Index, Lequesne Index, and Pain scores were analyzed. Biomarkers: serum nitrite, AGEs, thiobarbituric acid reactive substances, C-reactive protein, erythrocyte sedimentation rate, were also measured. Time taken to walk 20 m was also recorded. Patients were randomized to either AGEs inhibitor or placebo tablets as thrice-daily regimen.

RESULTS:

At 24 weeks, net decrease in pain score, -6.64±2.71 versus -8.20±1.28, P=0.003; total WOMAC score, -5.88±0.84 versus -8.26±1.24, P=0.013; Lequesne Index score, -0.60±0.06 versus -0.84±0.09, P=0.05; time taken for 20-m walk test, -5.0±1.39 versus -5.0±0.92 s, P=1.00, were observed in the placebo versus drug group, respectively. Net change in serum nitrite, -0.15±0.01 versus -0.79±0.12 µmol/L, P<0.001; AGEs, -0.12±0.02 versus -0.99±0.09, arbitrary florescence units, P=0.001; thiobarbituric acid reactive substances, -0.69±0.12 versus -1.80±0.12 nmol/L, P<0.01; C-reactive protein, -0.12±0.35 versus -2.45±0.60 mg/L, P<0.01, were observed in the placebo versus drug group, respectively.

DISCUSSION:

This study shows the efficacy of an AGE inhibitor on decreasing pain and inflammation, and increasing daily activity and mobility in OA patients.

 

[Nuke]

What about ALT-711? It is effective in the heart and circulatory system. That should include the brain's circulatory system (I hope). It may not break AGEs in all body tissues, but its a start.

 

http://www.ncbi.nlm....pubmed/15218393

[resveratrol_guy]

ALT711 sounds fantastic, but that was 2004. What went wrong?

Edited by resveratrol_guy, 29 June 2015 - 05:56 PM.

[Nuke]

Found this too. https://www.ncbi.nlm...pubmed/15812746

 

And then they killed it.

https://www.fightagi...-alagebrium.php

 

It still looks promising to me though. It is on my research list, but I have not spend time on it yet.

 

 

[resveratrol_guy]

Found this too. https://www.ncbi.nlm...pubmed/15812746

 

And then they killed it.

https://www.fightagi...-alagebrium.php

 

It still looks promising to me though. It is on my research list, but I have not spend time on it yet.

 

I wonder why there was such a disconnect between the heart trial and the studies which tried to replicate the rat results in humans, but failed. It could be that the open-label aspect of the human trial caused some sort of placebo effect in the experimental group, for example, they exercised more because they knew they had a fighting chance with help from the drug. Or maybe it only acts on the heart. It seems to me that this stuff does not belong in the dustbin, and indeed you can still acquire it, but maybe in the end what it tells us is that AGE-breakers are a winning strategy if you can customize them for humans. Perhaps there are improved versions now under testing.

[playground]

 

Found this too. https://www.ncbi.nlm...pubmed/15812746

 

And then they killed it.

https://www.fightagi...-alagebrium.php

 

It still looks promising to me though. It is on my research list, but I have not spend time on it yet.

 

I wonder why there was such a disconnect between the heart trial and the studies which tried to replicate the rat results in humans, but failed. It could be that the open-label aspect of the human trial caused some sort of placebo effect in the experimental group, for example, they exercised more because they knew they had a fighting chance with help from the drug. Or maybe it only acts on the heart. It seems to me that this stuff does not belong in the dustbin, and indeed you can still acquire it, but maybe in the end what it tells us is that AGE-breakers are a winning strategy if you can customize them for humans. Perhaps there are improved versions now under testing.

 

 

The fact that they've killed it, could be a clue that it's effective.

 

Big Pharma acts proactively to prevent anything damaging it's future profits.

 

Look at what happened to Rene Caisse with Essiac

Look at what happened to Gerson and the 'banning' of fruit and vegetable juices as a treatment for cancer ('banning' ??)

Look at what happened to Hoxsey's Remedy

Look at what happened to the Pancreas Enzymes threapy (currently associated with Dr Gonzalez)

 

Look what's still happening with  Stanislaw Burzynski.

Look at the current harassment of MSM vendors

It's still illegal to sell Laetrile and apricot kernels for the treatment of cancer (in the USA)... It's only vitamin B17 (WTF?)

 

Nothing has changed, It's business as usual.

 

Genentech is a big pharma company.

They are earning billions from the sale of existing medications.

In 1999 they dismissed progress with two drugs on the grounds that they 'lacked efficacy'.

One was rhNGF.... (did such spectacular things in all the animal studies, but does nothing in humans ???)

The other was aminoguanidine... (a highly effective blocker of AGEs... killed in phase 3 trials, lacks efficacy?)

 

There is another example.

There was a vaccine for Lime disease, it was pulled from the market because,  they said, they didn't

want to have to pay out for litigation against the vaccine (completely ignoring that insurance covers those risks)

Or.. .maybe it showed itself effective against other pathogens implicated in a variety of _really_ serious

diseases (like Chlamydia Pneumoniae, for example).

 

Big Pharma has shown itself very happy to profit from human suffering.

Let's not forget that we have cancer drugs that are less effective than no treatment.

We have toxic cancer drugs that are mandated ...  whilst natural cures based on

fruit and vegetable juices are forbidden (in the USA).  Big Pharma is clearly taking the piss.

 

The fact that they've killed it, could be a clue that it's effective.

 

Playground.
 

[playground]

 

Found this too. https://www.ncbi.nlm...pubmed/15812746

 

And then they killed it.

https://www.fightagi...-alagebrium.php

 

It still looks promising to me though. It is on my research list, but I have not spend time on it yet.

 

I wonder why there was such a disconnect between the heart trial and the studies which tried to replicate the rat results in humans, but failed. It could be that the open-label aspect of the human trial caused some sort of placebo effect in the experimental group, for example, they exercised more because they knew they had a fighting chance with help from the drug. Or maybe it only acts on the heart. It seems to me that this stuff does not belong in the dustbin, and indeed you can still acquire it, but maybe in the end what it tells us is that AGE-breakers are a winning strategy if you can customize them for humans. Perhaps there are improved versions now under testing.

 

 

It appears that this stuff _is_ available, despite being killed during trials.

http://www.iron-drag...products_id=172

 

They also have anti-AGE compound 'aminoguanidine'.

 

No NGF though.

 

playground.

 

 

 

[ceridwen]

I hate to put a spanner in the works but Alzheimers might be caused by too much tryptophan. That would fit quite neatly into the problem with AGEs. 

raypeat/articles/aging/tryptophan-serrotonin/aging.shtml

I compared this to what we already know and think it adds some important pieces to the puzzle. Hope this helps.

[kaskiles]

Vegan keto is going to be hard enough, now we need to add 'reduced tryptophan' into the mix?

[ceridwen]

It's a very complicated disease