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Tärkeimmät asiat: matala verenpaine, matala kolestroli ja hoikkuus

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Kokosin tohon paketin: noista kolmesta ku huolehditte niin pitäs pysyä terveenä. Tämä ketju laitetaan nyt tän alueen yläosaan pysyväksi.

 

 

 

 

 

1. Verenpaine matalla / viitearvoissa

 

http://fi.wikipedia.org/wiki/Verenpaine

 

 

VP-taulukko.gif

 

 

 

2. Kolestroli matalalla

 

http://www.sydanliitto.fi/kolesteroli#.VBbZsxaRbh4

 

 

 

Pyri kohti näitä arvoja

 

Kokonaiskolesteroli alle 5,0 mmol/l*

 

LDL-kolesteroli alle 3,0 mmol/l**

 

HDL-kolesteroli yli 1,0 mmol/l

 

Triglyseridit alle 2,0 mmol/l

 

 

 

 

 

 

 

3. Hoikkana olo tulee sitten seuraavana.

 

LS_taulukko_01.jpg

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Verenpaine kai alkaa olemaan selvästi haitallinen vasta, kun 140/90 ylittyy, eli paineelle on annettu tiukkoja ihannearvoja, mutta kolesterolille jostain syystä niin ei ole tuossa tehty. LDL 3,0 on jo aika korkea.

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Verenpaine kai alkaa olemaan selvästi haitallinen vasta, kun 140/90 ylittyy, eli paineelle on annettu tiukkoja ihannearvoja, mutta kolesterolille jostain syystä niin ei ole tuossa tehty. LDL 3,0 on jo aika korkea.

 

Minulla 190/144. Onko paha mitä se kertoo?

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Ei tässä oo sodasta kyse, eikä sellaseeen houkuttelusta. Ihan tavallisena pulliaisena oon vaan alkanut kiinnittää huomiota varsinkin tohon verenpaineeseen, korkea sellainen tekee melkosta tuhoa.

 

Joka tapauksessa alueelle oli hyvä laittaa tollanen pysyvä "kaikkein paras vinkki" yläosaan.

Nokialla yhdellä miehellä on erittäin alhainen kolesteroli ja silti suonet tukossa. 1,9 LDL ja kokonaiskole reilu 3.

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Sydäkohtauksen kannalta kolesteroli on merkittävämpi. Aivohalvauksen kannalta verenpaine on merkittävämpi.

 

Kokonaisuutena kolesteroli tappaa enemmän varsinkin miehiä.

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Eevertillä takki kääntynyt verenpaineen suhteen, koska aiemmin meuhkasi korkean verenpaineen vaarallisuudesta suu vaahdossa.

Kuulemma alkuasukkailla on verenpaine (yläpaine115) Onko oma paine noussut?

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Korkea hoitamaton verenpaine tekee pahaa tuhoa kuulemma jo 5 vuodessa. Kovettaa verisuonet...

 

sitten tukokset tulee helposti.

 

Jos kolesteroli on alhainen, niin verenpaine ei saa suoniin plakkia aikaiseksi. Se ilmeisesti jonkin verran kuitenkin paksuntaa ja jäykistää suonia. Sepelvaltimotautia ei pelkällä verenpaineella kuitenkaan saa aikaiseksi matalan kolen kundi.

 

Verenpainehan kai on esim. silmille haitallista.

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Sepelvaltimotautia ei pelkällä verenpaineella kuitenkaan saa aikaiseksi matalan kolen kundi.

 

Tämä siis pätee silloin, jos kolet on olleet matalat läpi elämän.

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Tämä siis pätee silloin, jos kolet on olleet matalat läpi elämän.

Lataa tutkimusta pöytään asian tiimoilta. Epäilen että ei löydy tutkimusta jossa on ihmisillä tutkittu heidän koletasoja läpi elämän.

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Itse en ainakaan yritä tiputtaa ldl kolesterolia kovinkaan alas, mulle riittää että pysyy 2-3, tai ei haittaa jos vähä yli 3 menee. Alhaisita kolesteroliarvoista on haittaa ja vaikuttaa hormoonitoimintaan negatiivisesti.

 

http://renegadehealth.com/blog/2014/09/12/five-reasons-why-you-dont-want-your-cholesterol-level-to-get-too-low

 

When Cholesterol Goes Too Low

 

Low cholesterol is associated with hyperthyroidism, adrenal insufficiency, liver disease, malabsorption, autism, and some cancers. Doctors know that extremely low cholesterol is a sign of severe deterioration of health. From my clinical experience, if my patients’ cholesterol levels go too low, their hormone levels drop, thinking gets fuzzy, and they’re tired all the time. What’s too low?

