After 150 comments have been made, maybe 6 people will stop to read this. But I feel compelled to contribute a bit of what I've learned about obesity.
I was the medical director of an obesity treatment clinic for 10 years, working with thousands of obese patients.
The most important lesson is that obesity is a disease, and each obese person has a different disease. Each case requires a unique treatment approach. "Cookie-cutter" methods won't cut it.
I'm convinced that obesity is the most complex disease the art and science of medicine has ever faced. I can't even begin to describe the mind-boggling complexity of the situation.
A minimalist outline: factor in participation of the endocrine system (insulin resistance, role of cortisol, thyroid, reproductive hormones), the immune system products promoting obesity, as well as adverse inflammatory effects of adiposity contributing to metabolic disarray, and the brain's functional role in metabolism involving highly intertwined connections of neuronal circuits regulating metabolism and sleep/circadian rhythms. And so I could go on for gigabytes on these subjects, even before citing the enormous list of references.
Short answer: all of these body systems (neural, endocrine, immune) are interactive. Think many:many relationship with "many"==trillions. Therein are the solutions to obesity. Small needles, huge haystack.
Short answer: all of these body systems (neural, endocrine, immune) are interactive. Think many:many relationship with "many"==trillions. Therein are the solutions to obesity. Small needle, huge haystack.
A few years ago it was mentioned at a conference that at the time over 250 human genes (and their peptide products) had been identified to play a role in obesity. Considering the multitude of known and potential gene/environment interactions, what simple "cause and effect" paradigm could we glean?
So yes, many obese patients respond favorably to low CHO, high N diets.
Altering PUFA intake to approximate a 1:1 intake of N3 and N6 EFA in adequate amounts is warranted. Elimination of physiologically incompatible trans-fatty acids in the diet is absolutely necessary. Mono-unsaturated or saturated fats within calorie constraints are not usually an issue. Behavioral approaches are always indicated.
Just remember, each of us is different, our systems are inherently quirky, and tremendous variation is common. The above general rules are fine to start with, but be prepared, understand the "reality paradox": exceptions are the rule and not the exception.
Interesting and quite dense post - I had some trouble with the terminology so, for the other five people reading this.. CHO = carbon hydrogen oxygen (ie carbohydrates), N = nitrogen (ie proteins & purines)? This was hard to figure out from google alone but seems to make sense..
Also, PUFA = Polyunsaturated Faty Acids, EFA = Essential Fatty Acids. n3/n6 are more commonly (less precisely?) known as omega 3/omega 6 fatty acids.
From my personal, anecdotal experience the first intervention has been effective (and this seems to accord with the received recommendations wrt better health outcomes for those eating more vegetables and fish). But how clear are we on the outcomes of these simple and broadly applicable interventions have been made clear and concrete so far? The first goal for the science should surely be to end the debate on the proliferation "diseases of civilisation" which, to my understanding, we should be able to do by proving a difference in outcomes for these interventions and correlating them to the dietary shifts of the last 30 years
Sorry, should have been more explicit, but you've correctly deciphered all the obscure abbreviations.
I think your questions point to the gist of the matter: obesity is not a simple problem to understand or to solve.
There certainly is evidence that obesity is a "disease of civilisation". Over the last 5 or 6 decades the real prevalence of obesity, diabetes, depression, autoimmune disorders have sharply risen in concert in the industrialized world, but far less so in third world nations.
While many hypotheses have been put forward, the reasons remain a mystery. It seems possible, even likely, the issues surrounding obesity will not be settled in my lifetime.
It seems to me that you're forgetting a very important cause to obesity. The marketing campaigns led by big corporations such as Mac Donald's, Coca Cola and so on...
No doubt many researchers would agree: the food industry has contributed to the problem. Evidence points to manufacturers adding large quantities of sugars (in many forms) to convenience and fast foods as a major culprit.
Physiological effects of this intake result in greater synthesis of fatty acids which are easily stored in fat depots. Over time in vulnerable individuals the cumulative result is excessive adiposity and obesity.
There has been a push to reduce the sugar content of foods and educate the public about the risks. Consumers should learn to read nutrition labels and avoid products with high sugar content.
I was the medical director of an obesity treatment clinic for 10 years, working with thousands of obese patients.
The most important lesson is that obesity is a disease, and each obese person has a different disease. Each case requires a unique treatment approach. "Cookie-cutter" methods won't cut it.
I'm convinced that obesity is the most complex disease the art and science of medicine has ever faced. I can't even begin to describe the mind-boggling complexity of the situation.
A minimalist outline: factor in participation of the endocrine system (insulin resistance, role of cortisol, thyroid, reproductive hormones), the immune system products promoting obesity, as well as adverse inflammatory effects of adiposity contributing to metabolic disarray, and the brain's functional role in metabolism involving highly intertwined connections of neuronal circuits regulating metabolism and sleep/circadian rhythms. And so I could go on for gigabytes on these subjects, even before citing the enormous list of references.
Short answer: all of these body systems (neural, endocrine, immune) are interactive. Think many:many relationship with "many"==trillions. Therein are the solutions to obesity. Small needles, huge haystack.
Short answer: all of these body systems (neural, endocrine, immune) are interactive. Think many:many relationship with "many"==trillions. Therein are the solutions to obesity. Small needle, huge haystack.
A few years ago it was mentioned at a conference that at the time over 250 human genes (and their peptide products) had been identified to play a role in obesity. Considering the multitude of known and potential gene/environment interactions, what simple "cause and effect" paradigm could we glean?
So yes, many obese patients respond favorably to low CHO, high N diets. Altering PUFA intake to approximate a 1:1 intake of N3 and N6 EFA in adequate amounts is warranted. Elimination of physiologically incompatible trans-fatty acids in the diet is absolutely necessary. Mono-unsaturated or saturated fats within calorie constraints are not usually an issue. Behavioral approaches are always indicated.
Just remember, each of us is different, our systems are inherently quirky, and tremendous variation is common. The above general rules are fine to start with, but be prepared, understand the "reality paradox": exceptions are the rule and not the exception.