Красное мясо убивает

Original Message From: "Виктор" <vict***@p*****.ru>

Интересно, что замена птичьим мясом лучше чем замена овощами.
Непонятно правда как там заменяли и насколько...

---------Судя по "средним дозировкам" всё сводится к рекомендации Майи
Плисецкой - "жрать надо меньше".

"Нехватка красного мяса в рационе вызывает депрессию у женщин"
http://science.compulenta.ru/668121/

19 марта 2012г. 23:24 пользователь Виктор <vict***@p*****.ru> написал:

Красное мясо и птицу не ем 17 лет, и никаких депрессийю

С уважением, Ольга

To: science.news.bessmertie <privatmemb***@y*****.com>
Sent: Wednesday, March 21, 2012 11:20 PM

"Нехватка красного мяса в рационе вызывает депрессию у женщин"
http://science.compulenta.ru/668121/

19 марта 2012г. 23:24 пользователь Виктор <vict***@p*****.ru> написал:

Original Message From: "Privatmember" <privatmemb***@y*****.com>

:-) Разумеется не у всех и по разному выражено, просто заметили связь
статистическую.
Может это временный эффект отмены, если в ходе эксперимента их просили не
сть, а они если до этого.

"Stas AV" написано 22.03.2012 11:26:46:

В переходный период, пока организм перестраивается, возможно, у кого-то и бывает,
но это же временно.
У алкоголиков после лишения дозы тоже депрессии возникают, однако ;-)
Не ем мясо (птицу, рыбу) и все продукты животного происхождения (яйца, молочное)
с 2008 года,
полёт отличный, настроение прекрасное, какие уж там депрессии...
Чаще замечаю беспричинные агрессии, депрессии у моих коллег, любителей покушать
мясо.

Очередная страшилка, для тех, кто доверяет кому угодно, только не своему родному
любимому организму, IMHO.

С Уважением,
Дмитрий

Дмитрий, завидую ;-). А как принимаете В12, сколько, в какой форме? Вычитала
на пабмеде, что можно и таблетки, схема описана, я уже на поддерживающей дозе
1 раз в месяц по 2000 микрограмм (4 шт. про 500). И что ещё надо: из витаминов
В, Д, К ?

Со спасибом и уважением Ольга

To: science.news.bessmertie <privatmemb***@y*****.com>
Sent: Monday, March 26, 2012 10:31 AM

"Stas AV" написано 22.03.2012 11:26:46:

В переходный период, пока организм перестраивается, возможно, у кого-то и бывает,
но это же временно.
У алкоголиков после лишения дозы тоже депрессии возникают, однако ;-)
Не ем мясо (птицу, рыбу) и все продукты животного происхождения (яйца, молочное)
с 2008 года,
полёт отличный, настроение прекрасное, какие уж там депрессии...
Чаще замечаю беспричинные агрессии, депрессии у моих коллег, любителей покушать
мясо.

Очередная страшилка, для тех, кто доверяет кому угодно, только не своему родному
любимому организму, IMHO.

С Уважением,
Дмитрий

-------Господа, а не проще ли иногда, в умеренном количестве, кушать (с
удовольствием) это самое страшное мясо?!

Опасаюсь, что пищеварение перестраивается, и мясо становится слишком крепким
орешком. Т.е., или регулярно, или ни гу-гу.

Со спасибом и уважением Ольга

To: science.news.bessmertie <privatmemb***@y*****.com>
Sent: Monday, March 26, 2012 11:13 AM

-------Господа, а не проще ли иногда, в умеренном количестве, кушать (с
удовольствием) это самое страшное мясо?!

Мясо поди тоже собственного производства на собственного производства
кормах? ;-)

---------К сожалению нет. Животноводство, в отличие от растениеводства,
слишком порабощает "хозяина". От скотины никуда не уедешь. И кушать она
хочет каждый день.
Но, во первых, я беру мясо не в супермаркетах, где красиво
подсвеченные брусочки хрен знает чего, а в небольших ларьках, которые
имеют постоянных поставщиков здесь же в районе (и постоянных покупателей),
во-вторых, беру там очевидно куски животного - с костями,
кусочками шкуры и сала, при наличии тут же всех остальных "деталей" от
сердца до гонад....
Наконец, в третьих, красное мясо составляет постоянный элемент
питания, но весьма редкий - мы едим его прибл. 3 - 6 раз в месяц...
---------Изредка бывает возможность купить мясо непосредственно в деревне,
где наша "фазенда". Там я хорошо вижу, чем питаются бычки на соседних
лугах, да и, так или иначе, знаю их хозяев.

----------Согласитесь, здесь что-то не то. Своим выбором мы ограничиваем
свои будущие возможности!?
Может просто регулярность сделать с большим периодом, чтобы всё же
не грохать значимую часть своих ферментных систем?

Так ведь ферменты, которые нужны для того, что я ем (овощи, фрукты, бобовые,
зерновые, кефир, яйца) , синтезируются нормальною Только неиспользованные мудрый
органон перестаёт выдедять - заче зря стараться.

Со спасибом и уважением Ольга

To: science.news.bessmertie <privatmemb***@y*****.com>
Sent: Monday, March 26, 2012 11:52 AM

----------Согласитесь, здесь что-то не то. Своим выбором мы ограничиваем
свои будущие возможности!?
Может просто регулярность сделать с большим периодом, чтобы всё же
не грохать значимую часть своих ферментных систем?

----------Так и я про то же. Если что-то существенное вы не едите долго,
атрофируются системы, обеспечивавшие производство нужных для этого
ферментов (может и не совсем, но "раскрутить" их производство по новой
будет сложно и долго). Т.е. ваши ресурсы выживания ограничиваются в связи
со специализацией. А уж надо ли это вам - выбор ваш!.

<Sergei.Lubars***@k*****.ru> написано 26.03.2012 16:14:50:

Да, похоже, что крупы не являются видовым питанием человека. По ощущениям
тяжеловатая пища. Скорее, как запасной вариант, в пророщенном виде. Мне кажется,
что "основанием" пирамиды питания должны быть овощи (и фрукты). Очень хорошо
усваиваются, питательны и вкусны. Я ещё люблю орехи, семена подсолнечника,
тоже дают много энергии, если сырые и замоченные (опять же по своим ощущениям).