Total cholesterol levels above 200 mg/dL are associated with increased risk for cardiovascular disease. In my clinical experience, patients with levels between 145 and 165 have very low risk of heart disease, and those as low as 135 to 145, have no incidence. Going lower does not further reduce your risk—how can you get better than zero risk?

LDL levels above 100 are associated with increased risk for cardiovascular disease. Desirable LDL cholesterol levels are between 70 and 80. This is an approximate number. There are individual variations, and some people without cardiovascular disease have much higher LDL levels. However, recent research and my clinical experience inform us that people with levels in approximately the 70 – 80 range are unlikely to have cardiovascular disease. Would even lower be better?

Heart disease remains the number-one killer of American men and women. But, this is very odd, because in traditional cultures heart disease is so rare that instead of number one on the death list, it’s at the bottom. Even in America, at the beginning of the twentieth century, heart attacks were uncommon.

Medical anthropologists found that our hunter-gatherer ancestors likely had LDL levels between 50 to 70 mg/dL. Indigenous groups like the Maasai and Inuit also have low LDL levels. Heart attacks among these people are non-existent. What would a paleo range work for modern people?

Strict vegetarians can also have LDL levels in this range. Some of my raw food vegan patients have LDL levels as low as 35 and total cholesterol levels below 100.

It’s hard to know what is too low, but if your LDL is below 65 mg/dL, your body may not function optimally. You probably won’t have symptoms, or those that you experience might get associated with other conditions like chronic fatigue syndrome. If your LDL levels are lower than 35 mg/dL, your brain might not fully function. Your energy could drop, you may feel depressed, and your behavior could be altered because low cholesterol has been associated with reduced serotonin activity in the brain. You may not be able to use sunlight to make vitamin D. Your body will not be able to make enough steroid hormones, including adrenal hormones.

The Dangers of Too Low Cholesterol and LDL:

Low vitamin D

Fatigue

Reduced libido

Mood changes

Memory loss

Increased risk for neurodegenerative disease

The Goldilocks Zone

Is there a total cholesterol and LDL number that is just right? Since so many factors are involved in health, searching for a perfect number for lipid levels might prove futile. However, you might discover your own personal “Goldilocks Zone”—a range for cholesterol and LDL that is just right for you.

It’s time we seized a new vision about cholesterol because of it’s life giving—and, life take away—value. Remember, cholesterol is life’s friend, not the enemy.

 

-Dr. JE Williams


Shakes are for fakes, eat steaks -Stan Efferding

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Lataa tutkimusta pöytään asian tiimoilta. Epäilen että ei löydy tutkimusta jossa on ihmisillä tutkittu heidän koletasoja läpi elämän.

 

Tarkoitin, että jos missään elämän vaiheessa plakki ei pääse kertymään, niin silloin verisuoni on puhdas. Aina, kun niin pääsee tapahtumaan(LDL yli 1,8), niin tapahtuu pysyvää vahinkoa, jota ei voi kumota kuin pieneltä osin. Ei ole keinoa puhdistaa suonta puhtaaksi, jolloin ehkäisy on tärkeää.

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Itse en ainakaan yritä tiputtaa ldl kolesterolia kovinkaan alas, mulle riittää että pysyy 2-3, tai ei haittaa jos vähä yli 3 menee. Alhaisita kolesteroliarvoista on haittaa ja vaikuttaa hormoonitoimintaan negatiivisesti.

 

http://renegadehealth.com/blog/2014/09/12/five-reasons-why-you-dont-want-your-cholesterol-level-to-get-too-low

In my clinical experience, patients with levels between 145 and 165 have very low risk of heart disease, and those as low as 135 to 145, have no incidence.

 

Medical anthropologists found that our hunter-gatherer ancestors likely had LDL levels between 50 to 70 mg/dL.

 

Käytännössä liian alhaista ei ole kenelläkään. Luolamiehen LDL 1,3-1,8, ei sepelvaltimotautia.

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Hyvä kirjoitus:

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3012294/

[h=2]IT'S THE CHOLESTEROL, STUPID![/h]During the 1992 presidential campaign in the USA, the Clinton campaign slogan was “It's the economy, stupid,” and that phrase apparently was helpful in getting Mr. Clinton elected president. Several recent publications have been highly critical of some lipid-lowering trials using statin drugs and also have debased the cholesterol “hypothesis” on atherosclerosis (13).

