Трансцендентальная апперцепция

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#1

Непрочитанное сообщение Д.С. » 03 сен 2015, 09:29

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#551

Непрочитанное сообщение Д.С. » 19 сен 2016, 13:58

Reversal of obesity and insulin resistance by a non-peptidic glucagon-like peptide-1 receptor agonist in diet-induced obese mice.

Abstract
BACKGROUND:
Glucagon-like peptide-1 (GLP-1) is recognized as an important regulator of glucose homeostasis. Efforts to utilize GLP-1 mimetics in the treatment of diabetes have yielded clinical benefits. A major hurdle for an effective oral therapy has been the difficulty of finding a non-peptidic GLP-1 receptor (GLP-1R) agonist. While its oral bioavailability still poses significant challenges, Boc5, one of the first such compounds, has demonstrated the attainment of GLP-1R agonism in diabetic mice. The present work was to investigate whether subchronic Boc5 treatment can restore glycemic control and induce sustainable weight loss in diet-induced obese (DIO) mice, an animal model of human obesity and insulin resistance.
METHODOLOGY/PRINCIPAL FINDINGS:
DIO mice were treated three times a week with Boc5 (0.3, 1 and 3 mg) for 12 weeks. Body weight, body mass index (BMI), food intake, fasting glucose, intraperitoneal glucose tolerance and insulin induced glucose clearance were monitored regularly throughout the treatment. Glucose-stimulated insulin secretion, β-cell mass, islet size, body composition, serum metabolic profiles, lipogenesis, lipolysis, adipose hypertrophy and lipid deposition in the liver and muscle were also measured after 12 weeks of dosing. Boc5 dose-dependently reduced body weight, BMI and food intake in DIO mice. These changes were associated with significant decreases in fat mass, adipocyte hypertrophy and peripheral tissue lipid accumulation. Boc5 treatment also restored glycemic control through marked improvement of insulin sensitivity and normalization of β-cell mass. Administration of Boc5 (3 mg) reduced basal but enhanced insulin-mediated glucose incorporation and noradrenaline-stimulated lipolysis in isolated adipocytes from obese mice. Furthermore, circulating leptin, adiponectin, triglyceride, total cholesterol, nonesterified fatty acid and high-density lipoprotein/low-density lipoprotein ratio were normalized to various extents by Boc5 treatment.
CONCLUSIONS/SIGNIFICANCE:
Boc5 may produce metabolic benefits via multiple synergistic mechanisms and may represent an attractive tool for therapeutic intervention of obesity and diabetes, by means of non-peptidic GLP-1R agonism.

http://www.ncbi.nlm.nih.gov/pubmed/21151924
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#552

Непрочитанное сообщение Joker » 19 сен 2016, 14:04

Д.С. писал(а): dietary-induced obese mice
Д.С. писал(а): Вы спросите, в чем проблема? Главным недостатком этого исследования является то, что ученые пришли к выводам касательно ТМАО на основании экспериментов, проведенных на мышах.
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#553

Непрочитанное сообщение Д.С. » 19 сен 2016, 14:22

Взаимно, дорогая.

Lakshmi писал(а): Только я не знала ничего про базальный (что он высок у тех, у кого много жира). Помог случай и теперь я знаю причину своего плато.

tro*

Д.С. писал(а): Роль базальной секреции инсулина заключается в следующем: снижение базальной продукции печенью, снижение уровня глюкозы натощак, снижение уровня СЖК.

): http://www.rmj.ru/articles/obshchie-sta ... z4KJcARCbr
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#554

Непрочитанное сообщение Микулишна » 19 сен 2016, 14:23

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#555

Непрочитанное сообщение Joker » 19 сен 2016, 14:50

А при чем здесь роль базальной секреции инсулина? :mocking: Я прекрасно знаю его физиологическую роль, я не знала про то, что он высок у людей с лишним весом.
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#556

Непрочитанное сообщение Joker » 19 сен 2016, 14:56

Я вообще про то, что если уж приводится в качестве контраргумента тот факт, что исследование произведено на мышах, и в связи с этим, имеет серьезный недостаток, тогда надо вообще все "звериные" исследования поудалять и не признавать.
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#557

Непрочитанное сообщение Д.С. » 19 сен 2016, 14:58

Lakshmi писал(а): Я вообще про то, что если уж приводится в качестве контраргумента тот факт, что исследование произведено на мышах, и в связи с этим, имеет серьезный недостаток, тогда надо вообще все "звериные" исследования поудалять и не признавать.
Извини.
У меня ни уйха нет времени попи*деть Vala_32 ниочём.
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#558

