Looking forward to it!

James

I've verified that I'm confirmed.  They're updating the online program as they go, and I'll appear on it at some point.  And I'll let the AHS reveal the topic, as my abstract is a far more articulate summary than anything I can say off the cuff!

JS

Awesome! Look forward to meeting you there.

I think the current program is preliminary and is being updated slowly. I had an email from Kamal Patel saying that a full program with abstracts would be available in April.

Per chance do we get a sneak preview of the title of your presentation?

James

My presentation was accepted, and I confirmed that I'll attend, so I'm not sure why I'm not on the online program.  I'll email them and ask.

JS

Notice your conspicuously missing from the current list of names on this years AHS pre-program? Will you be in attendance?

James

I'm glad we were able to communicate an understanding.  Thank you for the support...and if you find my work helpful, you can support it by picking up a copy of TGC, a T-shirt, or just buying some stuff through my Amazon link.

JS

Appreciate the closure, well worded and thought provoking. Love the blog. This is somewhat of a wasted comment but it would have been rude not to thank you for the response 😛

jesse

That's an interesting development (AFAIK uroguanylin was previously thought only to regulate fluid balance), but I don't know enough about its other interactions to write an article that gives my readers a useful takeaway.  Otherwise I'm just saying "Hey, look at this new satiety hormone we found, add it to the list." (along with CCK, PYY, GLP-1, etc.)

Also, I've fixed the part where my forum software munches URLs.

Sondra Rose:

I'm glad to hear of your success!  

Nutrition seems to be at the base of the health pyramid: fixing nutrition isn't a guarantee that our other problems will be fixed, but it seems to be a necessary precondition, and it often accomplishes a great deal on its own.

jesse:

OK, I think I understand what you're saying now.  Yes, the need for more energy substrate is absolutely a cause of hunger...and it's usually the primary driver!  (Most people think it's the only driver.)

Furthermore, in metabolically functional animals (including people) this drive is generally in balance with actual energy needs.  As I said in the speech and in my articles, "Any animal whose faulty perceptions and motivations caused it to become obese, emaciated, malnourished, or poisoned by excess would have been strongly selected against."

What I'm addressing in my articles, and my speech, are the situations in which hunger is out of balance with energy needs.  "I'm gaining fat, why am I still hungry all of the time?"  

There are several reasons I don't like speaking in terms of "energy balance."  

First, as I think I hammered home above, "calories" aren't an interchangeable currency.  As you note, for someone doing frequent, heavily glycolytic workouts, fat does not interchange for carbohydrate...so it's quite possible to be hungry for something that can replenish muscle glycogen even in a theoretical "calorie surplus".  

In contrast, a sedentary person who doesn't undergo glycolytic exercise has very little storage capacity for carbohydrate, so once their liver is replete, they'll be storing it in fat cells and revving up their metabolism to try and burn it off...and they'll generally be hungry again once this process completes, even though they're in "calorie surplus" and gaining weight.  Such a person should be eating more fat, which is supplying most of their energy needs at rest and at low exercise intensities (e.g. walking), and which won't result in metabolic spikes, blood sugar spikes, and then, inappropriate hunger.

Second, our bodies work very hard to adapt themselves to existing conditions, including food intake.  Eat insufficient salt and your body will conserve it: eat an excess and your body will excrete it.  Eat less energy substrate in general, and your basal metabolic rate will probably drop, as will your desire to expend energy via exercise.  Eat adequate calories but zero carbohydrate, and your RER will drop as your body adapts to greater availability of fat.  And so on.  

So yes, I agree that a requirement for energy substrate is the primary driver of hunger.  However, that drive is modulated by micronutritional state...

...and "calories" are not a fully interchangeable currency that satisfies a fixed need for energy.  

That being said, it's absolutely legitimate to make a judgment based on the state of the system at a specific time, e.g. "If you want to gain muscle mass, you need to consume enough energy substrate to synthesize the tissues as well as the amino acids and fats required to build them -- which is more than you consume in order to maintain your current weight at your current activity level."  

I believe that's what you're saying, and I agree.

However, what that does NOT mean is that if you ingest 500 more "calories" per day, you'll magically gain X pounds of mass per week.  Your body might rev up your BMR to burn it off as heat ("I feel really warm today"); it might store it as fat; or it might synthesize new muscle tissue, IF there is sufficient protein available, IF you're generating anabolic signals through resistance exercise and a sufficiency of the hundreds of other factors required.  Etc.