Вы не слишком верите в возможности своего организма. Если уж так случится, (тьфу
3 раза :)
что придётся выживать в местности, где кругом валяются дымящиеся колбасы, шашлыки
и бифштексы, а яблони и всё растительное выгорит на годы, то в конце концов
всё раскрутится, пусть даже сложно и долго.
Только стоит ли расширять ресурсы выживания организма на всякий случай,
регулярно "подтравливая" его тяжёлой и токсичной пищей?
"надо ли это вам - выбор ваш!"
Если я после 40 лет потребления мясного рациона без особых проблем
перестроился на растительный (перестроив ферментативную систему),
значит я могу без особого беспокойства ещё 40 лет так питаться,
не утратив полностью возможности вернуться обратно в случае форс-мажорных
катаклизмов. А там посмотрим.
А мясо - оно невкусное по сравнению с яблоком, уж поверьте человеку,
который действительно пробовал оба варианта.
;-)))

С Уважением,
Дмитрий

-------именно...(по ощущениям)!

дымящиеся колбасы, шашлыки и бифштексы, а яблони и всё растительное
выгорит на годы, то в конце концов всё раскрутится, пусть даже сложно и
долго.

-------Думаю, в моём случае раскручиваться будет тяжело, долго и не без
последствий.

-----На самом деле ресурсы пластичности организма не беспредельны, и есть
работы, где показано, что возврат не всегда прост и возможен в полной
мере.

-----------Поверьте человеку, который любит и умеет готовить и мясо, и
рыбу, и фрукты-овощи, и печенья-тортики - всё это вкусно, если хорошо
приготовлено из НАТУРАЛЬНЫХ продуктов и в меру (и в разумных сочетаниях).
Я обожаю шашлыки, но едим мы их максимум 3-4 раза в год.
----А вот курочка в собственном соку с гарниром из морковки, лука (можно
порея) и яблок - ММММММММММММММММММММ!

Tue, 27 Mar 2012 12:34:51 +0400 (MSD) от <Sergei.Lubars***@k*****.ru>:

Верю, конечно, сам был точно таким же в прошлой жизни :-)
А вы никогда не задумывались, сколько времени в жизни вы тратите на приготовление
блюд?
Даже если в сутки в среднем тратить только полчаса, то несложно подсчитать,
что за 10 лет вы "отработали" на кухне 5 месяцев по 12 часов.
А за 30-50 лет? Уже годы. А ведь это время можно было бы потратить более гармонично?
Неудивительно, что люди предпочитают травиться в общепите (рестораны, кафе, столовые),
либо покупая полуфабрикаты неизвестно кем приготовленные, т.е. приготовленные
не самим себе, а кому-то другому.

С Уважением,
Дмитрий

то несложно подсчитать, что за 10 лет вы "отработали" на кухне 5 месяцев
по 12 часов. А за 30-50 лет? Уже годы. А ведь это время можно было бы
потратить более гармонично?

приготовленные, т.е. приготовленные не самим себе, а кому-то другому.

--------Вы посчитайте ещё, сколько потрачено времени на сон.... И всегда
ли сэкономленное время идёт на "добрые дела" И потом - если приготовление
себе-любимому и близким является творческим процессом, то это отнюдь не
потеря времени......
---------Про общепит "вопросов нет"!!!

Здравствуйте, Sergei.
Good morning, afternoon, evening, Sergei.
Thursday, March 29, 2012
Вы писали 26 марта 2012 г., 14:35:41:
You wrote 26.03.2012, 14:35:41:

Атрофируются и в дальнейшем могут уже никгда не
выйти на прежний уровень.

--
Абсолютная истина, рождаясь в споре, часто умирает потом со смеху...

С уважением, Кондратьев Сергей.
Sincerely yours, Kondratiev S.V.
Thursday, March 29, 2012 mailto:kon***@a*****.ru

Отбросил (может, на время отодвинул, время покажет) все заморочки с БАДами
по причине:
1) к сожалению (не уверен, может и к счастью ;-) в нашем небольшом городе
(в Казахстане) доставать (и особенно на регулярной основе) рекомендуемые
БАДы как-то очень проблематично;
2) попробовав натуральное питание (4-й год сыроедение),
получил потрясающие результаты, которые переворачивают ВСЕ представления
о медицине, здоровье, молодости.
3)учёный мир очень часто меняет своё мнение, сегодня ставит "+", завтра "-",
и БАДы не исключение.

Тем не менее тема БАДов остался у меня под вопросом (но не отрицанием).
В наборе "Бессмертных" есть "солнце, воздух, вода, движение, и желание быть
молодым всегда". Но этим надо заниамться. Заниматься всю жизнь, что я и делал
с юности и по сей день, спасибо мне :-) Как это ни странно, "желание быть
молодым всегда" у меня было ещё школе :-))) Теперь я ещё добавил
натуральное питание. Взвесив все "за" и "против" я пришёл к выводу, что методы
натуропатии (солнце, воздух, вода, движение, натуральное питание) продуктивнее
и безопаснее БАДов.
Это, конечно, моё личное мнение, основанное на моих ощущениях.
В общем, у меня всё просто:-)

С Уважением,
Дмитрий

Mon, 26 Mar 2012 01:47:13 -0700 (PDT) от Privatmember <privatmemb***@y*****.com>:

бывает,

Кстати *0,1 таб.* LEF MIX содержит 100% RDA ~6мкГ витамина B12 в трёх
разных формах.
Усваивается В12 у многих далеко не радужно.
И я не слышал, что бы водорастворимые витамины значимо депонировались, то
есть принимать их раз в месяц - совршенно неразумнно по двум причинам.

Стас, почитайте:
http://www.ncbi.nlm.nih.gov/pubmed/16585128

http://www.ncbi.nlm.nih.gov/pubmed/21600388

http://www.ncbi.nlm.nih.gov/pubmed/19900336

Со спасибом и уважением Ольга

To: science.news.bessmertie <privatmemb***@y*****.com>
Sent: Monday, March 26, 2012 11:59 AM

Кстати *0,1 таб.* LEF MIX содержит 100% RDA ~6мкГ витамина B12 в трёх
разных формах.
Усваивается В12 у многих далеко не радужно.
И я не слышал, что бы водорастворимые витамины значимо депонировались, то
есть принимать их раз в месяц - совршенно неразумнно по двум причинам.