Непрочитанное сообщение Joker » 19 сен 2016, 15:03

Д.С. писал(а): У меня ни уйха нет времени попи*деть Vala_32 ниочём.
А я и не собиралась с тобой пи*деть, откуда такие фантазии? :mocking:
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#559

Непрочитанное сообщение Camel1000 » 19 сен 2016, 15:11

Lakshmi писал(а): тот факт, что исследование произведено на мышах
Процентов так 90 биологиchеских знаний добыто на мышах, крысах, chервяках, мухах и бактериях. И сhто?
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#560

Непрочитанное сообщение Д.С. » 19 сен 2016, 15:14

Lakshmi писал(а):
Д.С. писал(а): У меня ни уйха нет времени попи*деть Vala_32 ниочём.
А я и не собиралась с тобой пи*деть, откуда такие фантазии? :mocking:
Отлично.

А по мышей спроси у Стоппани. Это он автор.
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#561

Непрочитанное сообщение Joker » 19 сен 2016, 15:17

Camel1000 писал(а): И сhто?

Ничего. Просто Дмитрий привел статью в теме про ТМАО под авторством некоего Стоппани (источник статьи не указан). И автор высказал мнение, что исследования, проведенные на мышах имеют серьезный недостаток из-за того, что они произведены на мышах. :mocking:
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#562

Непрочитанное сообщение Д.С. » 19 сен 2016, 15:21

В смысле интерполяции работы/влияния чего на людей без дополнительных исследований - да нельзя переносить.
Как биологические факты и связи "вообще" - ну да. Их есть.
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#563

Непрочитанное сообщение Д.С. » 27 сен 2016, 18:13

Книга только что вышла, так что сп--ть её неоткуда пока.

Buddha's Diet: The Ancient Art of Losing Weight Without Losing Your Mind
Авторы: Tara Cottrell,Dan Zigmond


Отзывы
This is one of those books about losing weight without losing your mind and that when we eat is as important as what we eat and its not at all hours of the day as we do in society today. How we have become complacent and out of sync with our bodies, what we eat should be nourishing, so stop filling your emotional void with food. Its about changing the time you eat, metabolism and your eating clock.
The authors focus on the Buddha's instructions not about what to eat (there's not much there, apparently), but on when to eat. While he told his monks and nuns only to eat between dawn and noon, the authors expand the idea to include a meal later in the day. What I found most helpful about this model of intermittent fasting was: the research they mention in support of it; a specific, step-by-step path from our current way of eating (all the time, especially after dinner) to a more condensed eating schedule; and how our approach to eating provides multiple opportunities to deepen our Buddhist practice. It's the best Buddhist book I've read this year.
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#564

Непрочитанное сообщение Д.С. » 27 сен 2016, 19:05

Новости от vladimirfo.

Opposing Effects of Fasting Metabolism on Tissue Tolerance in Bacterial and Viral Inflammation

In Brief
Starve a fever, stuff a cold: why anorexia
helps the organism to tolerate bacterial
infections but makes viral infections hard
to endure.

Изображение

В зависимости от патогена, необходима разная диета.
Если у нас бактериальная инфекция, то кетоны уменьшают урон нейронов от реактивных видов кислорода (ROS).

С вирусной инфекцией всё наоборот. Глюкоза необходима для защитной реакции организма на вирусные инфекции.

*************************
Ага, довольно короткое и точное описание того, что происходит.

Было две модели воспалительных процессов:
бактериальная - заражали листериями;
вирусная - заражали гриппом

Важно то, что для инициации кетоза (а точнее блокирования метаболизма глюкозы) использовали 2-deoxy-d-glucose (2DG), последняя молекула заслуживает отдельного упоминания в разрезе кето-диеты.

Делали так: в каждом модели давали и глюкозу, и 2DG (то есть и блокировали метаболизм глюкозы) и смотрели разницу - где что отличается.

Администрация 2DG напрямую блокировала расплод листерий и шло подавление эндотоксемии (присутствия эндотоксина LPS в крови).
Администрация глюкозы имела противоположный эффект.
Смотрели разницу - нашли в количестве мертвых нейронов в мозгах мышей.
Во время бактериальной инфекции производится много реактивных видов кислорода (ROS).
С помощью 2DG активировали транскрипторный фактор PPAR-alpha, который отвечает за вход в кетоз.
Кетоны действовали как ингибиторы деацетилазы гистонов (разновидность анти-эпилептиков и стабилизаторов настроения, на которые по действию похожи кетоны) и источник энергии, что позволяло клеткам и тканям адаптироваться к бактериальной инфекции.

