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Cholesterol feeds prostate cancer

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General fitness, health and nutrition
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18 March 2005
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21 April 2005
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Roman Bystrianyk
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  1. http://www.healthsentinel.com/news.php?event=news_print_list_item&id=689

    "Cholesterol feeds prostate cancer", BBC News, March 18, 2005,
    Link: http://news.bbc.co.uk/2/hi/health/4359117.stm

    High cholesterol levels accelerate the growth of prostate tumours,
    research has found.

    A team from Boston's Children Hospital also found that
    cholesterol-lowering statin drugs may inhibit prostate cancer growth.

    The findings may help explain why prostate cancer is more common in the
    West, where diets tend to be high in cholesterol.

    Details are published in the Journal of Clinical Investigation.

    Rates of prostate cancer in rural parts of China and Japan, where low
    fat diets are the norm, are up to 90% less than in the West.

    Yet when Eastern men migrate to the West their chances of being
    diagnosed with prostate cancer increase.

    This has led doctors to suspect that environmental factors - such as
    diet - may play a significant role in the development of the disease.

    Mice experiments

    The Boston team injected human prostate cancer cells into mice and
    watched them grow.

    When the animals were fed high cholesterol diets, cholesterol was found
    to accumulate in the outer membranes of tumour cells.

    This appeared to alter chemical signalling patterns within the cells.

    As a result, they resisted signals telling them to commit suicide and
    instead continued to proliferate in the uncontrolled fashion seen in
    cancer.

    The increased cholesterol levels did not trigger new cancers in the
    mice.

    But six weeks after the tumour cells were injected, mice on the
    high-cholesterol diets had twice as many tumours as animals on ordinary
    diets.

    Their tumours were also much larger in size.

    When the cells were exposed to the cholesterol-lowering drug
    simvastatin, cell death increased and tumours stopped proliferating.

    But replenishing cell membranes with cholesterol caused the cancer to
    run out of control again.

    Lead researcher Dr Michael Freeman said: "Our study opens up a new
    paradigm in thinking about how cancer might be controlled
    pharmacologically by manipulating cholesterol.

    "Our data support the notion that cholesterol-lowering drugs - which
    are widely used and fairly safe - might be effective in prevention of
    prostate cancer, or as an adjunctive therapy."

    Chris Hiley, of the UK Prostate Cancer Charity, said: "This research is
    clearly at an early stage, as it was accomplished in mouse cells, not
    men, but it's heartening to see a plausible connection made between
    processes inside cells and the Westernised high fat diet that seem to
    increase the risk of prostate cancer occurring.

    "The results do open up thinking about new drug therapies.

    "But there is also a low tech option any man could attempt today.

    "Adopt a healthy low cholesterol diet and active lifestyle.

    "Cut down on saturated fats, reduce the total amount of fat eaten but
    eat oily fish, and eat a high fibre diet - with porridge oats, and
    plenty of fresh fruit and vegetables."

    Every year 27,000 men are diagnosed with prostate cancer and 10,000 men
    die from it.

  2. Wow - what a ridiculous experiment. Why not just take the serum
    cholesterol levels of men with prostate cancer, then see if progression
    is related to the cholesterol level? Even then, what should be
    measured is the oxysterol content of the serum, meaning oxidized
    cholesterol. The only thing I'd like to know is if the "researchers"
    bothered to determine whether the cholesterol they fed the tumors had
    high oxysterol contents. This seems to be the case, because the statin
    drug lowers inflammation, and cholesterol does too, if it's not
    oxidized. If it's oxidized it will create inflammation. It's amazing
    how so many "scientists" are ignorant of recent research.

  3. How does cholesterol become oxidized?

    Does this mean that those who eat cholesterol need to avoid rancid fats?

    "montygram" <[email hidden]> wrote in message
    news:[email hidden]...

    Quoted message said:

    Wow - what a ridiculous experiment. Why not just take the serum
    cholesterol levels of men with prostate cancer, then see if progression
    is related to the cholesterol level? Even then, what should be
    measured is the oxysterol content of the serum, meaning oxidized
    cholesterol. The only thing I'd like to know is if the "researchers"
    bothered to determine whether the cholesterol they fed the tumors had
    high oxysterol contents. This seems to be the case, because the statin
    drug lowers inflammation, and cholesterol does too, if it's not
    oxidized. If it's oxidized it will create inflammation. It's amazing
    how so many "scientists" are ignorant of recent research.

  4. "montygram" <[email hidden]> wrote in message
    news:[email hidden]...