На что именно обращать внимание, какие выводы?

Я ошибся, В12 - видимо единственный водорастворимый витамин, который
депонируется.

То есть его получается можно шамкать и раз в 2 недели.

General Information

Chemistry

Vitamin B12 (cobalamin, Cbl) is a water-soluble vitamin and a member of a
family of related molecules

known as corrinoids which contain a corrin nucleus made up of a
tetrapyrrolic ring structure. The centre

of the tetrapyrrolic ring nucleus contains a cobalt ion that can be attached
to methyl, deoxyadenosyl-,

hydroxo- or cyano- groups.

Natural occurrence

Vitamin B12 originates from bacteria, fungi and algae, and is present in
virtually all animal tissues. Plants

contain no vitamin B12 beyond that derived from microbial contamination.

Occurrence in food, food supplements and medicines

Major dietary sources of vitamin B12, mainly in the forms of methyl,
deoxyadenosyl- and

hydroxocobalamin, include meat (e.g. 0.1 mg/kg in lamb), particularly liver
( 0.1 mg/kg) and fish (e.g.

0.03-0.1 mg/kg in salmon, 0.01-0.03 mg/kg in tuna). Hydroxocobalamin and, in
particular, cyanocobalamin

are synthetic forms used in vitamin supplements, pharmaceuticals and in the
fortification of food. Methyl

cobalamin has been used therapeutically outside the UK, for example, in
Japan.

Recommended amounts

The RNI for vitamin B12 in adults in the UK is 0.0015 mg/day (COMA, 1991).
There is no increment

required during pregnancy but there is a recommended increment of 0.0005
mg/day for breast

feeding mothers.

Analysis of tissue levels and vitamin B12 status

Measurement of vitamin B12 in plasma is routinely used to determine
deficiency, but may not be a reliable

indication in all cases. In pregnancy, for example, tissue levels are normal
but serum levels are low.

Various other plasma markers have been identified (including methylmalonic
acid, homocysteine,

holotranscobalamin, anti-intrinsic factor antibodies) and methods devised
(Schilling test, cobalamin

absorbance test, serum gastrin deoxyuridine suppression test) to distinguish
different causes of deficiency.

Brief overview of non-nutritional beneficial effects

Results of studies in humans have suggested that large doses of vitamin B12
(particularly methyl

cobalamin) may influence biological rhythms and thus may be beneficial in
the treatment of sleep

disorders. Vitamin B12 has also been reported to increase light sensitivity
by affecting melatonin

secretion. Vitamin B12, in combination with folic acid, has been suggested
to be beneficial in certain

disorders, such as idiopathic osteoarthritis and vitiligo.

Expert Group on Vitamins and Minerals 2003

93

Risk Assessment Vitamin B12 1

Function

Vitamin B12 serves as a cofactor to at least two enzymes, methionine
synthase and methylmalonyl

CoA mutase. Methionine synthase is pivotal in one-carbon metabolism, being
crucial in the synthesis

of the universal methyl donor S-adenosyl methionine and in the cellular
import and metabolism of

folate. Methylmalonyl CoA mutase converts L-methylmalonyl CoA to succinyl
CoA and is important

in even-chained fatty acid synthesis.

Deficiency

Dietary deficiency is rare in younger people living in the community but
occurs more frequently in older

people, particularly those living in institutional environments. Individuals
adhering to vegan diets may

also be at risk. Deficiency is mostly attributable to inherited or acquired
defects resulting in

malabsorption or the impairment of transport of the vitamin within the body.
Deficiency impacts on

the haematopoietic and nervous systems. Associated diseases include
megaloblastic anaemia and

neuropathies typically sub-acute combined degeneration of the spinal cord.
Vitamin B12 deficiency can

lead to moderate hyperhomocysteinaemia, a possible risk factor for occlusive
vascular disease.

Oral supplements are indicated prophylactically where there is a likelihood
of deficiency in those

whose gastrointestinal function is normal e.g. in individuals who are strict
vegetarians. Inherited and

acquired disorders relating to vitamin B12 malabsorption are usually treated
by repeated injection.

However, oral administration of very high doses of vitamin B12 has been
shown to be effective in the

treatment of pernicious anaemia.

Interactions

Steroid drugs, such as prednisone, have been reported to increase the
absorption of vitamin B12 in

patients with pernicious anaemia. Excessive alcohol consumption and some
drugs may decrease

absorption of vitamin B12. Oral co-administration with ascorbic acid may
result in destruction of vitamin

B12. Concurrent administration of chloramphenicol may lead to antagonism of
the haematopoietic

response to vitamin B12.

Absorption and bioavailability

Vitamin B12 requires intrinsic factor (IF), secreted mainly from the gastric
parietal cells, to ensure

adequate absorption at normal dietary intake levels. Thus the absorption of
physiological doses of

vitamin B12 is limited to approximately 0.0015 - 0.002 mg/dose or meal, due
to saturation of the uptake

system. Regardless of dose, approximately 1.2% of vitamin B12 is absorbed by
passive diffusion and

consequently this process becomes quantitatively important at
pharmacological levels of exposure.

Protein binding in certain foods may reduce the bioavailability of the
vitamin, particularly in individuals

with impaired gastric acid and/or digestive enzyme secretion. The different
forms of crystalline

cobalamin appear to be absorbed or retained to different extents, depending
on the dose. Differences

are most apparent at low doses.

Ingested vitamin B12 is released from the food matrix by the action of
digestive enzymes and gastric acid

and becomes bound to salivary haptocorrin-binding proteins. As the pH rises
further along the gut, and

under the influence of pancreatic enzymes, vitamin B12 is released from the
salivary haptocorrin and

becomes complexed with intrinsic factor (IF). The cobalamin-IF complex binds
to a specific cell wall

Part 1 Water Soluble Vitamins

94

1

1

Expert Group on Vitamins and Minerals 2003

95

receptor of the ileal enterocyte and is internalised by endocytosis. Once
inside the cell, the IF is

degraded and the liberated vitamin is converted to the methyl or the
deoxyadenosyl form, is bound to

transcobalamin II (TC II) binding protein and then exported into the portal
blood. In the general

circulation, most cobalamin is bound to transcobalamin I (TC I) but the
majority of cobalamin available

for uptake into the tissues is that bound to TC II.