По время вирусной инфекции ингибирование утилизации глюкозы было летальным (при классическом диетарном кето нет ингибирования утилизации глюкозы).
Вирусная инфекция приводит к стрессу эндоплазматического ретикулума (ER). Отсутствие утилизации глюкозы приводит к большему стрессу этого органоида и возможному адопоптозу (программе клеточной гибели).
Вирусные инфекции стимулируют unfolded protein response (UPR) отчасти через путь PERK-eIF2a-ATF4-CHOP. Когда этот путь активирован, то клетка может либо адаптироваться, либо активировать программу смерти (адопоптоз).
Утилизация глюкозы необходима при вирусных инфекциях для цитозащитной реакции в нейронах.
Отсутствие глюкозы во время вирусных инфекций приводит к пониженному пульсу, более редкому дыханию, более низкой температуре тела.
Глюкоза активно забирается мозгом после вирусной инфекции, но не после бактериальной.


Изображение
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#565

Непрочитанное сообщение Микулишна » 28 сен 2016, 09:00

То есть, если я сейчас в соплях (стопудовый вирусняк) - я должна трескать плюшки с конфетками? :mocking2:
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#566

Непрочитанное сообщение Д.С. » 28 сен 2016, 12:12

Микулишна писал(а):То есть, если я сейчас в соплях (стопудовый вирусняк) - я должна трескать плюшки с конфетками? :mocking2:
Нет.
Отнюдь.
Но навернуть овощей-фруктов... И ещё чё-нибудь с низким ГИ - да.
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#567

Непрочитанное сообщение Д.С. » 28 сен 2016, 13:22

50 Years Ago, Sugar Industry Quietly Paid Scientists To Point Blame At Fat

In the 1960s, the sugar industry funded research that downplayed the risks of sugar and highlighted the hazards of fat, according to a newly published article in JAMA Internal Medicine.

The article draws on internal documents to show that an industry group called the Sugar Research Foundation wanted to "refute" concerns about sugar's possible role in heart disease. The SRF then sponsored research by Harvard scientists that did just that. The result was published in the New England Journal of Medicine in 1967, with no disclosure of the sugar industry funding.


The sugar-funded project in question was a literature review, examining a variety of studies and experiments. It suggested there were major problems with all the studies that implicated sugar, and concluded that cutting fat out of American diets was the best way to address coronary heart disease.

The authors of the new article say that for the past five decades, the sugar industry has been attempting to influence the scientific debate over the relative risks of sugar and fat.

"It was a very smart thing the sugar industry did, because review papers, especially if you get them published in a very prominent journal, tend to shape the overall scientific discussion," co-author Stanton Glantz told The New York Times.

Money on the line


In the article, published Monday, authors Glantz, Cristin Kearns and Laura Schmidt aren't trying make the case for a link between sugar and coronary heart disease. Their interest is in the process. They say the documents reveal the sugar industry attempting to influence scientific inquiry and debate.

The researchers note that they worked under some limitations — "We could not interview key actors involved in this historical episode because they have died," they write. Other organizations were also advocating concerns about fat, they note.

There's no evidence that the SRF directly edited the manuscript published by the Harvard scientists in 1967, but there is "circumstantial" evidence that the interests of the sugar lobby shaped the conclusions of the review, the researchers say.

For one thing, there's motivation and intent. In 1954, the researchers note, the president of the SRF gave a speech describing a great business opportunity.

If Americans could be persuaded to eat a lower-fat diet — for the sake of their health — they would need to replace that fat with something else. America's per capita sugar consumption could go up by a third.


But in the '60s, the SRF became aware of "flowing reports that sugar is a less desirable dietary source of calories than other carbohydrates," as John Hickson, SRF vice president and director of research, put it in one document.

He recommended that the industry fund its own studies — "Then we can publish the data and refute our detractors."

The next year, after several scientific articles were published suggesting a link between sucrose and coronary heart disease, the SRF approved the literature-review project. It wound up paying approximately $50,000 in today's dollars for the research.

One of the researchers was the chairman of Harvard's Public Health Nutrition Department — and an ad hoc member of SRF's board.

"A different standard" for different studies

Glantz, Kearns and Schmidt say many of the articles examined in the review were hand-selected by SRF, and it was implied that the sugar industry would expect them to be critiqued.