    Quoted message said:

    Wow - what a ridiculous experiment. Why not just take the serum
    cholesterol levels of men with prostate cancer, then see if progression
    is related to the cholesterol level? Even then, what should be
    measured is the oxysterol content of the serum, meaning oxidized
    cholesterol. The only thing I'd like to know is if the "researchers"
    bothered to determine whether the cholesterol they fed the tumors had
    high oxysterol contents. This seems to be the case, because the statin
    drug lowers inflammation, and cholesterol does too, if it's not
    oxidized. If it's oxidized it will create inflammation. It's amazing
    how so many "scientists" are ignorant of recent research.

    How ignorant you are!!!!!!

    Heart Vessels. 2005 Feb;20(1):8-12. Related Articles, Links

    Improvement of arterial stiffness by the antioxidant and anti-inflammatory
    effects of short-term statin therapy in patients with hypercholesterolemia.

    Matsuo T, Iwade K, Hirata N, Yamashita M, Ikegami H, Tanaka N, Aosaki M,
    Kasanuki H.

    National Hospital Organization, Yokohama Medical Center, Yokohama, Japan,
    [email hidden].

    The preventive effect of statins on coronary events is not only associated
    with the cholesterol-lowering effect of these drugs, but also various direct
    effects on the vascular wall, which include improvement of endothelial
    function, antioxidant activity, and anti-inflammatory activity. We
    investigated whether short-term statin therapy could improve arterial
    stiffness and assessed its mechanism of action in patients with
    hypercholesterolemia. We assessed arterial stiffness in 10 patients (mean
    age: 62.9 +/- 9.0 years) with hypercholesterolemia (total cholesterol >/=220
    mg/dl). The patients were treated with cerivastatin (0.15 mg/day) for 4
    weeks. Before and after 4 weeks of treatment, we determined arterial
    stiffness from brachial-ankle pulse wave velocity and the ankle-brachial
    blood pressure index (ABI) using a FORM apparatus (Colin, Komaki, Japan). We
    also measured the blood levels of high-sensitivity C-reactive protein
    (hsCRP) and malondialdehyde low-density lipoprotein (MDA-LDL) as markers of
    inflammation and oxidation, respectively. After statin therapy, both the
    right and left abPWV were significantly decreased from 1544.6 +/- 157.1 to
    1349.0 +/- 223.9 cm/s and from 1592.1 +/- 164.8 to 1424.8 +/- 245.2 cm/s,
    respectively (P < 0.05). However, the ABI was unchanged after 4 weeks of
    cerivastatin therapy. MDA-LDL decreased significantly (from 161.2 +/- 42.4
    to 119.4 +/- 33.5 U/l, P < 0.05) and hsCRP also decreased. Total cholesterol
    and LDL-cholesterol decreased, while triglycerides and high-density
    lipoprotein-cholesterol were unchanged. Blood pressure was not significantly
    altered from the baseline value by statin therapy. These results suggest
    that the preventive effect of statins on coronary events is partly
    associated with the various actions of these drugs on the vascular wall, and
    that statins are not only cholesterol-lowering agents but also
    antiatherosclerotic agents.

    PMID: 15700196 [PubMed - in process]

    Drugs Today (Barc). 2004 Dec;40(12):975-90. Related Articles, Links

    Antioxidant effects of statins.

    Stoll LL, McCormick ML, Denning GM, Weintraub NL.

    Department of Internal Medicine, Division of Cardiovascular Diseases, The
    University of Iowa, Iowa City, IA 52242, USA. [email hidden]

    Statins, a group of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA)
    reductase inhibitors, are widely used in clinical practice for their
    efficacy in producing significant reductions in plasma cholesterol and LDL
    cholesterol and in reducing morbidity and mortality from cardiovascular
    disease. However, several large clinical trials have suggested that the
    cholesterol-lowering effects of statins may not completely account for the
    reduced incidence of cardiovascular disease seen in patients receiving
    statin therapy. A number of recent reports have shown that statins may also
    have important antiinflammatory effects, in addition to their effects on
    plasma lipids. Since inflammation is closely linked to the production of
    reactive oxygen species (ROS), the molecular basis of the observed
    antiinflammatory effects of statins may relate to their ability block the
    production and/or activity of ROS. In this review, we will discuss both the
    inhibition of ROS generation by statins, through interference with NAD(P)H
    oxidase expression and activity, and the actions of statins that serve to
    blunt the damaging effects of these radicals, including effects on
    antioxidant enzymes, lipid peroxidation, LDL cholesterol oxidation and
    nitric oxide synthase. These antioxidant effects of statins likely
    contribute to their clinical efficacy in treating cardiovascular disease as
    well as other chronic conditions associated with increased oxidative stress
    in humans. (c) 2004 Prous Science. All rights reserved

    PMID: 15645009 [PubMed - in process]

    Quoted message said:
  5. First off, the worst dietary sources are powdered dairy and foods
    cooked while exposed to air. A recent expiment showed that steaming
    salmon was the worst cooking method. Fatty acid researcher Mary Enig
    also has warned about homogenization. Then there's fat that's gone
    rancid, which should be avoided entirely (I skim the yellowed sides off
    sticks of butter for this reason). Remember that cholesterol is a
    protein carrier of fat.