Distribution and metabolism

Vitamin B12 is distributed into the liver, bone marrow and virtually all
other tissues, including the

placenta and breast milk of nursing mothers. The liver is the predominant
storage site for vitamin B12.

Uptake into cells occurs through receptor mediated endocytosis involving
specific TC II cell wall

receptors. Once inside the tissues/cells, the complex is degraded by the
lysosomes, and the

released cobalamin is metabolised either to methyl-cobalamin in the cytosol,
where it binds to

methionine synthase, or to deoxyadenosyl-cobalamin in the mitochondria,
where it binds to

methylmalonyl CoA mutase.

Excretion

Excretion occurs mainly via the faeces and urine, but also through the
shedding of skin cells. Excretion is

very slow, with significant enterohepatic cycling.

Toxicity

Human data

There are a few case reports of adverse effects associated with ingestion of
vitamin B12, either as a

supplement, or following the consumption of yeast extract products, which
also contain

cyanocobalamin. Five cases of allergic reactions were reported, three of
which were recurrences of

symptoms in individuals who had been previously exposed to cobalamin by the
parenteral route. One

further case reported the occurrence of a skin eruption that resembled acne
rosacea. Vitamin B12

exposures were generally not specified.

No adverse effects were reported in an experiment designed to determine the
uptake of single oral

doses of cyanocobalamin (up to 100 mg). However, only three participants
were administered the very

high doses.

Oral studies have been conducted to investigate the effects of vitamin B12
on pernicious anaemia.

However, although no adverse effects are apparent, these studies are not
relevant to the general

population since absorption of vitamin B12 is reduced in this condition. The
effect of high oral-dose

cyanocobalamin on plasma homocysteine levels in healthy females of
child-bearing age and the

benefits of cyanocobalamin in patients with seasonal affective disorder have
been investigated. No

adverse affects related to treatment were reported in any study including
those in which individuals

received up to 4.5 mg/day cyanocobalamin for 14 days, 2.0 mg/day
cyanocobalamin for up to one year

or 1.0 mg/day cyanocobalamin for several years. Less information is
available following the oral

administration of the hydroxocobalamin form of vitamin B12. However, no
adverse effects were reported

1

in individuals administered 0.3 mg/day for up to 12 months. No adverse
effects were reported in a

controlled study in which 125 individuals received 6.0 mg/day
methylcobalamin for up to 12 weeks.

Adverse reactions (not specified) were reported in one of 16 and in one of
23 oligozoospermia patients

given 6 or 12 mg/day methyl cobalamin, respectively, for 16 weeks,
presumably via the oral route.

However, this study was not controlled.

Animal data

The data-base on the oral toxicity of vitamin B12 in laboratory animals is
limited. Doses of 1.5 to 3.0

mg/kg bw by intraperitoneal and subcutaneous administration were found to be
acutely toxic in mice

(CNS effects; convulsions, cardiac and respiratory failure and ultimately
death). However, much higher

doses ( 5 g/kg bw) cyanocobalamin appeared to be tolerated by mice
following oral administration.

There is no evidence relating to vitamin B12 and teratogenicity or adverse
effects on fertility or postnatal

development.

Carcinogenicity and genotoxicity

There is no evidence suggesting that vitamin B12 is carcinogenic or
genotoxic in vitro or in vivo. How ever,

although data are not consistent, there is some limited evidence to suggest
that high doses of vitamin

B12 may have tumour promoting activity.

Mechanisms of toxicity

No data have been identified.

Dose-response characterisation

No relevant data have been identified.

Vulnerable groups

No vulnerable groups have been identified.

Genetic variations

No genetic variations have been identified.

Part 1 Water Soluble Vitamins

96

1

1

Studies of particular importance in the risk assessment

(For full review see
http://www.food.gov.uk/science/ouradvisors/vitandmin/evmpapers or the

enclosed CD).

Waife et al., 1963

As part of a non-controlled supplementation trial in patients with
pernicious anaemia (n=27) no adverse

reactions were reported in individuals receiving 0.3 mg hydroxocobalamin/day
for up to one year.

Berlin et al., 1968

No adverse effects attributable to vitamin B12 (cyanocobalamin) were
recorded in a long-term clinical

trial of 64 patients with pernicious anaemia, and other types of vitamin B12
deficiency given a daily oral

dose of 0.5 mg rising to 1.0 mg of cyanocobalamin (without intrinsic factor)
for 10 to 70 months

(42 patients received treatment for over 4 years). However, as noted
previously, systemic absorption in

these patients is limited.

Juhlin and Olsson, 1997

One hundred patients with vitiligo were treated with oral folic acid (5 mg)
and vitamin

B12 (1.0 mg cyanocobalamin) twice daily, for up to 12 months. There were no
reports of adverse effects.

However, 27/100 and 48/100 participants had stopped taking the supplements
after 1 - 2 months and

3 - 6 months, respectively but reasons for withdrawal were not stated.

Takahashi et al., 1999

As part of a double-blind study to assess the therapeutic effect of methyl
cobalamin on sleep-wake

disorder, patients were administered either 6.0 (n=21) or 0.03 mg/day (n=27)
methylcobalamin for 8

weeks. The lower dose group was considered as a control group because
ethical permission was not

granted for the inclusion of a placebo control group. There was no report of
any adverse effects. The

route of administration was not clear from the information given. Data were
not available for all

patients at the end of 8 weeks (two of the 6.0 mg/day dose group and three
of the 0.03 mg/day group).

Exposure assessment

Total exposure/intake18:

Food Mean: 0.0062 mg/day

97.5th percentile: 0.020 mg/day (1986/7 NDNS)

Supplements up to 3.0 mg/day (Annex 4)

Estimated maximum intake: 0.020 + 3.0 = 3.0 mg/day

No potential high intake groups have been identified.

Expert Group on Vitamins and Minerals 2003

18 The survey data do not distinguish the different forms of vitamin B12.
Dietary vitamin B12 is mainly in the methyl, deoxyadenosyl and
hydroxocobalamin forms.