What is the evidence that “elevated cholesterol” causes atherosclerosis? There are four supporting arguments in my view (47). 1) Atherosclerotic plaques are easily produced experimentally in herbivores (e.g., rabbits, monkeys) simply by feeding these animals cholesterol (e.g., egg yokes) or saturated fats. Indeed, atherosclerosis is probably the second easiest disease to produce experimentally. (The first is an endocrine deficiency—simply excise an endocrine gland.) 2) Cholesterol is present in atherosclerotic plaques in experimentally produced atherosclerosis and in plaques in human beings. 3) Societies and individuals with high serum cholesterol levels (total and low-density lipoprotein [LDL] cholesterol) compared to populations and individuals with low levels have a high frequency of atherosclerotic events, a high frequency of dying from these events, and a large quantity (burden) of plaque in their arteries. (The best study in my view supporting this thesis is the Seven Countries study [8–10].) 4) Lowering total and LDL cholesterol levels decreases the frequency of atherosclerotic events, the chances of dying from these events, and the quantity of plaques in the arteries. No one has produced atherosclerosis experimentally by increasing the arterial blood pressure or glucose levels or by blowing smoke in the faces of rabbits their entire lifetime or by stressing these animals. The only way to produce atherosclerosis experimentally is by feeding high-cholesterol and/or high-saturated-fat diets to herbivores. (Atherosclerosis is not a disease of carnivores, and it is not possible to produce atherosclerosis in carnivores [dogs, cats, tigers, lions, etc.] unless the thyroid gland is removed or made dysfunctional before a high-cholesterol or high-saturated-fat diet is administered [11]).

 

Why has the proven causal relation between abnormal serum LDL cholesterol and atherosclerosis been so difficult to accept by so many extremely intelligent physicians? One factor, in my view, is that this cholesterol-atherosclerosis causal relation has been diluted by the concept of multiple atherosclerotic risk factors and the idea that atherosclerosis is a multifactorial disease. The Framingham study, which has taught us all so much, introduced the concept of “risk factors” and fostered the view that the greater the number of risk factors present, the greater the chance of atherosclerotic events (12). As a consequence, “elevated cholesterol” became just one of several risk factors and was perceived as essentially having no more influence than elevated systolic blood pressure, diabetes mellitus (“glucose intolerance”), cigarette smoking, abdominal obesity, lack of regular physical activity, family history, or left ventricular hypertrophy except in the younger patients (13). The view that atherosclerosis is a multifactorial disease has muddled the waters in my view. This is not to say that cigarette smoking, elevated blood pressure, diabetes mellitus, obesity, and inactivity are not harmful—of course they are—but if the serum LDL cholesterol is

 

A second factor is the introduction and propagation of the thesis that atherosclerosis is an inflammatory disease (15). Yes, a few mononuclear cells are regularly seen in experimentally produced atherosclerotic plaques but not commonly in plaques of patients with fatal coronary disease or in plaques excised by endarterectomy (16, 17). And, yes, some blood inflammatory markers are commonly elevated in persons with atherosclerotic events. But, many patients have atherosclerotic events when the high-sensitivity (hs) C-reactive protein (CRP) is normal (18). And patients with the next highest serum LDL cholesterol levels, namely those with heterozygous familial hypercholesterolemia, have atherosclerotic events often in their 30s and 40s.

A third factor preventing acceptance of the causal relation between abnormal serum LDL cholesterol and atherosclerosis has been the observation that among adults with nonfamilial hypercholesterolemia but similar levels of serum LDL cholesterol, some develop atherosclerotic events and others do not. It is in this group particularly in my view that the other “risk factors” as well as high-density lipoprotein (HDL) cholesterol levels come into play. Of two people of similar age and sex and similar serum LDL cholesterol levels, say 130 mg/dL, the patient whose systolic systemic blood pressure is 170 mm Hg versus the other patient with a systolic pressure of 115 mm Hg is at much greater risk of an atherosclerotic event. And cigarette smoking may work in a similar fashion. Nevertheless, if the serum LDL cholesterol is

 

Another factor may be the use of multiple atherosclerotic risk factors in the guidelines for whom to treat and whom not to treat with lipid-lowering drugs. Although the guidelines do focus on the serum LDL cholesterol level, the number of other “risk factors” present plays a prominent role in this therapeutic decision (19). If no other nonlipid risk factors are present or if only one non-LDL cholesterol risk factor is present and there have been no previous atherosclerotic events and diabetes mellitus is not present, the magical drug treatment number is an LDL cholesterol level >190 mg/dL. Refraining from drug intervention until this very high LDL cholesterol level is reached plays down or even nullifies the importance of cholesterol in preventing events. (It is important to realize that the lipid-lowering drug guidelines [1988, 1993, 2001, and 2004] have to do only with reducing atherosclerotic events. They do not concern themselves with preventing atherosclerotic plaques in the first place. Of course, if atherosclerotic plaques are prevented, atherosclerotic events do not occur!)

