Waking At 3 Each Morning

[tara]

I've been cutting some calories and fat to lose some belly fat. It's very slow which is fine. But maybe it has something to do with it. I'm normally not one to under eat.

Then maybe you have a choice between slowing it down even more, or having a tiny snack in the early morning, or a little more fat just before sleep? ~ 10 - 15 g carbs was often enough to get me back to sleep.

 

[Mito]

I've been cutting some calories and fat to lose some belly fat. It's very slow which is fine. But maybe it has something to do with it. I'm normally not one to under eat.

https://chrismasterjohnphd.com/2017/07/29/my-recommendations-for-better-sleep/
#2 eat enough food
#3 eat enough carbs

 

[James IV]

I've been cutting some calories and fat to lose some belly fat. It's very slow which is fine. But maybe it has something to do with it. I'm normally not one to under eat.

Sigh. You really should have mentioned that in the first place. This could be the whole problem.
That's like asking why your **** hurts and not telling us you replaced your toilet with a barbecue grill.

 

[ecstatichamster]

I will try eating a bit of fat before bedtime.

 

[DuggaDugga]

I've been cutting some calories and fat to lose some belly fat. It's very slow which is fine. But maybe it has something to do with it. I'm normally not one to under eat.

Increasing your thyroid function through good insulin sensitivity and decreased stress.
Fat is the primary energy source of myocytes at rest, so non-stressful exercise that stimulates muscle growth (weight lifting) is the best way to lower fat. Cortisol metabolizes skeletal muscle and promote fat deposition in the abdomen.
If you want to lose weight appropriately, fasting and carb-avoidance are probably not wise.

[Serum cortisol level variations in thyroid diseases]. - PubMed - NCBI
Fasting as a metabolic stress paradigm selectively amplifies cortisol secretory burst mass and delays the time of maximal nyctohemeral cortisol con... - PubMed - NCBI
Obesity and cortisol status. - PubMed - NCBI
Body fat distribution and cortisol metabolism in healthy men: enhanced 5beta-reductase and lower cortisol/cortisone metabolite ratios in men with f... - PubMed - NCBI
The relationship between cortisol, muscle mass and muscle strength in older persons and the role of genetic variations in the glucocorticoid receptor. - PubMed - NCBI
Interaction of the endocrine system with inflammation: a function of energy and volume regulation
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3978663/
Danny and Haidut can explain it far more eloquently:

 

[Wagner83]

Sigh. You really should have mentioned that in the first place. This could be the whole problem.
That's like asking why your **** hurts and not telling us you replaced your toilet with a barbecue grill.

 

[James IV]

Well, if you guys figure out how to mobilize and burn body fat without increasing cortisol, let me know. (Not being sarcastic)

In my experience you must allow cortisol to elevate to some degree in order to mobilize and burn body fat. I've found the absolute best time for this process to occur is while sleeping. Since cortisol is supposed to rise during sleep anyway according to the circadain rhythm's natural affect on hormones. Hence my recommendation for most carbs and calories consumed earlier in the day, and very little after dark or with the last meal. This is an actual applicable approach. So far I've only seen others telling you what not to do.

However, like I said, I'm open to a better approach.

 

[DuggaDugga]

Well, if you guys figure out how to mobilize and burn body fat without increasing cortisol, let me know. (Not being sarcastic)

The issue with cortisol liberating fatty acids is that they don't just get excreted. Much of it ends up getting deposited in "inappropriate" tissues like the liver.
The cortisol and high levels of fatty acids in the blood induce insulin resistance via the Randle cycle (not really a cycle, per se).
Skinny on Fat Metabolism: Lipolysis and Fatty Acid Utilization

Elevated circulating FAs are associated with obesity and thought to mediate insulin resistance. High serum FA levels can result in deposition of FA in non-adipose tissues leading to ectopic TAG storage in organs such as the liver and skeletal muscle, contributing to insulin resistance [54]. It is also postulated that other lipid metabolites such as DAG and ceramide, by activating serine kinases, may cause insulin resistance [55–56]. Furthermore, macrophage infiltration in adipose tissue may cause increased inflammatory cytokine production resulting in insulin resistance [56–57]. It has been reported that FA released from adipocytes themselves can activate toll-like receptors on adipocytes and macrophages, inducing inflammatory pathways and reducing insulin signaling [56, 58].