Hydroxo- and particularly cyanocobalamin are the forms usually present in
dietary supplements.

97

1

Part 1 Water Soluble Vitamins

1

Risk assessment

Vitamin B12 is a water-soluble vitamin. At physiological doses, as occurs in
food, the amount absorbed is

largely limited (approximately 0.002 mg/meal) by the capacity of the
intrinsic factor-wall receptor

uptake system. At pharmacological levels of dosing, diffusion becomes more
important as the route of

absorption. Vitamin B12 present in excess of the binding capacity of the
liver, plasma and other tissues is

excreted by glomerular filtration.

It is generally accepted that ingested vitamin B12 (cobalamin) has a very
low toxicity in humans. Most

available documented data are either in the form of case reports of possible
vitamin B12-associated

adverse effects or from clinical trials or supplementation studies designed
primarily to investigate

potential beneficial effects. The latter generally involve the use of the
cyanocobalamin or

methylcobalamin forms of vitamin B12 and do not always specifically report
an absence of adverse

effects.

The animal toxicity database for vitamin B12 is very limited. Doses of 1.5
to 3.0 mg/kg bw by

intraperitoneal and subcutaneous administration were found to be acutely
toxic in mice (CNS effects;

convulsions, cardiac and respiratory failure and ultimately death). However,
much higher doses ( 5

g/kg bw) cyanocobalamin appeared to be tolerated by mice following oral
administration.

ESTABLISHMENT OF GUIDANCE LEVEL

There are insufficient data from studies in humans and animals to set a Safe
Upper Level for vitamin B12.

Clinical studies have reported no adverse effects following administration
of up to 6.0 mg/day of

methylcobalamin for several weeks and up to 1.0 mg/day cyanocobalamin for
several years. Clinical

trials and supplementation studies involving up to 100 individuals to
investigate the beneficial effects of

oral cyanocobalamin have not reported any treatment-related adverse
reactions following doses of 0.3

to 4.5 mg for periods ranging from 14 days to several years. Cyanocobalamin
is the type of vitamin B12

most frequently included in supplements in the UK. The study by Juhlin and
Olsson (1997), supported by

the absence of an identified hazard and widespread clinical experience with
oral and parenteral

treatment, suggests that supplemental intakes of 2.0 mg cyanocobalamin/day
should not produce any

adverse effects and this intake can be used for guidance purposes. This is
equivalent to 0.034 mg/kg

bw/day in a 60 kg adult. No uncertainty factor is needed because human data
from large numbers of

individuals are available. However, it should be noted that this figure has
been established in particular

subgroups of the population, i.e. vitiligo suffers and those treated for
pernicious anaemia, and may not

be completely applicable to the general population.

98

1

References

Berlin, H., Berlin, R., Brante, G. (1968). Oral treatment of pernicious
anemia with high doses of vitamin B12

without intrinsic factor. Acta Medica Scandinavica 184, 274-258.

COMA (1991). Dietary Reference Values for Food Energy and Nutrients for the
United Kingdom. Report

of the Panel on Dietary Reference Values, Committee on Medical Aspects of
Food and Nutrition Policy.

HMSO, London.

Juhlin, L., Olsson, M.J. (1997). Improvement of vitiligo after oral
treatment with vitamin B12 and folic acid

and the importance of sun exposure. Acta Dermatol-venereologica 77, 460-462.

Takahashi, K., Okawa, M., Matsumoto, M., Mishima, K., Yamadera, H., Sasaki,
M., Ishizuka, Y., Yamada, K.,

Higuchi, T., Okamoto, N., Furuta, H., Nakagawa ,H., Ohta, T., Kuroda, K.,
Sugita, Y., Inoue, Y., Uchimura, N.,

Nagayama, H., Miike, T., Kamei, K. (1999). Double-blind test on the efficacy
of methylcobalamin on sleepwake

rhythm disorders. Psychiatry and Clinical Neurosciences 53, 211-213.

Waife, S.O., Jansen, C.J., Crabtree, R.E., Grinnan, E.L., Fouts, P.J.
(1963). Oral vitamin B12 without intrinsic

factor in the treatment of pernicious anemia. Annals of Internal Medicine
58, 810-817.

Это, наверное , старовато. Вот напр и доказательная медицина Кохрейн (для нас
- неврачей - падочка-выручалочка):
http://summaries.cochrane.org/CD004655/oral-vitamin-b12-versus-intramuscular-vitamin-b12-for-vitamin-b12-deficiency

С уважением Ольга

To: science.news.bessmertie <privatmemb***@y*****.com>
Sent: Monday, March 26, 2012 7:16 PM

General Information

Chemistry

Vitamin B12 (cobalamin, Cbl) is a water-soluble vitamin and a member of a
family of related molecules

known as corrinoids which contain a corrin nucleus made up of a
tetrapyrrolic ring structure. The centre

of the tetrapyrrolic ring nucleus contains a cobalt ion that can be attached
to methyl, deoxyadenosyl-,

hydroxo- or cyano- groups.

Natural occurrence

Vitamin B12 originates from bacteria, fungi and algae, and is present in
virtually all animal tissues. Plants

contain no vitamin B12 beyond that derived from microbial contamination.

Occurrence in food, food supplements and medicines

Major dietary sources of vitamin B12, mainly in the forms of methyl,
deoxyadenosyl- and

hydroxocobalamin, include meat (e.g. 0.1 mg/kg in lamb), particularly liver
( 0.1 mg/kg) and fish (e.g.

0.03-0.1 mg/kg in salmon, 0.01-0.03 mg/kg in tuna). Hydroxocobalamin and, in
particular, cyanocobalamin

are synthetic forms used in vitamin supplements, pharmaceuticals and in the
fortification of food. Methyl

cobalamin has been used therapeutically outside the UK, for example, in
Japan.

Recommended amounts

The RNI for vitamin B12 in adults in the UK is 0.0015 mg/day (COMA, 1991).
There is no increment

required during pregnancy but there is a recommended increment of 0.0005
mg/day for breast

feeding mothers.

Analysis of tissue levels and vitamin B12 status

Measurement of vitamin B12 in plasma is routinely used to determine
deficiency, but may not be a reliable

indication in all cases. In pregnancy, for example, tissue levels are normal
but serum levels are low.