In a letter, SRF's Hickson said that the organization's "particular interest" was in evaluating studies focused on "carbohydrates in the form of sucrose."

"We are well aware," one of the scientists replied, "and will cover this as well as we can."

The project wound up taking longer than expected, because more and more studies were being released that suggested sugar might be linked to coronary heart disease. But it was finally published in 1967.

Hickson was certainly happy with the result: "Let me assure you this is quite what we had in mind and we look forward to its appearance in print," he told one of the scientists.

The review minimized the significance of research that suggested sugar could play a role in coronary heart disease. In some cases the scientists alleged investigator incompetence or flawed methodology.

"It is always appropriate to question the validity of individual studies," Kearns told Bloomberg via email. But, she says, "the authors applied a different standard" to different studies — looking very critically at research that implicated sugar, and ignoring problems with studies that found dangers in fat.

Epidemiological studies of sugar consumption — which look at patterns of health and disease in the real world — were dismissed for having too many possible factors getting in the way. Experimental studies were dismissed for being too dissimilar to real life.

One study that found a health benefit when people ate less sugar and more vegetables was dismissed because that dietary change was not feasible.

Another study, in which rats were given a diet low in fat and high in sugar, was rejected because "such diets are rarely consumed by man."

The Harvard researchers then turned to studies that examined risks of fat — which included the same kind of epidemiological studies they had dismissed when it came to sugar.

Citing "few study characteristics and no quantitative results," as Kearns, Glantz and Schmidt put it, they concluded that cutting out fat was "no doubt" the best dietary intervention to prevent coronary heart disease.

Sugar lobby: "Transparency standards were not the norm"

In a statement, the Sugar Association — which evolved out of the SRF — said it is challenging to comment on events from so long ago.

"We acknowledge that the Sugar Research Foundation should have exercised greater transparency in all of its research activities, however, when the studies in question were published funding disclosures and transparency standards were not the norm they are today," the association said.

"Generally speaking, it is not only unfortunate but a disservice that industry-funded research is branded as tainted," the statement continues. "What is often missing from the dialogue is that industry-funded research has been informative in addressing key issues."

The documents in question are five decades old, but the larger issue is of the moment, as Marion Nestle notes in a commentary in the same issue of JAMA Internal Medicine:

"Is it really true that food companies deliberately set out to manipulate research in their favor? Yes, it is, and the practice continues. In 2015, the New York Times obtained emails revealing Coca-Cola's cozy relationships with sponsored researchers who were conducting studies aimed at minimizing the effects of sugary drinks on obesity. Even more recently, the Associated Press obtained emails showing how a candy trade association funded and influenced studies to show that children who eat sweets have healthier body weights than those who do not."


As for the article authors who dug into the documents around this funding, they offer two suggestions for the future.

"Policymaking committees should consider giving less weight to food industry-funded studies," they write.

They also call for new research into any ties between added sugars and coronary heart disease.
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#568

Непрочитанное сообщение Д.С. » 30 сен 2016, 10:36

Новости от vladimirfo

https://experiment.com/u/3f3C9gWhat did Dr. Owen and Dr. Cahill do? Why was this so important?

Объясняют исследование Оуэна и Кахилла в 60-х.
Брали больных ожирением и измеряли, чем питается из мозг сейчас и через 6 недель голодовки (вода + витамины + минералы).
Поставили катетеры на сонные артерии (через них снабжается мозг) и на яремную вену (кровь от мозга к сердцу) и меряли нутриенты.
Изначально мозг жирдяет поглощал в среднем 130 гр глюкозы в день.
Через 6 недель 1/3 глюкозы и 2/3 бета-гидроксибутирата (неудивительно).

Американский Институт Медицины это как-то извратил/перепутал и решил, что мозгу нужно 130 гр глюкозы в день.
И это стало одной из парадигм low-fat high-carb диеты.

**************
In the late 1960's, Drs. Oliver Owen and George Cahill did one of the fundamental experiments in brain metabolism. (Mea culpa-- I identified Dr. Owen as Robert Owen mistakenly, now corrected). They measured what the brain required, macronutrient-wise, and how much of it was needed per day. In particular, patients who were morbidly obese were hospitalized and placed on a zero calorie diet for six weeks for the purpose of weight loss. The patients received adequate hydration and vitamins and minerals, but that was all. Unsurprisingly the patients lost weight.

