Well, I’ve hit the dreaded “stall.” I am 8 months in and the scale hasn’t moved in 4+weeks. I’m OMAD, 23/1 for feeding window. Under 20 carbs. No nuts. Sleeping well, low stress. Not menopausal, walk/exercise 3x a week, lift mild weights 2 days a week.
IF isn’t helping. OMAD is just helping me maintain weight. I’m really not sure what to do to get the scale moving again. Or do I just suck it up and say that this is as good as it gets for me. I’d love to reach my goal weight but it doesn’t seem to be in the cards for me. Any suggestions of things I haven’t already tried appreciated.
(Gregory - You can teach an old dog new tricks.)
While keeping your carbs under 20, are you tracking your calories at all ?
Any reason to believe you are putting on any muscle?
You could be losing fat but not losing weight…
I’m not “tracking” my calories per say. Since I’m eating OMAD and I’ve been doing keto for 8 months, for the most part I know my portion sizes and basic calories. I suspect I’m around 1200 to 1400 calories, maybe less. Not more for sure.
I have lost a bit of weight via a measuring tape, so that is why I’m not freaking out, but it would be nice to see the scale move.
I am tracking my ketones via Keto Mojo and I average 1.8 to 4.0 depending on the day.
I don’t think I’m gaving tons of muscle, I just think my body is tired of losing weight. Lol
I think stalls after losing a bunch are a signal from your body that it needs time to adjust. Weight loss like that necessitates a lot of processes within your body to be adjusted. I am currently on a stall, and I just listen to my body - if hungry I eat. Time for skin to adjust, flab to grow firm, and lots of things we cannot see. Consider it a badge, and be nice to your body.
“…When the calories you burn equal the calories you eat, you reach a plateau. …” - Mayo Clinic
• Your metabolism has slowed down so your burning body fat much slower? (BMR/RMR/TEE -intramyocellular lipid build up at rest esp. gluteus maximus)
• All the energy that is being expended on trying to decrease body fat storage is now being concentrated on preserving storage capacity?
• Dietary fats (and amino acids) participate directly in energy metabolism of the mitochondria and make up the physical plasmic structure of the mitochondria membrane itself, especially saturated fatty acids SFA?
• Dietary carbohydrates do not participate directly in the energy metabolism of the mitochondria?
• The biogenesis of new mitochondria and increase in number of mitochondria is dependent on saturated fatty acids SFA. Which in turns forms newer and functional mitochondrial proton pumps for the production of higher energy expenditure of ATP and phosphorylation synthesis for the oxidation of carbohydrates within adipose cells and burning (oxidation) of body fat through components of adrenaline?
Originally I got the acronyms mixed up and confused short chained fatty acids SCFA with saturated fatty acids SFA; in this post (I orally dictate), sorry about that so I made more footnotes to clarify this at the bottom…
 “…Red blood cells are devoid of mitochondria and are therefore unable to oxidize neither fatty acids nor amino acids, relying only on glucose for ATP synthesis. …” …More
 “…Overall, the aforementioned mitochondrial membranes play an important role in the organelle’s functions and in maintaining cellular homeostasis. The composition of these membranes is very dynamic, especially the specialized IMM, and is tightly regulated but can be altered through the intake of dietary FAs. Alterations in the composition of membrane phospholipids will influence the biophysical properties of the membrane and thereby protein function (49). …” “… In mitochondrial membranes, the abundance of SFAs is significantly lower than the amount of unsaturated FAs. However, an increase in dietary intake of SFAs can increase the amount of FAs such as palmitic and stearic acids within the mitochondrial membranes, leading to potential impairments (113). In one study, SFAs were increased in rat liver mitochondria, particularly in cardiolipin, which led to the impaired release of cytochrome c (114). Although significantly less studied than unsaturated FAs in relation to mitochondria, SFAs likely play an important role in regulating mitochondrial membrane structure and function. Elucidating how SFAs influence mitochondrial biophysical organization is an area for future investigation. One possibility is that SFAs may counter-regulate the effects of unsaturated FAs by perturbing the diffusion of protein complexes and thereby their ability to execute optimal respiratory function (Figure 3). This would be driven by the ability of SFAs to increase membrane microviscosity and potentially increase the thickness of the membrane bilayer. …” …More