Various other plasma markers have been identified (including methylmalonic
acid, homocysteine,

holotranscobalamin, anti-intrinsic factor antibodies) and methods devised
(Schilling test, cobalamin

absorbance test, serum gastrin deoxyuridine suppression test) to distinguish
different causes of deficiency.

Brief overview of non-nutritional beneficial effects

Results of studies in humans have suggested that large doses of vitamin B12
(particularly methyl

cobalamin) may influence biological rhythms and thus may be beneficial in
the treatment of sleep

disorders. Vitamin B12 has also been reported to increase light sensitivity
by affecting melatonin

secretion. Vitamin B12, in combination with folic acid, has been suggested
to be beneficial in certain

disorders, such as idiopathic osteoarthritis and vitiligo.

Expert Group on Vitamins and Minerals 2003

93

Risk Assessment Vitamin B12 1

Function

Vitamin B12 serves as a cofactor to at least two enzymes, methionine
synthase and methylmalonyl

CoA mutase. Methionine synthase is pivotal in one-carbon metabolism, being
crucial in the synthesis

of the universal methyl donor S-adenosyl methionine and in the cellular
import and metabolism of

folate. Methylmalonyl CoA mutase converts L-methylmalonyl CoA to succinyl
CoA and is important

in even-chained fatty acid synthesis.

Deficiency

Dietary deficiency is rare in younger people living in the community but
occurs more frequently in older

people, particularly those living in institutional environments. Individuals
adhering to vegan diets may

also be at risk. Deficiency is mostly attributable to inherited or acquired
defects resulting in

malabsorption or the impairment of transport of the vitamin within the body.
Deficiency impacts on

the haematopoietic and nervous systems. Associated diseases include
megaloblastic anaemia and

neuropathies typically sub-acute combined degeneration of the spinal cord.
Vitamin B12 deficiency can

lead to moderate hyperhomocysteinaemia, a possible risk factor for occlusive
vascular disease.

Oral supplements are indicated prophylactically where there is a likelihood
of deficiency in those

whose gastrointestinal function is normal e.g. in individuals who are strict
vegetarians. Inherited and

acquired disorders relating to vitamin B12 malabsorption are usually treated
by repeated injection.

However, oral administration of very high doses of vitamin B12 has been
shown to be effective in the

treatment of pernicious anaemia.

Interactions

Steroid drugs, such as prednisone, have been reported to increase the
absorption of vitamin B12 in

patients with pernicious anaemia. Excessive alcohol consumption and some
drugs may decrease

absorption of vitamin B12. Oral co-administration with ascorbic acid may
result in destruction of vitamin

B12. Concurrent administration of chloramphenicol may lead to antagonism of
the haematopoietic

response to vitamin B12.

Absorption and bioavailability

Vitamin B12 requires intrinsic factor (IF), secreted mainly from the gastric
parietal cells, to ensure

adequate absorption at normal dietary intake levels. Thus the absorption of
physiological doses of

vitamin B12 is limited to approximately 0.0015 - 0.002 mg/dose or meal, due
to saturation of the uptake

system. Regardless of dose, approximately 1.2% of vitamin B12 is absorbed by
passive diffusion and

consequently this process becomes quantitatively important at
pharmacological levels of exposure.

Protein binding in certain foods may reduce the bioavailability of the
vitamin, particularly in individuals

with impaired gastric acid and/or digestive enzyme secretion. The different
forms of crystalline

cobalamin appear to be absorbed or retained to different extents, depending
on the dose. Differences

are most apparent at low doses.

Ingested vitamin B12 is released from the food matrix by the action of
digestive enzymes and gastric acid

and becomes bound to salivary haptocorrin-binding proteins. As the pH rises
further along the gut, and

under the influence of pancreatic enzymes, vitamin B12 is released from the
salivary haptocorrin and

becomes complexed with intrinsic factor (IF). The cobalamin-IF complex binds
to a specific cell wall

Part 1 Water Soluble Vitamins

94

1

1

Expert Group on Vitamins and Minerals 2003

95

receptor of the ileal enterocyte and is internalised by endocytosis. Once
inside the cell, the IF is

degraded and the liberated vitamin is converted to the methyl or the
deoxyadenosyl form, is bound to

transcobalamin II (TC II) binding protein and then exported into the portal
blood. In the general

circulation, most cobalamin is bound to transcobalamin I (TC I) but the
majority of cobalamin available

for uptake into the tissues is that bound to TC II.

Distribution and metabolism

Vitamin B12 is distributed into the liver, bone marrow and virtually all
other tissues, including the

placenta and breast milk of nursing mothers. The liver is the predominant
storage site for vitamin B12.

Uptake into cells occurs through receptor mediated endocytosis involving
specific TC II cell wall

receptors. Once inside the tissues/cells, the complex is degraded by the
lysosomes, and the

released cobalamin is metabolised either to methyl-cobalamin in the cytosol,
where it binds to

methionine synthase, or to deoxyadenosyl-cobalamin in the mitochondria,
where it binds to

methylmalonyl CoA mutase.

Excretion

Excretion occurs mainly via the faeces and urine, but also through the
shedding of skin cells. Excretion is

very slow, with significant enterohepatic cycling.

Toxicity

Human data

There are a few case reports of adverse effects associated with ingestion of
vitamin B12, either as a

supplement, or following the consumption of yeast extract products, which
also contain

cyanocobalamin. Five cases of allergic reactions were reported, three of
which were recurrences of

symptoms in individuals who had been previously exposed to cobalamin by the
parenteral route. One

further case reported the occurrence of a skin eruption that resembled acne
rosacea. Vitamin B12

exposures were generally not specified.

No adverse effects were reported in an experiment designed to determine the
uptake of single oral

doses of cyanocobalamin (up to 100 mg). However, only three participants
were administered the very

high doses.

Oral studies have been conducted to investigate the effects of vitamin B12
on pernicious anaemia.