But what Owen and Cahill also did is now the stuff of legend. They catheterized both carotid arteries (the arteries that supply the brain with blood flow) as well as the jugular veins (that take blood away from the brain toward the heart). And they measured blood nutrient levels in both blood vessels to determine, from the differences in concentrations, what the brain actually extracted from the blood.

They found that the initial blood specimens, performed under the patients' usual dietary intake circumstances (high carbohydrate), demonstrated that the brain utilized about 130 grams of glucose per day.

After six weeks of fasting, they found that the patients were fine mentally and emotionally (they tested them in a variety of ways) but their brain now utilized about 1/3 of the glucose compared with before. 2/3 of the brain's needs were now supplied by betahydroxybutyrate, the principle blood ketone body.

In short the brain had adapted to starvation, the most basic of ketogenic diets, and was fine.

Their data, after publication, were immediately misinterpreted by the American Institute of Medicine to say that the brain required 130 grams of glucose per day. Of course, this is exactly what they did not show, as the brain functioned perfectly well with 2/3 of its nutrient supply delivered as ketone bodies.

Sadly (and still mysteriously to me) the AIM's misinterpretation took hold with the traditional dietary community of the time and became a foundation principle of the low fat (high carb) paradigm. It's only now that we're seeing cracks form in that foundation.

An interested supporter, in a comment, was good enough to provide the complete reference for those interested in reading the original classic. I was remiss in not providing the ref, so much thanks:

Owen, O.E., Morgan, A.P., Kemp, H.G., Sullivan, J.M., Herrera, M.G. and Cahill Jr, G.F., 1967. Brain metabolism during fasting. Journal of Clinical Investigation, 46(10), p.1589.
Doi: Brain Metabolism during Fasting*
O. E. Owen, A. P. Morgan, H. G. Kemp, J. M. Sullivan, M. G. Herrera, and G. F. Cahill Jr.
First published October 1, 1967
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#569

Непрочитанное сообщение Д.С. » 04 окт 2016, 12:40

Триметазидин.
http://medical-diss.com/medicina/farmok ... o-sindroma


5. Использование триметазидина в комплексной терапии метаболического синдрома способствует оптимизации энергетического обмена, оцениваемого по активности сукцинатдегидрогеназы лимфоцитов, и восстановлению структуры компенсаторно-приспособительных реакций.

6. Метаболические эффекты триметазидина у пациентов с метаболическим синдромом характеризуются снижением уровня инсулинорезистентности при увеличении концентрации инсулина и оптимизацией липидного обмена в виде позитивной динамики уровня общего холестерина и уменьшения содержания в крови холестерина ЛПНП.

Заключение

Метаболический синдром, распространенность которого в мировой популяции составляет до 24%, значительно повышает риск сердечнососудистой заболеваемости и летальности [138; 160; 172], что делает актуальным проблему его своевременной диагностики и лечения, позволяющим предотвратить манифестацию у пациентов заболеваний атеросклеротического генеза и сахарного диабета 2 типа [109; 137; 190].



Медицинские Диссертации http://medical-diss.com/medicina/farmok ... z4M6jpMgWM...
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#570

Непрочитанное сообщение Д.С. » 05 окт 2016, 11:41

Compared with higher carbohydrate intakes, lowcarbohydrate
diets (35– 41.4% energy) increased the loss of
body mass, BF, and percentage BF, even after control for energy
intake as a covariate in the regression analyses. The mean total
carbohydrate intake in the low-carbohydrate studies ranged from
79 –97 g, depending on the analysis. Typically, a carbohydrate
intake of 100 g will cause ketosis (1). These results support the
apparent metabolic advantage of low-carbohydrate, ketogenic
diets (104). The additional body mass change is not likely due to
water loss, because the duration of the diet periods (6 –24 wk)
was too protracted (5, 75, 92) and estimations of total body water
tend to be similar between low-carbohydrate and low-fat diets
after 2 wk (5). The similar results of the analyses on body mass
and BF also supports the concept that the effect on body mass of
low-carbohydrate diets is an effect on FM rather than on body
water. Feinman and Fine (104) argued that low-carbohydrate
diets increase the demands on protein and amino acid turnover
for gluconeogenesis. Because this process has a high energy cost,
it would increase the energy deficit for a given energy intake,
thereby supporting the theory of a metabolic advantage of lowcarbohydrate
diets. In contrast, Buchholz and Schoeller (105)
averaged the results of 10 studies and reported no effect of lowcarbohydrate
diets on 24-h energy expenditure. However, none
of the studies they cited involved ketogenic diets, and most of the
studies were conducted with subjects in energy balance. A hypocaloric,
ketogenic diet would be expected to increase the demand
for gluconeogenesis because of the low energy and carbohydrate
availability. In contrast to this hypothesis, Brehm et al (4)
reported no differences in total energy expenditure when a lowcarbohydrate
diet was compared with a low-fat diet. However,
total energy expenditure was estimated rather than directly measured
with the use of a whole-body calorimeter or doubly labeled
water. Future research should focus on the effects of lowcarbohydrate
diets on energy expenditure with the use of these
measurement tools.