 How is fatty acyl CoA transported from the cytoplasm to the mitochondria for beta-oxidation? Cytoplasmic fatty acyl CoA is converted to fatty acyl carnitine by carnitine acyl transferase (CAT I), an enzyme of the inner leaflet of the outer mitochondrial membrane. Fatty acyl carnitine is then transported by an antiport in exchange for free carnitine to the inner surface of the inner mitochondrial membrane. There carnitine acyl transferase II (CAT II) reverses the process, producing fatty acyl CoA and carnitine. This shuttle mechanism is required only for longer chain fatty acids. Medium- and short chain fatty acids are carnitine-independent. They cross the mitochondrial membranes, and are activated in the mitochondrion. …More
 “…Short- and medium-chain fatty acids (SCFAs and MCFAs), independently of their cellular signaling functions, are important substrates of the energy metabolism and anabolic processes in mammals. SCFAs are mostly generated by colonic bacteria and are predominantly metabolized by enterocytes and liver, whereas MCFAs arise mostly from dietary triglycerides, among them milk and dairy products. A common feature of SCFAs and MCFAs is their carnitine-independent uptake and intramitochondrial activation to acyl-CoA thioesters. Contrary to long-chain fatty acids, the cellular metabolism of SCFAs and MCFAs depends to a lesser extent on fatty acid-binding proteins. SCFAs and MCFAs modulate tissue metabolism of carbohydrates and lipids, as manifested by a mostly inhibitory effect on glycolysis and stimulation of lipogenesis or gluconeogenesis. SCFAs and MCFAs exert no or only weak protonophoric and lytic activities in mitochondria and do not significantly impair the electron transport in the respiratory chain. SCFAs and MCFAs modulate mitochondrial energy production by two mechanisms: they provide reducing equivalents to the respiratory chain and partly decrease efficacy of oxidative ATP synthesis. …” …More
This means when your body is placed under stress, it find a way to adapt. In this case, as atomicspacebunny stated, “Your metabolism has slowed down…”
It’s a survival mechanism. You body believe you are starving and so it has decrease you metabolic rate, so that you don’t starve.
To get your weight loss back on track, one of two things needs to occur.
Decrease you caloric intake even more. However, at let’s say 1200 calories day, that isn’t the best option.
Losing weight is like taking a trip. You first need to find out where you are on the map so that you can plot the best course to get to your destination.
That means you first need to know how may calories you are consuming.
The best way to do that is to do that is a Three Day Recall, counting every thing you eat, then divide by 3 to determine you Daily Average Caloric Intake.
Resetting Your Metabolism
To reset your Metabolic Thermostat, you need to increase your your caloric intake approximately 20% above what you are now eating and maintain it for about two weeks.
This will increases your metabolic rate.
After those two weeks, drop you calorie intake back down 20%, to your present calorie intake for two weeks.
With your metabolic increased and you now in a calorie deficit, you’ll lose weight.
I realize this doesn’t seem right. Yes, you initially will gain some weight by increasing you caloric intake. However, you will lose that weight and more, once you drop you caloric intake 20% for the following two weeks.
It amounts to taking two step forward and one step back.
Bodybuilder use an aggressive form of this. Bulking (increasing calories) to increae muscle mass. Then Cutting (decreasing calories) to decease body fat, while maintaining muscle mass.
"…alternating 2-week blocks… resulted in greater weight loss (fat loss) without greater loss of FFM (Fast Free Mass/Muscle), attenuation of the reduction in REE (Resting Energy Expendidture), and superior weight loss retention after 6 months, compared with an equivalent ‘dose’ of continuous ER (Energy Restriction).
This makes sense. Do you think if I go back to 2 meals a day and increasing my calories just a bit would work. I’ve been OMAD for a while due to insulin resistance. But my insulin is down to 8.1 from 22, so I’m assuming my body could handle 2 meals a day for say a week or two and then drop back down to OMAD for a week or two. Maybe if my body is fed 2x a day it will feel like it’s not being starved but then I don’t have to drastically increase my calories. Thoughts?
Maybe try eating TMAD with a day or two of 24+ hours of water/salt fast a week. I actually seem to do better with this than I did with OMAD. I still OMAD some during the week just out of convenience, but try to throw in a couple of days with maybe even three meals a day to up the calories. You have to keep the body guessing or sometimes it will adapt.