However, although no adverse effects are apparent, these studies are not
relevant to the general

population since absorption of vitamin B12 is reduced in this condition. The
effect of high oral-dose

cyanocobalamin on plasma homocysteine levels in healthy females of
child-bearing age and the

benefits of cyanocobalamin in patients with seasonal affective disorder have
been investigated. No

adverse affects related to treatment were reported in any study including
those in which individuals

received up to 4.5 mg/day cyanocobalamin for 14 days, 2.0 mg/day
cyanocobalamin for up to one year

or 1.0 mg/day cyanocobalamin for several years. Less information is
available following the oral

administration of the hydroxocobalamin form of vitamin B12. However, no
adverse effects were reported

1

in individuals administered 0.3 mg/day for up to 12 months. No adverse
effects were reported in a

controlled study in which 125 individuals received 6.0 mg/day
methylcobalamin for up to 12 weeks.

Adverse reactions (not specified) were reported in one of 16 and in one of
23 oligozoospermia patients

given 6 or 12 mg/day methyl cobalamin, respectively, for 16 weeks,
presumably via the oral route.

However, this study was not controlled.

Animal data

The data-base on the oral toxicity of vitamin B12 in laboratory animals is
limited. Doses of 1.5 to 3.0

mg/kg bw by intraperitoneal and subcutaneous administration were found to be
acutely toxic in mice

(CNS effects; convulsions, cardiac and respiratory failure and ultimately
death). However, much higher

doses ( 5 g/kg bw) cyanocobalamin appeared to be tolerated by mice
following oral administration.

There is no evidence relating to vitamin B12 and teratogenicity or adverse
effects on fertility or postnatal

development.

Carcinogenicity and genotoxicity

There is no evidence suggesting that vitamin B12 is carcinogenic or
genotoxic in vitro or in vivo. How ever,

although data are not consistent, there is some limited evidence to suggest
that high doses of vitamin

B12 may have tumour promoting activity.

Mechanisms of toxicity

No data have been identified.

Dose-response characterisation

No relevant data have been identified.

Vulnerable groups

No vulnerable groups have been identified.

Genetic variations

No genetic variations have been identified.

Part 1 Water Soluble Vitamins

96

1

1

Studies of particular importance in the risk assessment

(For full review see
http://www.food.gov.uk/science/ouradvisors/vitandmin/evmpapers or the

enclosed CD).

Waife et al., 1963

As part of a non-controlled supplementation trial in patients with
pernicious anaemia (n=27) no adverse

reactions were reported in individuals receiving 0.3 mg hydroxocobalamin/day
for up to one year.

Berlin et al., 1968

No adverse effects attributable to vitamin B12 (cyanocobalamin) were
recorded in a long-term clinical

trial of 64 patients with pernicious anaemia, and other types of vitamin B12
deficiency given a daily oral

dose of 0.5 mg rising to 1.0 mg of cyanocobalamin (without intrinsic factor)
for 10 to 70 months

(42 patients received treatment for over 4 years). However, as noted
previously, systemic absorption in

these patients is limited.

Juhlin and Olsson, 1997

One hundred patients with vitiligo were treated with oral folic acid (5 mg)
and vitamin

B12 (1.0 mg cyanocobalamin) twice daily, for up to 12 months. There were no
reports of adverse effects.

However, 27/100 and 48/100 participants had stopped taking the supplements
after 1 - 2 months and

3 - 6 months, respectively but reasons for withdrawal were not stated

Takahashi et al., 1999

As part of a double-blind study to assess the therapeutic effect of methyl
cobalamin on sleep-wake

disorder, patients were administered either 6.0 (n=21) or 0.03 mg/day (n=27)
methylcobalamin for 8

weeks. The lower dose group was considered as a control group because
ethical permission was not

granted for the inclusion of a placebo control group. There was no report of
any adverse effects. The

route of administration was not clear from the information given. Data were
not available for all

patients at the end of 8 weeks (two of the 6.0 mg/day dose group and three
of the 0.03 mg/day group)

Exposure assessment

Total exposure/intake18:

Food Mean: 0.0062 mg/day

97.5th percentile: 0.020 mg/day (1986/7 NDNS)

Supplements up to 3.0 mg/day (Annex 4)

Estimated maximum intake: 0.020 + 3.0 = 3.0 mg/day

No potential high intake groups have been identified.

Expert Group on Vitamins and Minerals 2003

18 The survey data do not distinguish the different forms of vitamin B12.
Dietary vitamin B12 is mainly in the methyl, deoxyadenosyl and
hydroxocobalamin forms.

Hydroxo- and particularly cyanocobalamin are the forms usually present in
dietary supplements.

97

1

Part 1 Water Soluble Vitamins

1

Risk assessment

Vitamin B12 is a water-soluble vitamin. At physiological doses, as occurs in
food, the amount absorbed is

largely limited (approximately 0.002 mg/meal) by the capacity of the
intrinsic factor-wall receptor

uptake system. At pharmacological levels of dosing, diffusion becomes more
important as the route of

absorption. Vitamin B12 present in excess of the binding capacity of the
liver, plasma and other tissues is

excreted by glomerular filtration.

It is generally accepted that ingested vitamin B12 (cobalamin) has a very
low toxicity in humans. Most

available documented data are either in the form of case reports of possible
vitamin B12-associated

adverse effects or from clinical trials or supplementation studies designed
primarily to investigate

potential beneficial effects. The latter generally involve the use of the
cyanocobalamin or

methylcobalamin forms of vitamin B12 and do not always specifically report
an absence of adverse

effects.

The animal toxicity database for vitamin B12 is very limited. Doses of 1.5
to 3.0 mg/kg bw by

intraperitoneal and subcutaneous administration were found to be acutely
toxic in mice (CNS effects;

convulsions, cardiac and respiratory failure and ultimately death). However,
much higher doses ( 5

g/kg bw) cyanocobalamin appeared to be tolerated by mice following oral
administration.

ESTABLISHMENT OF GUIDANCE LEVEL

There are insufficient data from studies in humans and animals to set a Safe
Upper Level for vitamin B12.

