Relax. There is no need to get all testy and defensive. This topic is about leptin resistance, and the question of IF or not as a fix is legit. If Dr Kruse's practice for reversing leptin resistance doesn't sound like IF, then that's the way it is.
Originally Posted by Daemonized
The reason I stated that IF folks are out of control is because it is true! There is hardly any question on here about weight loss stalling or whatever where some amateur does not join in and start advocating IF as if it were some kind of magic bullet for everyone, no matter what. I'm interested in IF too, but I want to know some facts, like when it is appropriate, how long, and how often. The sites people are linking to are written by people who don't know what it's like to be working down from a very overweight condition. They are for fitness types looking to tune themselves up. What do these people know about being big and working their way down? They have only opinions.
I'm interested in Dr Kruse's info because he lost a lot of weight too. He's been there, done that. He's not some amateur skinny kid that pumped up and tells the world that IF is the magic bullet.
Funny, this way of eating seems familiar....
Originally Posted by js290
Here is the thread from yesterday.
Originally Posted by Robynbee
If you read through the comments on the Oprah post on his site, he responded to a comment I made about the eating within 30 minutes of waking up. There was a discussion here about that advice from Tim Ferriss in his new book about eating a bunch of protein within 30 minutes, but his book didn't address the science of that particular reasoning, just that it was important. So Dr. Kruse explains it in the comments on that post.
Originally Posted by Robynbee
Just a n00b
If you don't mind my asking, how much do you normally eat for each of your two meals? And what?
Originally Posted by Minxxa
in that same study posted:
They also show that animal-derived triglycerides impair leptin transport across the BBB, but not essential FFAs, plant-derived triglycerides, or milk proteins.
We directly tested the ability of triglycerides to inhibit leptin transport across the BBB. Three of four commercially available triglycerides (triolein, DPOG, and DSOG) inhibited uptake of I-Lep when injected intravenously at a dose that equaled the total triglyceride content of milk (Fig. 6A). A dose-response curve suggests that, at least in the case of triolein, lower doses are also effective. DMOG, the triglyceride that did not inhibit leptin transport, illustrates that the sn-1 position is important for the inhibitory effect. Myristate, as a medium-chain FFA, is only produced in by mammary alveolar cells; therefore, triglycerides containing it may not reflect diet or obesity (37). Additionally, it would not be expected to circulate in significant amounts in blood. These results suggest that leptin transport will be inhibited by triglycerides endogenous to blood.
These results show that serum triglycerides have a rapid and immediate effect on the transport of leptin. As such, they explain the inhibition in leptin transport seen with starvation. They also likely contribute to the inhibition seen with obesity. Triglycerides could produce their effect on leptin transport by binding leptin in the circulation or by acting directly on the leptin transporter. Other BBB transporters are known to be regulated by uncompetitive and noncompetitive mechanisms (38,39), and leptin transport is altered by α1-adrenergic agonists, glucose, and insulin (40,41). It may be that the leptin transporter possesses a regulatory site controlled by triglycerides.
These studies in wild baboons are consistent with the hypothesis that ancestral levels of leptin were much lower than those seen in Western civilization and that starvation was a more probable threat than obesity.Starvation-induced hypertriglyceridemia may have been so dominant an evolutionary pressure that leptin resistance induced by obesity-related hypertriglyceridemia was never selected against. Alternatively, it may be that the anorectic effect of leptin must be overridden to maintain an adequate intake of water-soluble vitamins, minerals, electrolytes, and other substances less efficiently stored than fat.
That Byron Mastering Leptin Guy explains this:
It is vital to create times during the day when small fat blobs, known as triglycerides, are cleared from your blood. If triglycerides build up during the day they physically clog leptin entry into your brain, causing leptin resistance ‚?? meaning that leptin cannot register properly in your subconscious command and control center. Your metabolism is not designed to deal with constant eating and snacking. Doing so confuses your metabolism and results in you eating much more than you really need. Eating too often is like a repetitive strain injury, like tennis elbow but in this case leptin elbow.
Yes, you are supposed to get a snack between meals ‚?? but it is supposed to come from your liver. This is how your body naturally clears triglycerides from your blood. Besides that fact that these fat blobs confuse leptin, they are also headed in the direction of your hips, thighs, and stomach. So breaking them down and clearing them out is vital, and this only happens when you allow 5-6 hours between meals. When you clear your circulatory highways of extra fat during the day then leptin works better. When you do a great job during the day then you are much more likely to break down and burn stored fat from your hips and thighs while you are sleeping.
Snacking turns out to be one of the worst things you can do. It doesn‚??t matter how many calories you snack on, when you snack you throw powerful hormonal switches that cause leptin to malfunction. The fictitious idea that snacking is needed to stoke your metabolism or maintain your blood sugar is in no small part behind dietary advice that has helped cause an epidemic of obesity.
Eating a protein rich breakfast can increase metabolism by 40 percentage preceding a meal, while a carbohydrate rich meal only increases it by about 5 %.
Why you should care about leptin resistance and such?
Cause leptin acts as the conductor in an orchestra, it coordinates the release of hormones like:
Thyroid hormones, growth hormones, Sex hormones, melatonin, etc. It also help to carry out immune system functions and to carry out rejuvenating sleep.
Effects of short-term carbohydrate or fat overfeed... [Int J Obes Relat Metab Disord. 2000] - PubMed result
There was no relationship between changes in leptin concentrations and changes in energy expenditure, suggesting that leptin is not involved in the stimulation of energy metabolism during overfeeding.
"In summary, the rapid decrease in serum leptin levels during fasting indicated that leptin release was regulated by factors other than changes in body fat mass. The lack of leptin changes during fasting, when basal insulin and glucose levels were maintained at basal levels, suggested that insulin and/or glucose may play a role in the regulation of leptin release."
Could you translate this? I'm not sure I get the reason this is here or where it came from.
Originally Posted by MalPaz