Maillard reaction in our bodies thanks to added fructose to foods?

At 23:33 minute of the 2013 video Dr Lustig says that fructose helps to brown bread better. I do not object against 'better'. This is due to the Maillard reaction, a non-enzymatic browning that is different from enzymatic browning, that happens when you cut an apple and observe how it goes brown within a minute. This is caused by enzymes. It is also different from a simple burning during baking, when the amino acids and starches react together, forming toxic acrylamides. Maillard reaction, on the other hand, is a chemical reaction between a reducing sugar and an amino acid, which can happen at a lower temperature than during baking. This process also happens in our bodies, when sugar found in blood react with proteins and produce haemoglobin A1c (HbA1c), which is used as a biomarker of poor glucose control in diabetics. You are right: glucose causes this reaction in our blood. 

I have heard Dr Lustig talking about the fructose effect on browning inside of our body. He once delivered an impressive piece of talk about it and showed the ground cartilage material of people who died at different age. There you could see at 11:42 minutes how their cartilage tissue became browner and browner the older they were: 

What is more, Dr Lustig kept repeating in various lectures how fructose is 7-times faster in the Maillard reaction than glucose. Impressed?

Well, let's look at a more complex picture. I would like to know how glucose fits into this. Do you remember Dr Lustig saying that 100% of fructose is metabolized by the liver, whereas 80% of glucose goes to the systemic circulation - the rest of the body? Unless we are talking about Maillard reaction in the liver caused by fructose, he is contradicting his own claims.

Actually, in another video at 52:50 he starts talking more in detail about how the fructose affects the proteins: when it binds to the protein it decreases its flexibility, causing a basement membrane thickening - leading to arterial wall thickening... which arterial wall? In the liver or the remaining body? 

How about the fact the concentrations of fructose in the systemic circulation are 10 - 1000 times lower than of glucose? 

Diabetics have even higher glucose concentrations when their diabetes is poorly controlled and that is why they are at risk of various health complications, including the arteriosclerosis leading to the cardiovascular diseases due to the damage to the arterial walls.

Does the 7 times faster Maillard reaction of fructose look so impressive now? 

I remember reading an article in some scientific magazine that even the ancient Egyptians had atherosclerosis. What from when they did not consume so much sugar and fructose within as we do today?

In another video of Dr Lustig talked in a more detail about this fructose issue. From 46:10 onward you can hear and see to which tissues this fructose apply. Firstly the 7 times faster results were achieved in vitro, in the laboratory, not a real body:

In a real and living body tissue or organ the body produces natural antioxidants which help to prevent this damaging oxidative processes or lower their impact on the living cell. We produce oxidative stress at every second in our body. Without it we would not be alive. So bathing some albumin (a protein) in a sugary water truly cannot be representative of the living body system. There even exists an adaptation to higher oxidative stress when the body is constantly and repeatedly exposed to it. It is the most prevalent and known in athletes: because they produce higher oxidative stress in their body, they are also more efficient to fight off the higher formation of free radicals by improving their own antioxidant capacity

Secondly, you could hear how sucrose is responsible for the diseased livers of rats while those on a complex carbohydrates (starch) were not suffering, illustrated by this image: 

Well, I would have two comments on this: 

1. I do not know what kind of starch was used. There is starch that is easily digested, producing high glycaemic index, and there are resistant starches that do not rise the blood glucose as high and are partly fermented by the gut bacteria, which is healthy for our colon and metabolic health overall. 
2. The abbreviations for MCD and MCS refer to the methionine and choline deficient or sufficient rats. Methionine is an essential amino acid which we need to build proteins from which other tissues or more complex formation are synthesized in the body. Choline is also an essential nutrient which is needed for healthy cell membranes. Therefore the animals and also humans can gradually become ill when deficient from one or both of these nutrients. You could see that those rats who had these nutrients in sufficient amounts were not affected by sucrose. 

Just because the animals had the liver damaged by the consumption of sucrose while deficient of these two essential nutrients does not mean that those fed on starch would not become ill a bit later. I did not read the study itself, but I know that the laboratory tests on animals are often feeding the poor creatures toxic amounts of the tested substances and the studies do not last for too long because of the funding reasons and sometimes the rush to report the findings. The scientists often find what they were looking for and end the experiment. And I suspect this was the case here, too. 

Moreover, you could also hear Dr Lustig saying in another video at 51:18 minute that when the animal is deficient in these two nutrients, the effect occurs. I have looked at when the diet can be deficient in choline and found out that this rarely happens - because even the processed food can supply this nutrient. Similarly for methionine, the diet rich in proteins, especially of animal origin, cannot be deficient in methionine. And you and me already know that the western population consumes more animal protein that they actually need. So, even if people have a rubbish junk food diet, they should rarely experience the deficiency of these two nutrients and therefore they should be protected against the negative effect of sugar in this sense. 

Another image, which illustrate the findings on humans consuming sugar reports higher incidence of liver fibrosis while having a lower incidence of steatosis with a daily consumption of sugar (from which they assessed the consumption of fructose): 

However, this study was a cross-sectional study, not a clinical intervention study and the links are just associations, not properly controlled for the confounders. In fact, as the abstract of the study says, these people were ALREADY SUFFERING the non-alcoholic fatty liver disease (NAFLD). All the scientists controlled for was: age, sex, BMI, and total calorie intake. Do you see alcohol intake anywhere? The fact that these patients had NAFLD does not mean that some of them did not consume alcohol as well. And you could see in another article of mine that with the increased consumption of sugars among the adult population, there was almost identical increase of alcohol consumption for several years. 

Moreover, the abstract of the study also says that the higher fructose was associated with a lower age, but the more prevalent damage in form of liver inflammation and hepatocytes ballooning was found at people older than 48 years of age. This just does not add up, does it? In fact, look at the diagram again: while the fibrosis was increased among people consuming the soft drinks daily, the steatosis - fatty liver was significantly DECREASED. What a surprise! So why Dr Lustig said that these two conditions were the same in another video presenting the same material at 51:40? Especially when you could read elsewhere, that:

"...a small number of cases, steatosis can develop into a fibrosis that can lead to cirrhosis..."

So is it the same thing or not? The study itself reported in the abstract that these people had increased prevalence of fibrosis but decreased prevalence of steatosis. What is going on here? The study only captured a snapshot in time, it did not follow the population over time so that those with steatosis would develop fibrosis. The same applies on a possible development of fibrosis in people over time: young people consuming more sugar than older people, but developing fibrosis over time, when their sugar intake is not as high. The study had no potential to assess and confirm this. 

You could also read in the abstract that people with higher fructose consumption had a lower serum glucose levels... nothing was said about insulin and insulin resistance although Dr Lustig repeatedly said that it is fructose that drives the insulin resistance and metabolic issues via promoting hyperglycemia. 

You were not said all these things. Instead, he explicitly said: 

"The amount of sugar consumed correlates in humans with the amount of liver disease."

Is the non-alcoholic fatty liver disease not a disease? Those people were already having NAFLD and the amount of fructose was positively correlated with the further damage in a form of fibrosis but negatively correlated with the accumulation of lipids in their livers. Only those over 48 years of age had the liver cells ballooning, which I understand as accumulation of liver fat but these were not the highest consumers of fructose. 

Keep your eyes open, folks.