And that is why it's counterproductive to think purely in terms of "calories".  There is no biological system that has, as its input, a "calorie".  

JS

I don't feel I've been able to get my point acknowledge, though it seems simple and non-controversial. It seems possibly even trivial, yet a part of the whole picture that I don't think should be ignored. Perhaps it's the limits of text communication or perhaps I'm living in my own world. I'll take one more stab at it because I think you have continued to refine your responses in a way that gives me a better toolset.

First: pointing out that a need for energy substrate is pretty much a need for macronutrients. By the same token that you ignore the inefficient conversions of various macronutrients into other macronutrients which are more suitable for fuel (glycogen, fatty acids, aminos), I can ignore the energy value of micronutrients (and even some of the macronutrients by the definition you used). In that, if they provide any energy it is negligible and not worth mentioning in a high level discussion.

Secondly: You have obliterated your point that we can have sufficient calories, and yet remain hungry due to needs for specific nutrients (macro/micro/nano, whichever). But haven't conceded the point that you could be replete in all specific nutrient needs and yet still need less specific nutrients as substrate for your long mountain bike treks, or my weight lifting sessions and soccer matches. It seems that you want to lump that into a nutrient need, like "i need glycogen", and I can kind of see that... but at the same time it seems like a purposeful aversion to addressing energy needs as a specific requirement. I wouldn't blame you because any nod towards energy balance could be a slippery slope like you mentioned above with the "fluid balance" analogy. But we have to be careful how we choose our models. Admitting that simple energy needs (typically glucose or fat) could be the driver for food cravings can alleviate the angst someone may feel if they are trying to eat low-carb or reduced calorie and still have cravings. Many people end up in that situation when they go to a paleo diet which is devoid of tubers/starches/rice/grains/dairy and low in fruit and are trying to do athletic endeavors. People trying to gain muscle mass need a lot more calories than they need anything else. I won't quote the source but I read a muscle-head analysis that it takes 35,000 calories to build a pound of muscle, independent of the fat, protein and glycogen needed for the actual structure of the muscle. So that is a pure energy need. I believe lumping certain nutrients into a category of "usable as energy substrate" is a reasonable thing to do. And then believing that we could crave those nutrients for exactly that reason is also reasonable.

I'm throwing the towel in here because it's kind of just going back and forth. If this doesn't clarify my point well enough then I'm OK with it not being settled, or even having it assumed settled from your perspective but not from mine. By the way, thanks for linking those articles by Jamie, I think he offers a good perspective on it. He does make a lot of assertions to build his case that I'm not sure are true. Of course I'm not sure they are not true either and I'm willing to believe that they are, just that they come across as assertive arguments that aren't common knowledge and thus would require some references/backing in a more rigorous setting!

take care J!

jesse

I have known this intuitively for some time and see the positive results in my clients constantly. No more cravings/binging once we sort out their gut health concurrently with focusing on nutrient density.

I discovered this personally when I was sorting out my FODMAPs intolerance. I dropped a lot of veggies from my diet and started eating more liver/cheese/seafood/bone broth. My absorption improved and Voila! More nutrient density = less hunger (after a few months) = finally dropping those last 5 lbs.

'Thus, for over 20 years, guanylin and uroguanylin have been well-known key paracrine players in intestinal ion and water balance. Another piece to the already intricate puzzle of obesity has now been provided by Valentino et al.,2 who identify uroguanylin as a gut-derived satiety factor. The ground-breaking finding comes from the identification of uroguanylin as an endocrine signal with a physiological role in energy homeostasis, thereby expanding the gut–brain axis by an additional factor.
Uroguanylin, a 16-amino-acid hormone secreted by enterochromaffin cells in the duodenum and proximal small intestine, was shown to be released after nutrient ingestion.2 Both guanylin and uroguanylin are secreted as prohormones, which require enzymatic conversion to yield the active hormones that act as agonists of GC‑C. Lack of GC‑C decreased satiation, leading to an elevated body weight due to increased visceral and subcutaneous adiposity in both male and female mice.2 GC‑C knockout mice also exhibited impaired glucose tolerance with hyperglycemia and hyperinsulinemia, together with marked liver steatosis. No differences between GC‑C knockout and wild-type mice were observed in lipid absorption, distribution and clearance, as well as in energy mobilization and expenditure. Thus, obesity was attributable to increased food intake, independent of the type of dietary nutrients and caloric content.'

The point is that uroguanylin works by activating the enzyme guanylate cyclase, which has a requirement for manganese or magnesium. It much prefers manganese.