The wiki page on the Randle cycle is decent:
Randle cycle - Wikipedia

The thing with fat is that your body is always using fat for energy, even when you're at rest. Some tissues do it more than others, on the high-end is the heart and skeletal muscle.

Fatty acid metabolism in adipose tissue, muscle and liver in health and disease. - PubMed - NCBI

Fat is the largest energy reserve in mammals. Most tissues are involved in fatty acid metabolism, but three are quantitatively more important than others: adipose tissue, skeletal muscle and liver. Each of these tissues has a store of triacylglycerol that can be hydrolysed (mobilized) in a regulated way to release fatty acids. In the case of adipose tissue, these fatty acids may be released into the circulation for delivery to other tissues, whereas in muscle they are a substrate for oxidation and in liver they are a substrate for re-esterification within the endoplasmic reticulum to make triacylglycerol that will be secreted as very-low-density lipoprotein.

Role of fatty acid uptake and fatty acid beta-oxidation in mediating insulin resistance in heart and skeletal muscle. - PubMed - NCBI

Fatty acids are a major fuel source used to sustain contractile function in heart and oxidative skeletal muscle. To meet the energy demands of these muscles, the uptake and beta-oxidation of fatty acids must be coordinately regulated in order to ensure an adequate, but not excessive, supply for mitochondrial beta-oxidation.

It's important to keep in mind that adipocytes are not just dead weight; they're metabolically active cells that respond to signals like any other cell in your body.
Obesity and insulin resistance

Adipocytes are well known for their essential role as energy storage depots for triglycerides, from which energy is called forth at times of need in the form of FFAs and glycerol. However, data emerging over the past several years have established an additional role for the adipocyte, that of secretory cell (Figure (Figure2).2). Adipocytes express and secrete numerous peptide hormones and cytokines, including TNF-α; plasminogen-activator inhibitor-1, which helps maintain hemostasis; angiotensinogen, whose proteolytic product regulates vascular tone; and leptin, which plays a central role in regulating energy balance. Adipose tissue can also produce active steroid hormones, including estrogen and cortisol (30, 31). Through such secreted products, adipocytes possess the capacity to influence local adipocyte biology, as well as systemic metabolism at sites as diverse as brain, liver, muscle, β cells, gonads, lymphoid organs, and systemic vasculature. This realization raises many possibilities for additional links between adipose function or mass and insulin resistance, independent of the adipocyte’s roles in energy storage and release (Figure (Figure11).

The short answer on how to lose weight: anabolic stimulus, insulin sensitivity, pro-thyroid, low-fat diet, low stress, nutrient-dense foods. The living organism knows how to regulate its metabolism and composition. Obesity is a human disease because humans expose themselves to nutritional deficiencies, stress, and environmental toxicities. It's in each of our body's capacity to resolve this when we resolve deficiencies and remove toxicities.

In addition to Danny Roddy's video I posted above, here's another good resource to understanding the role of carbs, fat, and insulin to directing a pro-metabolic state.
https://chrismasterjohnphd.com/2017/07/22/biochemistry-insulin-doesnt-make-fat/

 

[Wagner83]

The thing with fat is that your body is always using fat for energy, even when you're at rest. Some tissues do it more than others, on the high-end is the heart and skeletal muscle.

So what is the issue with fat in the diet?

 

[DuggaDugga]

So what is the issue with fat in the diet?

Excess dietary fat-- even saturated-- will lead to insulin resistance with the repercussions mentioned previously.
Fat oxidation does not support anapleurotic reactions, those that support the intermediates of the TCA cycle; oxaloacetate is produced from the pyruvate dehydronase complex, derived from glycolysis, the initial step of the metabolism of glucose. That's where the saying "fat burns in the flame of carbohydrates" comes from. High fat feeding also moves the glutathione redox status in the direction of oxidation.

