Skipping breakfast means you’ll eat LESS, not more
Is it a good idea to eat breakfast every morning if you want to lose weight? This is an extremely common claim when it comes to dieting. The idea is that you’ll get so much hungrier if you skip breakfast that you’ll eat more throughout the day. But this claim lacks reasonable scientific support, and is at best based on inconclusive questionnaire studies.
A recent well-designed interventional study showed that skipping breakfast means you’ll eat less throughout the day. A similar previous study showed the same thing.
Skipping a meal generally means you’ll eat less food. Hardly surprising, or what do you think?
New Study: A Low-Carb Diet and Intermittent Fasting Beneficial for Diabetics!
But that's just me!
I try not to skip breakfast because I've found that I don't really "wake up" until I've eaten something, hence I get NOTHING done until I have food in the morning. Eating for me is about having energy to do stuff. I have problems with low blood sugar (although less now than they were) so my metabolism always needs a little kick in the morning to get going.
I've stopped worrying about reaching some specific weight--I want to feel good and do the stuff that I want to do. If my ideal energy/happiness/productivity level means I'm heavy for the rest of my life, so be it.
Today I was up at 04:45, my egg/butter breakfast at 06:30, lugging a heavy camera around a film set all day and running around like crazy to get things done on time, home at 6pm (early finish!) and not particularly hungry. And plenty of energy too, so certainly not starving.
So maybe it is related to what you eat and/or your current keto state?
On standard diet, I was feeling pretty bad when skipping breakfast.
Morning I drink a rich coconut milk coffee blended that keep me full until 1pm, light dinner at 6pm. That's it.
So yes, LCHF + breakfast skipping = eating less
I have lost 20 lbs in 3 weeks! I am just on the start of my weight loss journey and I never expected it to be so easy. When I think of all the diets I have tried over the years, I feel like I have come home.
As always, biology is all about rates. Someone with surplus fat should be able to produce energy (release fat from adipose tissue) at a sufficient rate for sedentary life. Otherwise, if fat metabolism is impaired, they may develop an energy deficit and ravenous hunger at or before lunch and eat way too much. (People panic eat when they sense food shortage.) If the activity level during the day is higher, thereby raising the rate of energy demand, I expect a dietary source of food might be required to keep the rate of fuel availability (stored fat release rate + ingestion rate) at or above the rate of energy demand.
I would also expect that once one's percent body fat is much lower, energy from stored fat would be made available at a slower rate. Therefore the first ten pounds is easier to burn off than the last extra ten pounds. So for someone who is thin, eating some fat at breakfast may be a good idea, as the activity burn rate is more likely to exceed the aggregate release rate from adipose tissue. I would expect hunger to be a good guide, unless appetite signalling has been distorted by high-carb eating.
But I seem to be less hungry during the evening. I'm actually losing weight (maybe because I don't go out and have less beer).
In the summer, I bike outdoors for several hours every morning and never have breakfast before cycling. I truly love the ketogenic lifestyle.
(We all know that calories are rather meaningless, right?)
But I do find that if I eat my low carb porridge (my own mix) at about 09h30 in the morning, that I just cannot manage lunch except for my protein shake.
From the many articles it seems no clesr eidnc or conclusions as of now!
Remember when 6 meals and low fat was the gospel according to so called experts?
Now heevidence seems to support various versins of intermittent fasing and of curse low to no carbs and eating lots of the formerly shunned anima fats and avoiding the man made high omega 6 oils like corn, soy, etcetera
My opinion is twice a day in the AM and PM may prove optimal. Add to high animal fat and low carbs seems to produce optimal or more optimal biomarkers.
Cn some fr of intermittent fasting be addd? Who knows! Maybe?
Maybe alternate days for protein to induce autophagy? Maybe not as HFLC diets that are ketogenic also increse autophagy BUT is it the exact same biologica;l path? isthere a synegistic effect? Place your bets via what you eat and when and how and hope to see you in a thousand years. Eric
Combining mutants results in 5-fold lifespan extension in C. elegans
Research highlights possibility of combination therapy for aging
What are the limits to longevity? New research in simple animals suggests that combining mutants can lead to radical lifespan extension. Scientists at the Buck Institute combined mutations in two pathways well-known for lifespan extension and report a synergistic five-fold extension of longevity in the nematode C. elegans. The research, done at the Buck Institute and published online in Cell Reports on December 12, 2013, introduces the possibility of combination therapy for aging and the maladies associated with it.
The mutations inhibited key molecules involved in insulin signaling (IIS) and the nutrient signaling pathway Target of Rapamycin (TOR). Lead scientist and Buck faculty Pankaj Kapahi, PhD, said single mutations in TOR (in this case RSKS-1) usually result in a 30 percent lifespan extension, while mutations in IIS (Daf-2) often result in a doubling of lifespan in the worms – added together they would be expected to extend longevity by 130 percent. "Instead, what we have here is a synergistic five-fold increase in lifespan," Kapahi said. "The two mutations set off a positive feedback loop in specific tissues that amplified lifespan. Basically these worms lived to the human equivalent of 400 to 500 years."
Kapahi said the research points to the possibility of using combination therapies for aging, similar to what is done for cancer and HIV. "In the early years, cancer researchers focused on mutations in single genes, but then it became apparent that different mutations in a class of genes were driving the disease process," he said. "The same thing is likely happening in aging." Kapahi said this research could help explain why scientists are having a difficult time identifying single genes responsible for the long lives experienced by human centenarians. "It's quite probable that interactions between genes are critical in those fortunate enough to live very long, healthy lives."
