Obesity does not cause metabolic syndrome; insulin resistance causes obesity. True?

I have already discussed my concerns about whether obesity is a disease or not and here we have another attempt of Dr Lustig to make the obesity irrelevant, pronouncing it as only an associated factor with the metabolic syndrome (MetS). He believes that not obesity causes insulin resistance but that insulin resistance causes obesity. He also believes that it is only the abdominal fat (inside the abdomen) that is a factor for the insulin resistance development whereas the subcutaneous fat is not the cause of anything.  

I agree that fat deposits in different body parts represent a different risk of metabolic diseases. However, does that make the excess subcutaneous fat irrelevant, so that we could ignore the obesity and focus only on the MetS features? I doubt so. 

Just a recap: 80% of obese people still suffer metabolic diseases (that is 4 out of 5) and as Dr Lustig said, so does the 40% of those having a 'normal weight'. However, about 50% of these 'normal weight' are actually overweight. So, is the obesity and excess adiposity under the skin really irrelevant? What percentage of these overweight would actually suffer metabolic issues in contrast to those really of a normal weight? 

Dr Lustig insists that firstly there is an insulin resistance, leading to leptin resistance, which leads to obesity and when this insulin issue is fixed, then the leptin issue is fixed, and then the obesity will be fixed as well: 

Because:

You know what? I AGREE with that. Partly. People tend to develop metabolic issues as they are becoming overweight and obese. In this mechanism it is really difficult to distinguish to what extent it is a marker (due to wrong diet and lifestyle) and to what extent it is a cause. Meanwhile, it is individual for each person WHEN and at what level of excess adiposity they will qualify for the diagnosis of MetS.

Just think: if people were not constantly in a positive energy balance for weeks and months - would they develop metabolic disturbances? Would they get high cholesterol, high blood pressure, would they become insulin resistant, because the muscles cannot take any more energy molecules in? I bet that most of them would not and as you may be aware, in many people, who reduce their body weight, their metabolic markers also improve. Slim people do not tend to suffer metabolic syndrome at such a large scale as obese and overweight people do. 

Should we therefore dismiss the link between obesity and metabolic diseases just because some thin people become ill and 1 in 5 obese does not?

Dr Lustig made it clear: people develop metabolic diseases irrespectively of the excess of subcutaneous body fat and he did it via this slide: 

He said that insulin resistance is what the obesity and lipodystropy have in common. However, you might have already read my objections against using this lipodystrophy case. It was because these people are genetically predisposed for insulin resistance which makes them too different from the rest of us. In addition, these familial partial dystrophy cases are rare. In the nutshell, the lipodystrophy means abnormal distribution of body fatness and represents a group of various diagnoses that are characteristic with lipodystropny. People are either genetically predisposed or they acquire this condition as a consequence of other condition such as being HIV positive and treated with various medication of having a history of autoimmune disease. 

The lipodystrophy is a specific condition and is rather rare in comparison to the prevalent overweight and obesity cases which mostly occur due to simply overeating and having low levels of physical activity. People suffering from lipodystrophy are often overeating due to leptin deficiency, while overweight and obese people become leptin resistant due to constantly positive energy balance, often leading to insulin resistance, too. What they have in common is that both cases: lipodystrophic and obese people have disturbed metabolism of energy. However, there is difference: 

• lipodystrophic people are unable to store fat in some body parts (under the skin in limbs), but  they can store it in other body parts (neck, face, around the organs), which makes them to look slim, but in fact they are metabolically ill and obese inside. The inability to store fat under the skin and excess adiposity in other places affects the whole endocrine system, sometimes also leading to overeating, which further worsens the condition. This is what Dr Lustig has been describing. Nonetheless, the whole condition is caused by some other condition, as mentioned above. Overeating is a consequence of reduced subcutaneous fat tissue and low leptin levels and the insulin resistance develops as a consequence of this.
• obese people, on the other hand, usually develop metabolic disturbances as a consequence of simply consuming too much energy, (or unhealthy diet as such, this is a broader topic) while they were initially healthy and metabolically normal. They become insulin resistant and as such, because the elevated insulin interferes with leptin receptors of hypothalamus, they also become leptin resistant as a consequence. And so they continue eating like they did from the time when they were slim, because they love food, it is cheap, plenty of it and unaware of its energy content. And the leptin resistance does not make them stop even if they have increased leptin concentrations in blood. Therefore the mechanism is the opposite than in people suffering various forms of lipodystrophy. 