Effects of variation in protein and carbohydrate intake on body mass
and composition during energy restriction: a meta-regression1–3. February 2006
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#571

Непрочитанное сообщение Д.С. » 05 окт 2016, 22:01

Parsley & Cilantro Remove Heavy Metals, Here’s What They Didn’t Tell You

Хм.. в петрушке и кинзе уже могут быть тяжелые металлы из почвы. (Думаю, с морской всякой травкой может быть то же самое, нужны сертификаты)

More Strategic Ways To Remove Heavy Metals From The Body
Apple cider vinegar ё//* is a powerful and beneficial heavy metal chelator. It contains acetic acid which is known to detoxify heavy metals effectively and quickly. It’s a stronger solution than parsley or cilantro but you can dilute ACV in water and make it a consistent daily action to remove heavy metals.

Make sure that your magnesium levels are adequate when doing any heavy metal detoxification protocol. Magnesium plays an important role in relaxing the body, nerves and arteries to allow for detoxification and removal to take place. Magnesium is a detoxification supporting mineral in and of itself as well. I always have a natural calm magnesium supplement on hand. Over 80% of the population is deficient in magnesium so having a good all natural pure magnesium supplement on hand is beneficial for many reasons.

Essential oils can also be beneficial in the detoxification process to remove heavy metals. Thankfully doterra has certified pure therapeutic grade cilantro essential oil. Essential oils such as this one from doterra (which is pure) are void of heavy metals because an essential oil is only the chemicals from the plant, not the actual contents. The plant chemicals that benefit heavy metal detoxification are in this essential oil, but void of the heavy metals.

Make sure to keep your magnesium levels high by eating plenty of organic green veggies, cacao is a great source also. Take plenty of vitamin C rich foods as this benefits the heavy metal detoxification process also. Drink plenty of water and use apple cider vinegar diluted in water along with a few drops of cilantro essential oil each day to see both short and long term heavy metal detoxification benefits.

I hope you found this article informative, educating and makes you think twice about using only parsley and cilantro to detoxify heavy metals.
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#572

Непрочитанное сообщение Д.С. » 05 окт 2016, 22:29

Aluminum Protection Protoc
Aluminum Protection Protocol

Here are 5 foods to include in your diet that will not only nourish the body, they detoxify heavy metals like mercury and aluminum:

Cilantro a Wonderful Aluminum Detoxifier

“We found that cilantro accelerated the elimination of mercury, lead and aluminum thru the urine. If given before mercury filling removal procedure the mercury can be eliminated in 2 to 3 weeks by giving cilantro four times a day.” Omura et al 1995

1. ALA

2. Apples and other fruit with Malic ac

3. Garlic

4. Hungarian Peat *** (See Hungarian Peat Protocol)

5. Cilantro (See Cilantro Protocol)

6. Ginger

7. Iodine (See Iodine Protocol)

8. Magnesium (See Magnesium Protocol)

9. Malic Acid (See Malic Acid Protocol)

10. MSM (See MSM Protocol)

11. Silica (See Silicon Protocol)

12. Sulfur


Чтобы посмотреть протоколы нужно быть членом cb6a6 .
Vitamin C (See Vitamin C Protocol)
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#573

Непрочитанное сообщение Vetchinka » 05 окт 2016, 22:33

Все тайцы юзают эти дезодоранты-кристаллы из оксида алюминия. Я привозила, да раздарила ... ;)
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#574

Непрочитанное сообщение Д.С. » 05 окт 2016, 22:38

Vetchinka писал(а):Все тайцы юзают эти дезодоранты-кристаллы из оксида алюминия. Я привозила, да раздарила ... ;)
А у мамы алюминиевую посуду изъяла?! db3*
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#575

Непрочитанное сообщение Vetchinka » 05 окт 2016, 22:44

Д.С., западло им такой пользоваться ;) чугун наше все ;)
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