 

Such high guideline drug treatment levels keep, in my view, many persons deserving of lipid-lowering drug therapy from receiving these magical agents (20). The danger of high cholesterol levels to longevity was recognized by the life insurance companies in the 1930s but not by physicians. The normal range of serum total cholesterol in laboratory reports for decades was listed as 150 to 300 mg/dL. In 1972, one of the world's most prominent lipidologists reported that his total cholesterol “worry level” for patients was a value >300 mg/dL. If the expert uses such high numbers, what importance can be placed on cholesterol by the nonexpert community? Incidentally, for the first several decades of the Framingham study, an “elevated cholesterol” was defined as a serum total cholesterol >250 mg/dL. At this level, it is easy to understand how this “risk factor” did not separate itself from the others.

 

It is time to move on from a goal “to decrease risk” to a goal “to prevent plaques” (21). To do so requires much lower levels of LDL cholesterol than advocated by the guideline publications. My goal for all individuals worldwide is a serum LDL cholesterol at least 40%, indeed nearly 50%, including a reduction in stroke by 48%! This trial beautifully shows that we can drastically reduce or even prevent atherosclerotic events and expensive procedures by taking a single pill every day and do it safely. Most Americans will not reach the JUPITER treatment levels (LDL cholesterol 55 mg/dL) by diet alone. The statin drugs have been ingested by humans now for nearly 30 years, and their safety and thus benefit/risk ratio may be the best of any proven useful medication. The toxicity resides mainly in atherosclerosis, not in the drug.

 

I consider it unfortunate that there continues to be so much criticism of statin drugs, which I consider to be the best cardiovascular drug ever created.lowast.gif These drugs can prevent first and subsequent atherosclerotic events, they can reduce cardiovascular and all-cause mortality rates, they have the capacity to reduce the quantity of atherosclerotic plaques already present, and by decreasing the frequency of myocardial infarcts they reduce the frequency of heart failure and malignant ventricular arrhythmias. Their ability to reduce the serum levels of CRP may have benefits not yet fully appreciated. The discoverer of the first statin drug (Akira Endo, PhD) is deserving of the Nobel Prize for medicine!

 

The lower the LDL cholesterol the better, and this principle has been established repeatedly despite the voices of the anticholesterol, antistatin fallacy mongers! It's the cholesterol, stupid!

 

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Raportissa otettu tutkimuskohteeksi yksi 70 vuotias kuollut nainen, ja siitä on sitten vedetty johtopäätöksiä kolesterolin suhteen. Vegaanipiireille käy tutkimuskohteeksi näköjään tämä yksittäistapaus. Lisäksi raportissa paistaa läpi vegaanipropaganda, vegaaniruoka suosituksineen.


Shakes are for fakes, eat steaks -Stan Efferding

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Raportissa otettu tutkimuskohteeksi yksi 70 vuotias kuollut nainen, ja siitä on sitten vedetty johtopäätöksiä kolesterolin suhteen. Vegaanipiireille käy tutkimuskohteeksi näköjään tämä yksittäistapaus. Lisäksi raportissa paistaa läpi vegaanipropaganda, vegaaniruoka suosituksineen.

 

Toi nainen oli vain äärimmäinen esimerkki familiaalisesta hypobeetalipoproteinemiasta. Ei se ollut mikään johtopäätösten perusta.

 

Veganismiin tuo ei liity mitenkään.

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Kävin 2 - vuotta siten verikokeissa ja söin paljon lohta ja omega3 tuotteita ja kolet oli kok 5,2 HDl 1,5 ja LDL 3,3[ATTACH=CONFIG]8017[/ATTACH]

 

Nyt kävin taas ja ajattelin että varmaan nouseet kun joka päivä paistettua kanamunia, voita ja juustoa. Ja lisäksi syön ainakin kerran viikossa paskaruokaa sekä jäätelö vähintään 1 litra. Kok 4,2, HDL 1,5 ja LdL 2,4. LDL vähentynyt 30 % ja en syö enää kalaa tai omega3 tuoteita.

[ATTACH=CONFIG]8018[/ATTACH]

 

Lääkäri sanos et ihan sama mitä teet niin jatka samaan malliin.

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