    Also, if you eat cholesterol and also polyunsaturated fatty acids (and
    some forms of monounsaturated fatty acids, like canola, which really
    depletes antioxidant resources), the cholesterol can become oxidized
    inside your body. Eating berries, dark chocolate, etc. help to some
    degree. I boil eggs, which is okay because the cholesterol can't
    become oxidized unless oxygen is present. The presence of iron can
    speed up the process too (and copper, in particular ways). Even though
    the evidence is overwhelming, and even a spokesman for the AHA has
    recently pointed out that only oxidized cholesterol is a problem in any
    physiologically normal state, the word has not reached most of the
    "talking heads" in the mainstream media.

  6. -but isn't "hypercholesterolemia" levels like 800?

    "Robert" <[email hidden]> wrote in message
    news:[email hidden]...

    Quoted message said:


    "montygram" <[email hidden]> wrote in message
    news:[email hidden]...

    Quoted message said:

    Wow - what a ridiculous experiment. Why not just take the serum
    cholesterol levels of men with prostate cancer, then see if progression
    is related to the cholesterol level? Even then, what should be
    measured is the oxysterol content of the serum, meaning oxidized
    cholesterol. The only thing I'd like to know is if the "researchers"
    bothered to determine whether the cholesterol they fed the tumors had
    high oxysterol contents. This seems to be the case, because the statin
    drug lowers inflammation, and cholesterol does too, if it's not
    oxidized. If it's oxidized it will create inflammation. It's amazing
    how so many "scientists" are ignorant of recent research.

    How ignorant you are!!!!!!

    Heart Vessels. 2005 Feb;20(1):8-12. Related Articles, Links

    Improvement of arterial stiffness by the antioxidant and anti-inflammatory
    effects of short-term statin therapy in patients with


    hypercholesterolemia.

    Quoted message said:


    Matsuo T, Iwade K, Hirata N, Yamashita M, Ikegami H, Tanaka N, Aosaki M,
    Kasanuki H.

    National Hospital Organization, Yokohama Medical Center, Yokohama, Japan,
    [email hidden].

    The preventive effect of statins on coronary events is not only associated
    with the cholesterol-lowering effect of these drugs, but also various


    direct

    Quoted message said:

    effects on the vascular wall, which include improvement of endothelial
    function, antioxidant activity, and anti-inflammatory activity. We
    investigated whether short-term statin therapy could improve arterial
    stiffness and assessed its mechanism of action in patients with
    hypercholesterolemia. We assessed arterial stiffness in 10 patients (mean
    age: 62.9 +/- 9.0 years) with hypercholesterolemia (total cholesterol
    /=220
    mg/dl). The patients were treated with cerivastatin (0.15 mg/day) for 4
    weeks. Before and after 4 weeks of treatment, we determined arterial
    stiffness from brachial-ankle pulse wave velocity and the ankle-brachial
    blood pressure index (ABI) using a FORM apparatus (Colin, Komaki, Japan).


    We

    Quoted message said:

    also measured the blood levels of high-sensitivity C-reactive protein
    (hsCRP) and malondialdehyde low-density lipoprotein (MDA-LDL) as markers


    of

    Quoted message said:

    inflammation and oxidation, respectively. After statin therapy, both the
    right and left abPWV were significantly decreased from 1544.6 +/- 157.1 to
    1349.0 +/- 223.9 cm/s and from 1592.1 +/- 164.8 to 1424.8 +/- 245.2 cm/s,
    respectively (P < 0.05). However, the ABI was unchanged after 4 weeks of
    cerivastatin therapy. MDA-LDL decreased significantly (from 161.2 +/- 42.4
    to 119.4 +/- 33.5 U/l, P < 0.05) and hsCRP also decreased. Total


    cholesterol

    Quoted message said:

    and LDL-cholesterol decreased, while triglycerides and high-density
    lipoprotein-cholesterol were unchanged. Blood pressure was not


    significantly

    Quoted message said:

    altered from the baseline value by statin therapy. These results suggest
    that the preventive effect of statins on coronary events is partly
    associated with the various actions of these drugs on the vascular wall,


    and

    Quoted message said:

    that statins are not only cholesterol-lowering agents but also
    antiatherosclerotic agents.

    PMID: 15700196 [PubMed - in process]

    Drugs Today (Barc). 2004 Dec;40(12):975-90. Related Articles, Links

    Antioxidant effects of statins.

    Stoll LL, McCormick ML, Denning GM, Weintraub NL.

    Department of Internal Medicine, Division of Cardiovascular Diseases, The
    University of Iowa, Iowa City, IA 52242, USA.