Therefore, in my opinion, this example of lipodystrophy should not have been used to disprove the link between the body fatness and metabolic diseases in the population not affected by the lipodystrophy.

The Reframing the debate slide ended with this: 

Does this disprove the close link between excess body weight (or the process of gaining weight) and various features of metabolic syndrome? I do not think so. I see this initiative as messing around because at the end, there will again be FRUCTOSE. 

Going back to The Reality image, I have already highlighted that the metabolic dysfunction cannot be the cause of obesity for people who are metabolically normal and start to gain weight because of the obesogenic environment. And you could see that I gained weight without the symptoms of the metabolic disturbances just because I enjoyed the palatable and fattening foods too much and did not bother to move to burn the extra energy. I halted this trend when I reached BMI 27+ but if I did not do so I would most likely follow the fate of my close family who suffer a whole spectrum of metabolic dysfunctions, including obesity, hypertension, high cholesterol, cardiovascular diseases, fatty liver, type 2 diabetes, etc. I currently suffer none of these as a result of my lifestyle, I never did and I hope I will successfully avoid such conditions in the future. 

What Dr Lustig was talking about were his obese patients who struggled to lose weight because of having their biochemistry already affected for various reasons: hypothalamic trauma, specific genetic condition, being obese for some time already, unhealthy lifestyle, etc.

What I am saying is that although for many people the insulin resistance makes them to fail losing weight, but for them to gain weight firstly the insulin resistance is not a necessary factor. It tends to work the other way around: as people are gaining weight, they become insulin resistant in the process of gaining weight or when they finally become obese, because having this extra amount of fat in the body is not healthy at all. 

Fixing obesity does not improve metabolic health?

Everybody knows that when they gain weight, they are at a higher risk of metabolic diseases and many were lucky enough to reduce their medication for blood pressure or to lower their blood glucose or cholesterol levels when losing some weight. 

Yet Dr Lustig calls this connection a dogma: 

He also said that they (American authorities) have been trying this for 30 years and it did not work, because the number of obese children has tripled since 2001. 

So, what does not work? Reduction of obesity or reduction of metabolic diseases with the reduced body weight? I am getting confused.

Then the slide adds two more lines: 

I have already written a short article about how the obesity can be fixed even without interfering with the biochemistry by drugs, which is Dr Lustig's field. He is a doctor after all. I am a nutritionist.

He gave an equal sign between the obesity and leptin resistance. He said that within 12 hours in an attempt to lose weight the levels of leptin are 25% lower, which he called leptin deficiency and claimed it makes things worse because on top of the leptin resistance, there is also this leptin deficiency and the brain sees it as starvation. How flawed this very simplistic picture is you can realize after reading a short article here. 

Then two more lines were added to the slide: 

Dr Lustig said that if leptin was working people would not be obese. Really? Is it the only reason for obesity? Not the palatable and caloric food that makes people eat more than they normally would? It was well documented that people feel the satiety later when eating palatable food. Other behavioral research also found that people eat more when the food is well presented food while they are socializing. 

I accept that in many diseased people fixing the metabolic dysfunction will improve their obesity. However, does this apply to everybody? Take an individual who has just started to live a comfortable life with abundance of palatable food, which will inevitably lead to increased body weight. Is his metabolism dysfunctional already or not? Yes, there are people who have very strong homeostatic mechanism for maintaining stable body weight, but others do not seem to have it as strong. Is that a metabolic dysfunction? We have evolved on laying the fat deposits when the food was abundant because it was not the case for the whole year and there were periods with reduced access to food when the stored energy was a life saver. The problem is we do not experience a true hunger anymore. But we still have the physiology of our distant ancestors. 

The doctor used to say that it is the trick of the food industry to make people eating (and buying) more of the energy dense and processed food by making it palatable and irresistible. Is that not true anymore? Or, does this apply on those who have not yet developed insulin and leptin resistance, or these were not included in the model of metabolic dysfunction? 

For now we have the official statements of many health bodies that reducing body weight of obese people cuts their risks of disease or even death. In fact, I have just found this study, which compared the metabolically healthy obese and diseased obese people. You know what? They both were at a higher risk of death whether of all causes or due to the cardiovascular disease, in contrast to overweight. How completely different from what Dr Lustig has been presenting to you.