Clinical studies have reported no adverse effects following administration
of up to 6.0 mg/day of

methylcobalamin for several weeks and up to 1.0 mg/day cyanocobalamin for
several years. Clinical

trials and supplementation studies involving up to 100 individuals to
investigate the beneficial effects of

oral cyanocobalamin have not reported any treatment-related adverse
reactions following doses of 0.3

to 4.5 mg for periods ranging from 14 days to several years. Cyanocobalamin
is the type of vitamin B12

most frequently included in supplements in the UK. The study by Juhlin and
Olsson (1997), supported by

the absence of an identified hazard and widespread clinical experience with
oral and parenteral

treatment, suggests that supplemental intakes of 2.0 mg cyanocobalamin/day
should not produce any

adverse effects and this intake can be used for guidance purposes. This is
equivalent to 0.034 mg/kg

bw/day in a 60 kg adult. No uncertainty factor is needed because human data
from large numbers of

individuals are available. However, it should be noted that this figure has
been established in particular

subgroups of the population, i.e. vitiligo suffers and those treated for
pernicious anaemia, and may not

be completely applicable to the general population.

98

1

References

Berlin, H., Berlin, R., Brante, G. (1968). Oral treatment of pernicious
anemia with high doses of vitamin B12

without intrinsic factor. Acta Medica Scandinavica 184, 274-258.

COMA (1991). Dietary Reference Values for Food Energy and Nutrients for the
United Kingdom. Report

of the Panel on Dietary Reference Values, Committee on Medical Aspects of
Food and Nutrition Policy.

HMSO, London.

Juhlin, L., Olsson, M.J. (1997). Improvement of vitiligo after oral
treatment with vitamin B12 and folic acid

and the importance of sun exposure. Acta Dermatol-venereologica 77, 460-462.

Takahashi, K., Okawa, M., Matsumoto, M., Mishima, K., Yamadera, H., Sasaki,
M., Ishizuka, Y., Yamada, K.,

Higuchi, T., Okamoto, N., Furuta, H., Nakagawa ,H., Ohta, T., Kuroda, K.,
Sugita, Y., Inoue, Y., Uchimura, N.,

Nagayama, H., Miike, T., Kamei, K. (1999). Double-blind test on the efficacy
of methylcobalamin on sleepwake

rhythm disorders. Psychiatry and Clinical Neurosciences 53, 211-213.

Waife, S.O., Jansen, C.J., Crabtree, R.E., Grinnan, E.L., Fouts, P.J.
(1963). Oral vitamin B12 without intrinsic

factor in the treatment of pernicious anemia. Annals of Internal Medicine
58, 810-817.

Original Message From: "Privatmember" <privatmemb***@y*****.com>

это несравнимые материалы, кокрановцы только расследуют употребление
лечебной дозы через рот и внутримышечно, а я прислал полную информаци, все
аспекты может кому надо.

На заключение: перорально ничуть не хуже, чем внутримышечно. но дозы гораздо
выше, т.к много В12 разлагается в кислой среде желудка. (кроме людей с нарушением
всасывания в ЖКТ).
Дозы указаны. Что касается депонирования, то В12 депонируется в печени, поэтому
можно постепенно прейти на раз в месяц. Точная схема наезда на "раз в месяц"
вроде в техте первой статьи, могу найти.
Со спасибом и уважением Ольга

To: science.news.bessmertie <privatmemb***@y*****.com>
Sent: Monday, March 26, 2012 6:47 PM

На что именно обращать внимание, какие выводы?

--------Это значит - для не очень замороченных - кушать говядину несколько
раз в месяц. И вкуснее(если хорошо приготовить), и дешевле, и польза...

Да нет, таблетки дешевле говядины :-), но дело, видите-лью не в томю

С уважением Ольга

To: science.news.bessmertie <privatmemb***@y*****.com>
Sent: Tuesday, March 27, 2012 10:23 AM

--------Это значит - для не очень замороченных - кушать говядину несколько
раз в месяц. И вкуснее(если хорошо приготовить), и дешевле, и польза...

-------Поддерживаю. Пользовался в разное время разными "витаминками", но
последние годы тоже сосредоточился на выстраивании структуры обеспечения
себя качественными продуктами питания. Это далеко ещё не законченный
процесс - в перспективе самообеспечение себя яблоками(весь год),
виноградом, абрикосами, орехами....
------Придерживаюсь тезиса о "всеядности" человека, но с акцентом на
растительную, прежде всего живую пищу. Считаю, что "пирамида питания" с
"основанием" из круп и зерновых неверна и отражает скорее доступность этих
продуктов. В основании должны быть овощи (и фрукты). В этом плане прошлый
год меня хорошо поддерживали "зелёные коктейли". В данный момент, несмотря
на метровый снег на огороде, я уже засеял тепличку в основном
холодостойкими зеленными и редиской. Опыт прошлого сезона показывает, что
для нас одинаково ценно практически всё, что может вырасти - и почти все
сорняки, и ботва редиски и т.д. Поэтому мне по большому счёту неважно, что
вырастет - важнее, что я могу выиграть примерно месяц времени и реально
получить витаминную пищу к середине апреля (не по пучочку нитратного
укропа, а по литру и более коктейля (плюс салаты) в день. Знания позволяют
получать биомассу, используя в качестве удобрения лишь прелые опилки,
старую солому и немного золы!!!).

Здравствуйте, Дмитрий_S.
Good morning, afternoon, evening, Дмитрий_S.
Thursday, March 29, 2012
Вы писали 26 марта 2012 г., 13:36:47:
You wrote 26.03.2012, 13:36:47:

На паразитов не пробовали проверяться? :)
Опять же, эпидемия поноса в Германии с отмиранием
печени... :)))

Риски....

--
Говорила мне мама: "Иди в гинекологи - всю жизнь руки в тепле будут".

С уважением, Кондратьев Сергей.
Sincerely yours, Kondratiev S.V.
Thursday, March 29, 2012 mailto:kon***@a*****.ru

потрясающие результаты, которые переворачивают ВСЕ представления о
медицине, здоровье, молодости.

------Ну. что вы, право... Человеку хорошо, а вы опять о грустном.

Здравствуйте, Sergei.
Good morning, afternoon, evening, Sergei.
Friday, March 30, 2012
Вы писали 29 марта 2012 г., 22:56:44:
You wrote 29.03.2012, 22:56:44:

Тогда надо просто увеличить
дозу транквилизаторов. :))) Кстати, на Ютубе много роликов есть
про паразитов для наглядности. :)))

--
Иногда должны погибнуть добро и милосердие, чтобы жило все остальное

С уважением, Кондратьев Сергей.
Sincerely yours, Kondratiev S.V.
Friday, March 30, 2012 mailto:kon***@a*****.ru