Почему люди, нечувствительные к лептину не могут похудеть:
When someone is not responsive to the receptor signaling of leptin in the hypothalamus, they become unable to burn their excess calories off as pure heat so they remain overweight. They find it very difficult to lose the weight, even when they restrict calories to starvation levels. This will change when they become leptin sensitive once again.
Ну а то, как можно сжечь энергию в виде тепла рассказано вот тут по-русски: http://vvk.pp.ru/2013/02/23/why-is-oprah-still-obese-leptin-part-3/
Почему надо заканчивать кушать за 4-5 часов до сна:
The significance of the prolactin surge (especially in older people) is made clear if you eat carbs within 4 hours of going to sleep. Prolactin release is yoked to the dark/light conditions in most mammals. If you do not think prolactin is important for a natural sleep cycle watch this 4 minute TED video. It is also tied to NPY and to inflammatory cytokine signals in the brain. If you eat a large amount of carbs after dark it is spikes NPY, IL-6, TNF alpha, and raises sdLDL release at our liver. This has multiple effects on the system. The sdLDL blocks the ability of leptin to enter the hypothalamus at its evolutionary appointed time, 4 hours after you last eat or 4 hours after darkness falls. Il-6 and TNF alpha block the effects of leptin in the brain, liver and at muscles. The more carbs one eats, the higher NPY levels remain in the brain as well and this causes the carbohydrate cravings that most people report when they are leptin resistant.
We should now get back to discussing the neuro-humeral response of the brain to leptin; Timing is more critical than any other factor in the Leptin Rx. The reason for this is we are using multiple circadian cycles to reset the hypothalamus when it is flying blind due to brain inflammation at the receptor site. When we eat our last meal of the day as light levels begin to fall, leptin needs a minimum of four hours to be able to act on its receptor to signal the brain to our current energy status. The reason for this appears to be the biphasic insulin response from our last eaten meal, namely dinner. Any spike of insulin blocks the ability of leptin to enter the hypothalamus to give the brain this signal. This is why I tell you not to snack post dinner at all. Once leptin binds to the receptor, it then blocks dopamine’s control over the releasing factors in the pituitary. Pituitary prolactin secretion is regulated by dopamine to act on the dopamine-2 receptors Prolactin cells, causing inhibition of prolactin secretion. Once leptin binds, it blocks this inhibition and allows for prolactin to be released and to act to release growth hormone. Prolactin is the trigger for growth hormone release in humans. 90% of a humans growth hormone is released during sleep, if prolactin is allowed to act. Women in menopause have major prolactin releasing problems, and this is why they have sleep complaints, and why they get more belly fat at this point in their life. GH decreases abdominal fat while simultaneously increasing your lean muscle mass. It does this by increasing protein synthesis for renewal during autophagy. This is the hormone responsible for body composition in large part with the sex steroid hormones. If you have a bad body composition, you can bet that you have a leptin problem. This is why the mirror test works in most cases without testing. GH levels fall off a cliff for most women after age 40 (peri-menopause) and for men after age fifty. Any increase in inflammation for any reason generally makes menopause or andropause happen more quickly. When this happens, there is a corresponding drop in the quality of sleep as well the amount of autophagic repair. This is why I always ask a patient about sleep. It is a cardinal sign of a serious metabolic problem at the brain level. This reduction in autophagic repair is why people age and why disease increases as we age too. These biologic facts are widely reported in the literature. This is why older people tend to sleep less than younger people. It is also why babies sleep so long. They are growing and learning, and require more autographic repair as they trim all their newly laid down hard wired tracts. Babies release a ton of GH as they sleep to grow and evolve to get everything working optimally.
По поводу перепрограммирования нейронных путей контроля энергетической составляющей тела:
We can achieve leptin sensitivity after the hypothalamus is damaged, if we teach the brain how to use our older evolutionary non-leptin neural circuits. Yoking eating to light and day, and making timing to sleep and wakefulness and to the visceral sensations of distention of the gut via the vagus nerve are precisely how the Leptin Rx is designed to work. Taking full advantage of how certain macro-nutirents are tied to light cycle further helps reset hypothalamus in two to three months. The more inflammation that is present, the longer the reset may take. Instead of relying on optimal functioning of the hypothalamic leptin receptor, we can re-teach the hypothalamus to pay attention to the light levels, awakening time, time we sleep and face dark, when our gut is distended and filled with food and when it is not. We can also load the diet with protein and fat at certain times, to take full advantage of the existing working neural circuits in the brainstem and hypothalamus that accounts for carbohydrates, to our advantage in resetting how the brain can more fully perceive our energy status when the leptin receptor is not functioning. This science is precisely how a cochlear implant works in a neural deaf patient. It is not opinion, it is merely applying what we know works in one part of the brainstem, and using it another part using the natural circadian rhythms to allow the brain to re learn how to account for macronutrients correctly once again. It is also how neuroscientists have taught blind people to see using their tongue or tactile skin receptors to read (Paul Bach Y Rita work and braille as examples).