Anaplerotic reactions - Wikipedia
Mitochondrial glutathione depletion reveals a novel role for the pyruvate dehydrogenase complex as a key H2O2 emitting source under conditions of nutrient overload

Once regarded as “byproducts” of aerobic metabolism, the production of superoxide/H2O2 is now understood to be a highly specialized and extensively regulated process responsible for exerting control over a vast number of thiol-containing proteins, collectively referred to as the redox-sensitive proteome. Although disruptions within this process, secondary to elevated peroxide exposure, have been linked to disease, delineation of the sources and mechanisms regulating increased peroxide burden remain poorly defined and as such difficult to target using pharmacotherapy. Here we identify the pyruvate dehydrogenase complex (PDC) as a key source of H2O2 within skeletal muscle mitochondria under conditions of depressed glutathione redox buffering integrity. Treatment of permeabilized myofibers with varying concentrations of the glutathione depleting agent 1-chloro-2,4-dinitrobenzene (CDNB) led to a dose-dependent increase in pyruvate-supported JH2O2 emission, with emission rates eventually rising to exceed those of all substrate combinations tested. This striking sensitivity to glutathione depletion was observed in permeabilized fibers prepared from multiple species and was specific to PDC. Physiological oxidation of the cellular glutathione pool following high fat feeding in rodents was found to elevate PDC JH2O2 emission, as well as increase the sensitivity of the complex to GSH depletion. These findings reveal PDC as a potential major site of H2O2 production that is extremely sensitive to mitochondrial glutathione redox status.

Oxidation of the GSH/GSSG redox couple has been reported in a variety of chronic pathophysiological states, including, aging, diabetes and obesity-induced insulin resistance [23-26], as well as under even more acute (4 h) high dietary fat overload states in humans [25].

Effect of insulin and oral glutathione on glutathione levels and superoxide dismutase activities in organs of rats with streptozocin-induced diabetes. - PubMed - NCBI
The effects of glutathione, insulin and oxidative stress on cultured spermatogenic cysts

Glycolysis also produces an additional molecule of CO2 that the production of acetyl-CoA from beta-oxidation can't provide. Producing additional CO2 means increasing the Bohr effect, meaning quicker respiration. Glucose is water-sparing (carbo-*hydrate*; glucose is C6H12O6, an oxygen for every two hydrogen). Glycogen stores are the primary signal to the liver whether or not to convert T4 to T3, active thyroid hormone. Glucose increases respiration.

In thinking of an advantage to fat, I really can't come up with one outside of very rare, specific instances that involve lung injury and need to avoid exhaling. Happy to hear what others have to say.

 

[Colin Nordstrom]

my experience has correlated pretty well with James. I got disastrous results from the Carb backloading approach (no carbs early, all carbs post-workout/at night). When I switched to early day carbs (reducing starch/increasing sugar intake), things calmed down for me. My sleep is better when I move away from late day carbs. I would get a constant 3AM body alarm if I didn't switch to night fat-burning. Again, like James said, forget the Dugga Dugga science, and self-experiment. To me, anecdotal trumphs science everyday (science is wonderful but don't make it a religion).

 

[ecstatichamster]

Ray has said you can work through carb loading and sleep through the night as I recall. Wake up for a few days to consume some milk then a week later you no longer have to

 

[Colin Nordstrom]

this stuff is so individualized, any suggestions are warranted. when you work with clients, the science goes out the window. science can provide a rough guide, but man is the body a complex beast.

 

[James IV]

All this extensive science is great. But minutia is really fairly useless in application. Personally, I don't believe it helps actual people to accomplish health goals. But I am glad you share it for those individuals versed enough to find it useful.

However, regardless of the plethora of resources posted, none of that negates the fact that you have to mobilize bodyfat (Free Fatty Acids) in order to burn it. Cortisol is the primary signal to mobilize FFA. Fat doesn't just disappear from your fat reserves, even if you have the metabolism of a hummingbird. It must be mobilized and burned. So my statements stand. You will not lower bodyfat levels without cortisol mobilizing FFA. The best (least demanding on the body) time for this to occur is when you are sleeping.

I'm not one to say if you should or should not "try" to reduce bodyfat. That's up to the individual. It's obviously more beneficial to do this when your metabolism is strong, and you are healthy. But it doesn't negate the fact that lowering bodyfat necessitates the need for "stress" hormones in all scenarios.