Former Buck postdoctoral fellow Di Chen, PhD, now an associate professor at the Model Animal Research Center, Nanjing University, China, lead author of the study, said that the positive feedback loop (DAF-16 via the AMPK complex) originated in the germline tissue of worms. The germline is a sequence of reproductive cells that may be passed onto successive generations. "The germline was the key tissue for the synergistic gain in longevity – we think it may be where the interactions between the two mutations are integrated," Chen said. "The finding has implications for similar synergy between the two pathways in more complex organisms."
Kapahi said ideally the research would move into mice as a way of determining if the lifespan-extending synergy extends into mammals. "The idea would be to use mice genetically engineered to have suppressed insulin signaling, and then treat them with the drug rapamycin, which is well-known to suppress the TOR pathway."
Other Buck Institute researchers involved in the study include Patrick Wai-Lun Li, Emma Lynn Thomas, and Simon Melov. Other contributors include Benjamin A. Goldstein and Alan Hubbard from the School of Public Health, University of California, Berkeley and Waijiao Cai, from the Institute of Traditional Chinese and Western Medicine, Huashan Hospital, Fudan University, Shanghai. The work was supported by the National Institutes of Health (P30AG025708)( RO1AG038688), (RL1AAG032113) and (3RL1AG032113-03S1); the American Federation for Aging Research and the Hillblom Foundation.
Citation: "Germline Signaling Mediates the Synergistically Prolonged Longevity by Double Mutations in daf-2 and rsks-1 in C. elegans"; publishing online December 12, 2013 in Cell Reports.
You do not need rapamycin, Eric, LCHF does it as well and in continuos, natural way.
Epilepsia. 2011 Mar;52(3):e7-11. doi: 10.1111/j.1528-1167.2011.02981.x. Epub 2011 Mar 3.
The ketogenic diet inhibits the mammalian target of rapamycin (mTOR) pathway.
McDaniel SS, Rensing NR, Thio LL, Yamada KA, Wong M.
Department of Neurology and the Hope Center for Neurological Disorders, Washington University School of Medicine, St Louis, Missouri 63110, USA.
The ketogenic diet (KD) is an effective treatment for epilepsy, but its mechanisms of action are poorly understood. We investigated the hypothesis that the KD inhibits mammalian target of rapamycin (mTOR) pathway signaling. The expression of pS6 and pAkt, markers of mTOR pathway activation, was reduced in hippocampus and liver of rats fed KD. In the kainate model of epilepsy, KD blocked the hippocampal pS6 elevation that occurs after status epilepticus. Because mTOR signaling has been implicated in epileptogenesis, these results suggest that the KD may have anticonvulsant or antiepileptogenic actions via mTOR pathway inhibition.
Both studies cited looked at energy intake after one meal (or skipping the meal) which tells you virtually nothing about the long-term effects and potential compensatory reactions by the body. There was some data on the remainder of the day and intake, but again, we don't really care what happens in one day, we want presumably want to know what happens over time, which these studies don't address.
Even on SAD, even at my heaviest, I never really wanted to eat in the morning. That should have been a major clue to my insulin-resistant brain: never hungry after my longest (sleep-imposed) fast. I was burning fat and had no shortage. As soon as I did eat, whether it was forced morning breakfast or snack/lunchtime carbs, it was off to the races.
Out in the world, I'm always hearing others complain "Maaan, I just had a bagel/donut/Danish/etc 2 hours ago and I'm already starving again!" I remember what feeling "hangry" is like, but it's a bit amusing now that I'm in my 3rd year of one-meal-per-day IF + moderate LCHF & can go all day without food pretty much effortlessly. I do think overall intake normalizes over time, though--that one meal is definitely a BIG meal!
@ Rozzy. How can leaving breaking your overnight fast until a few hours later be a starvation diet?
Might work for some but not all. Everything should be tailored to the individual you are working with.
Do you think that I'm less hungry because I'm burning more body fat and that skipping breakfast is causing ketosis? I don't have a scale right now, so I can't monitor my weight that well. I lost 25 pounds on LCHF and will only eat LCHF, but I started plateauing a few months ago and then gained a few pounds back recently. I decided to start skipping breakfast because I needed to try something to start losing weight again.
Since going LCHF one year ago I have settled into no breakfast, eat when I am hungry and lost all the extra pounds I was carrying around. Plus the usual side effects of feeling great, almost super human.
Poor lady sitting next to me on the plane has Cheerios and a banana everyday and was overweight and complaining of memory loss from her Statins. I was eating bacon and eggs, I don't think I could have convinced her that what I was eating was healthier. She had been brainwashed all those years with advice from the pharmacy, USDA, and grocery manufacturers.
The day will come, too many people are starting to see the benefits of LCHF. I am shouting from the rooftops! Some people listen, some don't.
I eat between noon and 8 p.m. and eat about 1600 cal/day. Before I started this schedule I was eating around 1850/day, which is too much for me to lose weight. I had some difficulty adjusting to the change at first, but now I don't even think about food before noon. The desire to overeat always hits at night, so stopping my eating at 8 p.m. keeps me out of the danger zone. I'm also testing higher ketones as a result of the extended fast.
This whole "breakfast is the most important meal of the day" nonsense is more-or-less a junk-science ploy by Big Cereal to sell us fortified sugar pellets.
Bjarte - Team Diet Doctor