When the leptin receptor is not working well ,we can try to bypass it by using other neural pathways that leptin does also monitor but rarely uses any longer. This retraining allows the brain to relearn perception. The experiments of Dr. Merzenich cutting the median nerve completely and seeing the brain re map its sensory territory opened my eyes to this possibility.
When we eat meals, the sensation of physically eating is perceived by the vagus nerve. This nerve controls the entire GI tract down to the transverse mesocolon. It also monitors the hypothalamic parotid axis in the mouth that monitors carbohydrate contents in food in the mouth. This signal is an early detection system for the incretin gut hormone (ghrelin, PYY, CCK, agouti, glucagon) system that readies the gut for digestion. If one eats with a certain regularity (Leptin Rx) and makes sure it is tied to the sleep wake cycle, we can retrain the brain to account for food using older evolutionary pathways. The leptin receptor in the hypocretin neurons are newly adapted evolutionary speaking compared to the ones that rely on circadian signals. This has been demonstrated in Dr. LeCea’s work on sleep and leptin in narcolepsy. Leptin function, however, is found widespread in the animal kingdom, and has been used for long periods of time in evolution. The difference for humans today is how our neural circuitry has evolved to incorporate the leptin receptor for use in our brain to accounts for energy status. It appears we humans still have the “old wiring diagrams” in place, but we don’t use it these days because we evolved a “better” mechanism to account for food electrons from macronutrients. Moreover, it appears that today’s standard American diet causes a mismatch in how the currently evolved leptin receptor works over time. These new receptors are mismatched to our current diet and can cause our leptin receptor to fail when the signaling is overwhelmed with inflammation.
We are adapted to use the new system because of the positive reinforcement of these tracts from 0-6 years old. This hard wiring is not set in stone for a lifetime. But we rarely use it past this age. It becomes the preferred neural circuit because it is used chronically while the alternative pathways are not reenforced.
И к сожалению, я никак не могу найти статью, где я читала про большой завтрак у него на сайте... Очень грубо говоря, большое кол-во белка блокирует в мозге центры отвечающие за голод. Ну а насыщенный жир позволяет еде дольше перевариваться и оказывает протекторное действие на сосуды.
Из всего вышесказанного, очень краткое резюме:
Когда у тебя много жира, он выделяет туеву хучу лептина, в итоге организм становится к нему нечувствительным. Через 5-7 лет развивается инсулинорезистентность, далее метаболический синдром. Т.к. нейронные пути, которые мозг определил в возрасте 0-6 лет для регуляции твоего веса перестают работать из-за лептинорезистентности, можно показать ему другие пути, а именно - через корреляцию твоего режима со световым днём. Этот путь более древний (животные так живут постоянно), но такой же эффективный.
Углеводы могут нормально переноситься организмом в более длинные световые дни и при достатке витамина Д. Грубо говоря, если ты живешь на экваторе и загараешь - ты можешь больше есть фруктов и другий углей. Если ты где-нить в Эстонии зимой - переходи на жиры и белки. (кстати потребление вит Д в виде добавки так же эффективно)
Питаться надо 2-3 раза в день и НИКАКИХ ПЕРЕКУСОВ, потому что печень должна заново научиться сохранять и использовать сохраненные питательные вещества, пока ты не ешь или спишь.
Почему важно не есть за 4-5 часов до сна. Чтобы лептин начал вырабатываться в ответ на твой ужин должно пройти примерно 4 часа. Лептин блокирует ингибирование пролактина в мозге, т.е. начинает вырабатываться пролактин. Последний активирует выработку гормона роста (12-2) и работу щитовидной железы. Короче, запускается целый каскад реакций, которые поддерживают тебя молодым, здоровым, сжигают жир и растят мышцы. Но лептин блокируется инсулином, т.е. весь этот каскад обрубается на корню, если ты перед сном захаваешь что-нить сладкое. Ну а т.к. инсулин всётаки вырабатывается на любой прием пищи в том или ином кол-ве - лучше не перекусывать после 20:00.
Ещё могу добаивть, что нужен источник омега-3 жирных кислот. т.е. жирная рыба и морепродукты. И полное исключение гиброгенезированного растительного жира - маргарина. Так же нужно по максимуму убрать омега-6 ЖК (подсолнечное масло). В общем, жиры в рационе должны быть: животные (насыщенноые), растительные мононенасыщенные (оливковое масло, авокадо) и животные омега-3 (жирная рыба), при том именно животные омега-3, потому что растительные омега-3 (льняное масло) практически бесполезны для организма.