    [email hidden]

    Quoted message said:


    Statins, a group of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA)
    reductase inhibitors, are widely used in clinical practice for their
    efficacy in producing significant reductions in plasma cholesterol and LDL
    cholesterol and in reducing morbidity and mortality from cardiovascular
    disease. However, several large clinical trials have suggested that the
    cholesterol-lowering effects of statins may not completely account for the
    reduced incidence of cardiovascular disease seen in patients receiving
    statin therapy. A number of recent reports have shown that statins may


    also

    Quoted message said:

    have important antiinflammatory effects, in addition to their effects on
    plasma lipids. Since inflammation is closely linked to the production of
    reactive oxygen species (ROS), the molecular basis of the observed
    antiinflammatory effects of statins may relate to their ability block the
    production and/or activity of ROS. In this review, we will discuss both


    the

    Quoted message said:

    inhibition of ROS generation by statins, through interference with NAD(P)H
    oxidase expression and activity, and the actions of statins that serve to
    blunt the damaging effects of these radicals, including effects on
    antioxidant enzymes, lipid peroxidation, LDL cholesterol oxidation and
    nitric oxide synthase. These antioxidant effects of statins likely
    contribute to their clinical efficacy in treating cardiovascular disease


    as

    Quoted message said:

    well as other chronic conditions associated with increased oxidative


    stress

    Quoted message said:

    in humans. (c) 2004 Prous Science. All rights reserved

    PMID: 15645009 [PubMed - in process]

    Quoted message said:
  7. "Roman Bystrianyk" <[email hidden]> wrote in message
    news:[email hidden].

    This study supports the contention that if you watch your diet, you will be
    healthier.

    I think the conclusion that cholesterol lowering drugs will help prevent
    prostate cancer or decrease its spread is premature.

    Cholesterol is used in the synthesis of testoerone and sex hormones (both
    male and female). This may also be related to the results.

    Jeff

  8. Yes, watch the food instead of eat it - that is supported by the
    studies on calorie restriction.

  9. On 18 Mar 2005 12:17:15 -0800, "montygram" <[email hidden]>

    Quoted message said:

    some forms of monounsaturated fatty acids, like canola, which really
    depletes antioxidant resources), the cholesterol can become oxidized

    Interesting, so the label Canola oil is a switch that turn on C18:1
    omega-9 toxic while label olive oil turn this effect off. Very
    interesting.

    Canola oil do not contain C20:1 omega-9
    Could you repeat that??

  10. montygram said:


    First off, the worst dietary sources are powdered dairy and foods
    cooked while exposed to air. A recent expiment showed that steaming
    salmon was the worst cooking method.

    Yet steaming exposes it to the air less than other methods.

    I don't know whether you read the actual paper, but the lipid oxidation
    was unchanged and only cholesterol oxidation increased. Since the
    steaming was carried on for far longer than the other cooking methods it
    was probably due to duration.

    Quoted message said:

    Fatty acid researcher Mary Enig
    also has warned about homogenization. Then there's fat that's gone
    rancid, which should be avoided entirely (I skim the yellowed sides off
    sticks of butter for this reason). Remember that cholesterol is a
    protein carrier of fat.

    What's that supposed to mean? Cholesterol isn't protein and it isn't a
    carrier of fat.

    Quoted message said:

    Also, if you eat cholesterol and also polyunsaturated fatty acids (and
    some forms of monounsaturated fatty acids, like canola, which really
    depletes antioxidant resources), the cholesterol can become oxidized
    inside your body. Eating berries, dark chocolate, etc. help to some
    degree. I boil eggs, which is okay because the cholesterol can't
    become oxidized unless oxygen is present.

    Oxygen isn't a requirement for oxidation. Boiling is better mostly
    because the temperature is limited, athough the fact that hot oil and
    high surface area aren't involved makes a big difference.

    Quoted message said:

    The presence of iron can
    speed up the process too (and copper, in particular ways).

    Iron and copper can oxidise biomolecules directly with the presence of
    oxygen, although they will also generate oxygen radicals and thence
    hydroxyl radicals.

    MattLB

  11. On Mon, 21 Mar 2005 18:26:46 +0000, MattLB <[email hidden]>

    Quoted message said:
    Quoted message said:

    sticks of butter for this reason). Remember that cholesterol is a
    protein carrier of fat.

    What's that supposed to mean? Cholesterol isn't protein and it isn't a
    carrier of fat.

    right. Cholesterol is a fat. By being a carrier of fatty acids.
    But in HDL and LDL it is helped by lipid binding proteins, that is,
    proteins binding also cholesterol esters.

    But unesterified cholesterol could be questioned whether being fat or
    not.

  12. re: SKEPTICAL ENQUIRER article about cholesterol

    I went to website, but couldn't find the cholesterol article that's
    referred.

    B-T-W: Years ago I subscribed (by snail mail) to the magazine for about
    $16 a year

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