 

[ecstatichamster]

All this extensive science is great. But minutia is really fairly useless in application. Personally, I don't believe it helps actual people to accomplish health goals. But I am glad you share it for those individuals versed enough to find it useful.

However, regardless of the plethora of resources posted, none of that negates the fact that you have to mobilize bodyfat (Free Fatty Acids) in order to burn it. Cortisol is the primary signal to mobilize FFA. Fat doesn't just disappear from your fat reserves, even if you have the metabolism of a hummingbird. It must be mobilized and burned. So my statements stand. You will not lower bodyfat levels without cortisol mobilizing FFA. The best (least demanding on the body) time for this to occur is when you are sleeping.

I'm not one to say if you should or should not "try" to reduce bodyfat. That's up to the individual. It's obviously more beneficial to do this when your metabolism is strong, and you are healthy. But it doesn't negate the fact that lowering bodyfat necessitates the need for "stress" hormones in all scenarios.

But don't fat cells burn fat at rest? If you eat a low-fat diet, will your fat cells end up just consuming the fat and you lose weight without mobilizing free fatty acids?

 

[Diokine]

dem kidneys tho.

 

[James IV]

But don't fat cells burn fat at rest? If you eat a low-fat diet, will your fat cells end up just consuming the fat and you lose weight without mobilizing free fatty acids?

No. It doesn't work that way.

 

[Braveheart]

James...I always value your input and often agree, but today I'm confused regarding your view on cortisol...thought the goal was to lower it if concerned about weight?

Cortisol inhibits metabolism in fat tissue

 

[DuggaDugga]

All this extensive science is great. But minutia is really fairly useless in application. Personally, I don't believe it helps actual people to accomplish health goals. But I am glad you share it for those individuals versed enough to find it useful.

However, regardless of the plethora of resources posted, none of that negates the fact that you have to mobilize bodyfat (Free Fatty Acids) in order to burn it. Cortisol is the primary signal to mobilize FFA. Fat doesn't just disappear from your fat reserves, even if you have the metabolism of a hummingbird. It must be mobilized and burned. So my statements stand. You will not lower bodyfat levels without cortisol mobilizing FFA. The best (least demanding on the body) time for this to occur is when you are sleeping.

I'm not one to say if you should or should not "try" to reduce bodyfat. That's up to the individual. It's obviously more beneficial to do this when your metabolism is strong, and you are healthy. But it doesn't negate the fact that lowering bodyfat necessitates the need for "stress" hormones in all scenarios.

You are so lost, my friend. Please-- please-- do any amount of research. It's for your benefit.

No. It doesn't work that way.

Yes, it sort of does actually. It's a bit more complex, but I've already provided the basic physiology multiple times. Can you actually step up and refute it? Or will you turn a blind eye again? Let's make this constructive.

But don't fat cells burn fat at rest? If you eat a low-fat diet, will your fat cells end up just consuming the fat and you lose weight without mobilizing free fatty acids?

Yes, they do, and so does muscle (as a primary source even). I provided multiple studies that explain the mechanism. @James IV for whatever reason insists on saying the exact opposite but fails to apply any actual physiology. I even explained the repercussions to liberating FFA using cortisol and, again, he glosses right over it, stating the exact opposite, not providing evidence.

Feels like I'm on a paleo forum right now or something.

 

[tara]

Hence my recommendation for most carbs and calories consumed earlier in the day, and very little after dark or with the last meal.

I seem to have to have some later in the day, but I too seem to find it best to have most of the carbs and calories earlier. And I've been assuming, as you say, that that's because it fits in with the natural cortisol cycle.

science can provide a rough guide, but man is the body a complex beast.

+1

But don't fat cells burn fat at rest? If you eat a low-fat diet, will your fat cells end up just consuming the fat and you lose weight without mobilizing free fatty acids?

I don't think fat cells are very hungry - low maintenance organ, good for long term energy storage.
Muscles burn fat at rest, and I think they require more energy.
Seems to me, I do want to have a natural cirdcadian cortisol cycle, with it somewhat higher at night than during the day, allowing some fat to be burned to sustain me through the night, but not to get to extreme levels, or to remain at chronically elevated levels.
[eta:]But I don't think everyone necessarily needs to go to extremes of eating high (or low) fat to have it work optimally.